PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2938256-3	1986	These cells, when mixed with lymphocytes from rats with EAMG in vitro, strongly suppressed the antibody response to AChR.	eamg	56-60	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	116-120
35154091-5	2022	In both models, administration of CRIg/FH could significantly reduce the complement-mediated end-plate damage and suppress the development of EAMG.	eamg	142-146	V-set and immunoglobulin domain containing 4	Homo sapiens	34-38
3264006-2	1988	Unilateral limb denervation, a procedure known to increase the AChR content of muscle, "protected" the denervated leg against antibody-mediated AChr loss in acute EAMG induced by passive transfer of mAb 35 directed against the main immunogenic region.	eamg	163-167	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	144-148
3264006-3	1988	Also in chronic EAMG, brought about by immunizing rats with AChR in complete Freund"s adjuvant, the AChR loss of the denervated leg was about one fourth (13.5 vs. 53%) of the control leg.	eamg	16-20	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	60-64
3264006-3	1988	Also in chronic EAMG, brought about by immunizing rats with AChR in complete Freund"s adjuvant, the AChR loss of the denervated leg was about one fourth (13.5 vs. 53%) of the control leg.	eamg	16-20	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	100-104
3264006-4	1988	In both acute and chronic EAMG the amount of AChR complexed with antibody was lower in the denervated leg.	eamg	26-30	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	45-49
3264006-11	1988	Results show increased AChR synthesis to protect against chronic EAMG both in terms of clinical disease (nandrolone) as well as AChR loss (nandrolone, denervation).	eamg	65-69	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	23-27
3264006-12	1988	In addition it was shown that nandrolone increases serum C4 consumption which in the complement-dependent acute EAMG model causes enhancement of the severity of clinical disease and increased AChR loss.	eamg	112-116	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	192-196
3495549-3	1987	All four mAbs directed at the MIR which were tested were very efficient in inducing EAMG: within 2 days the rats became moribund or very weak and their muscle AChR content decreased to about 50% of normal.	eamg	84-88	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	159-163
6332854-3	1984	Lymph node cell cultures from rats with EAMG pretreated with ricin toxin-AChR conjugates exhibited suppressed T helper cell proliferation and B cell antibody synthesis in response to the subsequent addition of AChR.	eamg	40-44	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	73-77
3871377-5	1985	Treatment of ongoing EAMG resulted in a reduction of AChR antibody by more than 50%.	eamg	21-25	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	53-57
2578165-5	1985	Conventionally immunized animals showed the classical signs of EAMG: elevated antibody titers against nicotinic acetylcholine receptor and a reduction of the number of alpha-bungarotoxin-binding sites, as well as reduction of the number of acetylcholine-operated ionic channels.	eamg	63-67	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	102-134
6332854-3	1984	Lymph node cell cultures from rats with EAMG pretreated with ricin toxin-AChR conjugates exhibited suppressed T helper cell proliferation and B cell antibody synthesis in response to the subsequent addition of AChR.	eamg	40-44	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	210-214
6354071-2	1983	Rats with EAMG were treated with a protocol consisting of three components: (1) A single high dose of cyclophosphamide (200 mg/kg) was used to produce a rapid and sustained fall in the anti-AChR antibody levels by preferential destruction of antibody-producing B-lymphocytes.	eamg	10-14	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	190-194
6611231-11	1984	The anti-AChR antibodies eluted from muscles of rats with EAMG showed similar binding patterns to anti-receptor antibodies in rats" sera.	eamg	58-62	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	9-13
6085187-3	1984	Both the clinical and the electromyographic manifestations of EAMG was affected by AFP treatment.	eamg	62-66	alpha fetoprotein	Homo sapiens	83-86
6354071-8	1983	Rats with EAMG treated with this combined protocol showed a prompt and sustained fall in the anti-AChR antibody levels and had no anamnestic response to a challenge with AChR.	eamg	10-14	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	98-102
7165999-7	1982	In rats with EAMG, AChR contents was reduced in both denervated (1.1 +/- 1.0) and innervated muscles (1.3 +/- 0.9).	eamg	13-17	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	19-23
73154-7	1977	We suggest that EAMG in rabbits induced by Torpedo AChR differs serologically from myasthenia gravis in patients, probably owing to antigenic differences between Torpedo and human AChR, and that antigenic differences also exist between junctional and extrajunctional receptors.	eamg	16-20	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	51-55
6982313-4	1982	At both control and EAMG end-plates, AChR is internalized by endocytosis.	eamg	20-24	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	37-41
6982313-7	1982	AChR disappeared more rapidly from the EAMG than from the control end-plates.	eamg	39-43	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	0-4
6982313-9	1982	These data suggest that end-plate AChR is at a steady state in chronic EAMG.	eamg	71-75	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	34-38
6243761-2	1980	Postsynaptic response to epinephrine was defective in chronic EAMG with high titers of antibody, suggesting that active Na-K transport system modulated by cyclic adenosine monophosphate (AMP) may be affected primarily by antibody.	eamg	62-66	TANK binding kinase 1	Homo sapiens	120-124
6243761-5	1980	Normal response to insulin occurred in all phases of EAMG.	eamg	53-57	insulin	Homo sapiens	19-26
6176166-2	1981	AFP also inhibits the AChR and mitogen induced in vitro proliferative response of lymphocytes obtained from animals with EAMG.	eamg	121-125	alpha fetoprotein	Homo sapiens	0-3
182896-8	1976	The amount of AChR extracted from muscle of rats with EAMG was diminished.	eamg	54-58	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	14-18
182896-12	1976	Thus, both a decrease in amount of AChR  and the formation of antibody-AChR complexes contribute to impairment of neuromuscular transmission in rats with EAMG.	eamg	154-158	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	35-39
182896-11	1976	At least half of the AChR remaining in animals with chronic EAMG was complexed with antibody.	eamg	60-64	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	21-25
182896-12	1976	Thus, both a decrease in amount of AChR  and the formation of antibody-AChR complexes contribute to impairment of neuromuscular transmission in rats with EAMG.	eamg	154-158	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	71-75
33556668-5	2021	During the development of EAMG, the increase of follicular helper T cells (Tfh) 1, Tfh 17 cells and decrease of follicular regulatory T cells (Tfr) were reversely altered after leflunomide administration.	eamg	26-30	transferrin receptor	Homo sapiens	143-146
182897-5	1976	Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells.	eamg	64-68	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	25-29
182897-5	1976	Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells.	eamg	105-109	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	25-29
182897-12	1976	Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased.	eamg	72-76	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	5-9
182897-12	1976	Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased.	eamg	72-76	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	141-145
1085587-6	1976	Lymph node cells from rats sensitized to AChR  were capable of transferring EAMG to normal recipients.	eamg	76-80	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	41-45
1127382-5	1975	The presence of antibodies to syngeneic rat muscle AChR in the serum of rats with EAMG documents the existence of autoimmunity in the experimental disease.	eamg	82-86	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	51-55
29944018-3	2018	The data from this study showed that exogenous recombinant rat IL-9 (rrIL-9) acted as an IL-9 receptor antagonist, reduced the incidence of EAMG in rats, alleviated the severity of the disease, and reduced the anti-acetylcholine receptor (AChR) IgG antibody levels by altering the Th-subset distribution.	eamg	140-144	interleukin 9	Rattus norvegicus	63-67
31884963-14	2019	It was CXCR5- NK cells but not CXCR5+ NK cells that suppressed Tfh cells and inhibited the autoimmune response in EAMG models.	eamg	114-118	C-X-C motif chemokine receptor 5	Rattus norvegicus	7-12
30796753-9	2019	Based on these results, we hypothesize that an AChR-specific Tfh cell-mediated humoral immune response contributes to the development of EAMG.	eamg	137-141	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	47-51
32109680-7	2020	Intraperitoneal injection of OPN revealed the early incidence of EAMG, and more serious disease.	eamg	65-69	secreted phosphoprotein 1	Rattus norvegicus	29-32
24589747-4	2014	C57BL/6 (B6) mice immunized with 30mug of recombinant human MuSK in incomplete or complete Freund"s adjuvant (CFA) showed significant EAMG susceptibility (>80% incidence).	eamg	134-138	muscle associated receptor tyrosine kinase	Homo sapiens	60-64
29205338-3	2018	Functional sphingosine-1-phosphate (S1P) antagonists like fingolimod and siponimod (BAF312) are successfully used for the treatment of multiple sclerosis, and fingolimod was shown to prevent the development of myasthenic symptoms in experimental autoimmune myasthenia gravis (EAMG), the standard model of MG.	eamg	276-280	sphingosine-1-phosphate receptor 1	Mus musculus	36-39
26071315-6	2015	RESULTS: We found that caspase-1 inhibitor improved EAMG clinical symptom, which was associated with decreased IL-17 production by CD4+ T cells and gammadelta T cells, lower affinity of anti-R97-116 peptide IgG.	eamg	52-56	interleukin 17A	Rattus norvegicus	111-116
23042232-3	2013	METHODS: EAMG was induced with monoclonal antibody to the acetylcholine receptor (AChR) in Daf1(-/-) , CD59ab(-/-) , Daf1(-/-) CD59ab(-/-) , and wild-type C57Bl/6 mice.	eamg	9-13	CD55 molecule, decay accelerating factor for complement	Mus musculus	91-95
24731953-3	2014	Studies corroborating the evidence show that the complement (C3-C6)-deficient or complement inhibitor (anti-C1q, soluble CR1, anti-C6, and C5 inhibiting peptide)-treated animals are highly resistant to EAMG induction, whereas the deficiency of the naturally occurring complement inhibitors, such as the decay-accelerating factor (DAF), increases EAMG susceptibility.	eamg	202-206	complement C1q A chain	Homo sapiens	108-111
24731953-3	2014	Studies corroborating the evidence show that the complement (C3-C6)-deficient or complement inhibitor (anti-C1q, soluble CR1, anti-C6, and C5 inhibiting peptide)-treated animals are highly resistant to EAMG induction, whereas the deficiency of the naturally occurring complement inhibitors, such as the decay-accelerating factor (DAF), increases EAMG susceptibility.	eamg	202-206	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	121-124
23042232-3	2013	METHODS: EAMG was induced with monoclonal antibody to the acetylcholine receptor (AChR) in Daf1(-/-) , CD59ab(-/-) , Daf1(-/-) CD59ab(-/-) , and wild-type C57Bl/6 mice.	eamg	9-13	CD55 molecule, decay accelerating factor for complement	Mus musculus	117-121
23042232-10	2013	The NMJ of EAMG-induced Daf1(-/-) and CD59ab(-/-) mice demonstrated similar AChR density.	eamg	11-15	CD55 molecule, decay accelerating factor for complement	Mus musculus	24-28
21035305-5	2011	Surprisingly, when EAMG was induced in young (2 month-old) mice, EAMG was milder in Aire KO than in WT mice for several weeks until the age of about 5 months.	eamg	19-23	autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)	Mus musculus	84-88
23278585-4	2012	However, when EAMG was induced in young mice, Aire(-/-) mice presented a milder disease that wild-type (WT) controls.	eamg	14-18	autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)	Mus musculus	46-50
23278585-5	2012	In contrast, when EAMG was induced in older mice, Aire(-/-) mice were more severely affected than WT mice.	eamg	18-22	autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)	Mus musculus	50-54
23278585-6	2012	The relative resistance to EAMG in young Aire(-/-) mice correlated with increased numbers of T(reg) cells in their spleens compared to young controls.	eamg	27-31	autoimmune regulator (autoimmune polyendocrinopathy candidiasis ectodermal dystrophy)	Mus musculus	41-45
21636248-6	2011	The inborn or acquired deficiencies of IL-6, TNF-alpha and TNF receptor functions are associated with the lowest EAMG incidences.	eamg	113-117	interleukin 6	Homo sapiens	39-43
21636248-6	2011	The inborn or acquired deficiencies of IL-6, TNF-alpha and TNF receptor functions are associated with the lowest EAMG incidences.	eamg	113-117	tumor necrosis factor	Homo sapiens	45-54
22626443-4	2012	LPS abrogated EAMG resistance in CD4-/- mice by increasing high-affinity anti-AChR IgG2b in sera and enhancing immune complex deposition in muscle.	eamg	14-18	CD4 antigen	Mus musculus	33-36
22539289-3	2012	This report demonstrates reduced A2AR expression by both T cells and B cells residing in spleen and lymph nodes following EAMG induction.	eamg	122-126	adenosine A2a receptor	Rattus norvegicus	33-37
22539289-7	2012	An EAMG-preventive treatment regimen was established that consisted of (2-(p-(2-carbonylethyl)phenylethylamino)-5-N-ethylcarboxamidoadenosine) (CGS21680; A2AR agonist) administration 1 day prior to EAMG induction.	eamg	3-7	adenosine A2a receptor	Rattus norvegicus	154-158
18567851-9	2008	EAMG can be suppressed by treatment with denatured, bacterially expressed mixtures of extracellular and cytoplasmic domains of human alpha1, beta1, gamma, delta, and epsilon subunits.	eamg	0-4	BCL2 related protein A1	Homo sapiens	133-173
18207575-4	2008	EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4(+)CD25(+) cell ratios in lymph nodes.	eamg	0-4	interleukin 6	Mus musculus	60-64
18207575-4	2008	EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4(+)CD25(+) cell ratios in lymph nodes.	eamg	0-4	interleukin 10	Mus musculus	69-74
19025128-2	2008	Anti-C1q antibody administration before or following acetylcholine receptor immunization suppresses EAMG development by reducing lymph node cell IL-6 production and neuromuscular junction IgG, C3 and C5b-C9 deposition.	eamg	100-104	complement component 1, q subcomponent, alpha polypeptide	Mus musculus	5-8
19768385-11	2010	(3) Treatment with RelB-silenced DCs effectively reduced myasthenic symptoms and levels of serum anti-acetylcholine receptor autoantibody in mice with ongoing EAMG.	eamg	159-163	avian reticuloendotheliosis viral (v-rel) oncogene related B	Mus musculus	19-23
18502693-2	2008	In this study, we show that EAMG induced by repeated immunizations with acetylcholine receptor (AChR) protein in C57BL6 mice is effectively suppressed by GM-CSF treatment administered at a stage of chronic, well-established disease.	eamg	28-32	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	154-160
18567870-5	2008	Therefore, EAMG/MG could be treated by blocking the activation of classical complement pathway (CCP) and/or IL-6.	eamg	11-15	interleukin 6	Mus musculus	108-112
16034147-3	2005	We tested the therapeutic effect of human recombinant IL-1 receptor antagonist (IL-1ra) in C57BL/6 mice with EAMG.	eamg	109-113	interleukin 1 receptor antagonist	Homo sapiens	54-78
17618568-13	2007	The development of EAMG and production of AChR specific Ab in NK1.1(+) cell-depleted mice were decreased obviously after treating with anti-IFN-gamma antibody.	eamg	19-23	interferon gamma	Mus musculus	140-149
16725279-8	2006	Also, alpha9 was present in the CNS in widespread locations and the binding pattern of anti-alpha9 antibody was reminiscent of that of serum samples of some of the mice with EAMG.	eamg	174-178	UDP glucuronosyltransferase 1 family, polypeptide A6B	Mus musculus	6-12
16034147-3	2005	We tested the therapeutic effect of human recombinant IL-1 receptor antagonist (IL-1ra) in C57BL/6 mice with EAMG.	eamg	109-113	interleukin 1 receptor antagonist	Homo sapiens	80-86
15380483-10	2004	With EAMG, immunoreactivity for Crry and DAF increased at diaphragm junctions and for DAF at EOM junctions.	eamg	5-9	complement component (3b/4b) receptor 1-like	Mus musculus	32-36
15843529-6	2005	These up-regulations were observed in immune response effector cells, namely, lymph node cells, and in the target organ of the autoimmune attack, the muscle of myasthenic rats, and were significantly reduced after suppression of EAMG by mucosal tolerance induction with an AChR fragment.	eamg	229-233	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	273-277
15843529-10	2005	Our results demonstrate a positive association of IP-10/CXCR3 signaling with the pathogenesis of EAMG in rats as well as in human MG patients.	eamg	97-101	C-X-C motif chemokine ligand 10	Rattus norvegicus	50-55
15843529-10	2005	Our results demonstrate a positive association of IP-10/CXCR3 signaling with the pathogenesis of EAMG in rats as well as in human MG patients.	eamg	97-101	C-X-C motif chemokine receptor 3	Rattus norvegicus	56-61
16116977-7	2005	The results suggest that iDCs could be generated by inducing bone marrow precursors in low dose of GM-CSF, AchR-pulsed iDCs could induce tolerance of EAMG.	eamg	150-154	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	107-111
15380483-10	2004	With EAMG, immunoreactivity for Crry and DAF increased at diaphragm junctions and for DAF at EOM junctions.	eamg	5-9	CD55 molecule, decay accelerating factor for complement	Mus musculus	41-44
15380483-10	2004	With EAMG, immunoreactivity for Crry and DAF increased at diaphragm junctions and for DAF at EOM junctions.	eamg	5-9	CD55 molecule, decay accelerating factor for complement	Mus musculus	86-89
12097416-5	2002	EAMG resistance in IL-6(-/-) mice was associated with a significant reduction in germinal center formation and decreased serum complement C3 levels.	eamg	0-4	interleukin 6	Mus musculus	19-23
12554700-2	2003	In MG and EAMG, we detected serum AChE-R accumulation.	eamg	10-14	acetylcholinesterase	Rattus norvegicus	34-38
12682276-3	2003	Compared with wild-type C57BL6 mice, B7-1 and B7-1/2 KO mice were resistant to EAMG development.	eamg	79-83	CD80 antigen	Mus musculus	24-50
12097416-5	2002	EAMG resistance in IL-6(-/-) mice was associated with a significant reduction in germinal center formation and decreased serum complement C3 levels.	eamg	0-4	complement component 3	Mus musculus	127-140
11034361-1	2000	We recently demonstrated that oral or nasal administration of recombinant fragments of the acetylcholine receptor (AChR) prevents the induction of experimental autoimmune myasthenia gravis (EAMG) and suppresses ongoing EAMG in rats.	eamg	190-194	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	91-113
11960640-2	2002	IL-5 KO mice had a significantly reduced incidence and severity of EAMG.	eamg	67-71	interleukin 5	Mus musculus	0-4
11918681-7	2001	DC from healthy rats, modified in vitro by exposure to IFN-gamma or TGF-beta1, effectively suppress ongoing EAE and EAMG when given by the subcutaneous route.	eamg	116-120	interleukin 18	Rattus norvegicus	55-64
11918681-7	2001	DC from healthy rats, modified in vitro by exposure to IFN-gamma or TGF-beta1, effectively suppress ongoing EAE and EAMG when given by the subcutaneous route.	eamg	116-120	transforming growth factor, beta 1	Rattus norvegicus	68-77
11034361-1	2000	We recently demonstrated that oral or nasal administration of recombinant fragments of the acetylcholine receptor (AChR) prevents the induction of experimental autoimmune myasthenia gravis (EAMG) and suppresses ongoing EAMG in rats.	eamg	190-194	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	115-119
11034361-1	2000	We recently demonstrated that oral or nasal administration of recombinant fragments of the acetylcholine receptor (AChR) prevents the induction of experimental autoimmune myasthenia gravis (EAMG) and suppresses ongoing EAMG in rats.	eamg	219-223	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	91-113
11034361-1	2000	We recently demonstrated that oral or nasal administration of recombinant fragments of the acetylcholine receptor (AChR) prevents the induction of experimental autoimmune myasthenia gravis (EAMG) and suppresses ongoing EAMG in rats.	eamg	219-223	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	115-119
11034361-6	2000	On the other hand, oral administration of the less native fragments Halpha1-205 or denatured Trx-Halpha1-210 suppressed ongoing EAMG and led to opposite changes in the immunological parameters.	eamg	128-132	thioredoxin	Homo sapiens	93-96
10201893-8	1999	These results indicate that IFN-gamma promotes systemic humoral responses in EAMG by up-regulating the production and the affinity of anti-AChR autoantibodies, thereby contributing to susceptibility to EAMG in C57BL/6-type mice.	eamg	77-81	interferon gamma	Mus musculus	28-37
10606626-3	1999	This fragment, corresponding to the extracellular domain of the human AChR alpha-subunit (Halpha1-205), protected rats from subsequently induced experimental autoimmune myasthenia gravis (EAMG) and suppressed ongoing EAMG when treatment was initiated during either the acute or chronic phases of disease.	eamg	188-192	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	70-74
10606626-4	1999	Prevention and suppression of EAMG were accompanied by a significant decrease in AChR-specific humoral and cellular responses.	eamg	30-34	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	81-85
10393952-6	1999	These effects on EAMG were accompanied by a marked reduction in the proliferative T-cell response and IL-2 production in response to AcChoR, in reduced anti-self AcChoR antibody titers and in an isotype switch of AcChoR-specific antibodies, from IgG2 to IgG1.	eamg	17-21	interleukin 2	Homo sapiens	102-106
10201893-8	1999	These results indicate that IFN-gamma promotes systemic humoral responses in EAMG by up-regulating the production and the affinity of anti-AChR autoantibodies, thereby contributing to susceptibility to EAMG in C57BL/6-type mice.	eamg	202-206	interferon gamma	Mus musculus	28-37
9182902-6	1997	Since IFN-gamma, IL-4 and IL-10 promote the development of EAMG, the low expression of these cytokines might contribute to EAMG resistance in young Lewis rats.	eamg	59-63	interferon gamma	Rattus norvegicus	6-15
9743346-3	1998	Recently, we have demonstrated that IFN-gamma is necessary for the initiation of tAChR-induced EAMG in mice.	eamg	95-99	interferon gamma	Mus musculus	36-45
9743346-6	1998	Following immunization with Torpedo (t) AChR, the IL-4(-/-) mice readily developed signs of muscle weakness and succumbed to clinical EAMG with kinetics similar to the susceptibility of IL-4(+/+) mice.	eamg	134-138	interleukin 4	Mus musculus	50-54
9270663-9	1997	The results of this study indicate that the age-related susceptibility to EAMG is influenced by factors determined by the immune attack as well as mechanisms at the level of the neuromuscular junction.	eamg	74-78	renin binding protein	Rattus norvegicus	44-47
9190955-7	1997	Furthermore, EAMG in TCR transgenic mice was prevented by treatment with mAb to TCRBV8, which depleted BV8-expressing T cells.	eamg	13-17	T cell receptor alpha variable 6-3	Mus musculus	21-24
9190955-7	1997	Furthermore, EAMG in TCR transgenic mice was prevented by treatment with mAb to TCRBV8, which depleted BV8-expressing T cells.	eamg	13-17	T cell receptor beta, variable 8	Mus musculus	80-86
9190955-7	1997	Furthermore, EAMG in TCR transgenic mice was prevented by treatment with mAb to TCRBV8, which depleted BV8-expressing T cells.	eamg	13-17	prokineticin 2	Mus musculus	83-86
10102528-6	1999	In three out of ten Lewis rats injected with purified AChR, the EAMG models were established.	eamg	64-68	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	54-58
10102528-9	1999	In conclusion, the EAMG models were successfully established and the CD5+ B-lymphocyte expression in peripheral blood increased in EAMGs.	eamg	19-23	Cd5 molecule	Rattus norvegicus	69-72
9879680-2	1998	A transient burst of TNF-alpha, IL-1beta and IL-6 mRNA expressing cells was detected during the early phase of EAMG.	eamg	111-115	tumor necrosis factor	Rattus norvegicus	21-30
9879680-2	1998	A transient burst of TNF-alpha, IL-1beta and IL-6 mRNA expressing cells was detected during the early phase of EAMG.	eamg	111-115	interleukin 1 alpha	Rattus norvegicus	32-40
9879680-2	1998	A transient burst of TNF-alpha, IL-1beta and IL-6 mRNA expressing cells was detected during the early phase of EAMG.	eamg	111-115	interleukin 6	Rattus norvegicus	45-49
9842901-3	1998	Compared to wild-type mice, the CD28-/- mice became less susceptible, and CD40L-/- mice were completely resistant to EAMG induction.	eamg	117-121	CD40 ligand	Mus musculus	74-79
9842901-7	1998	Thus, CD28 and CD40L are differentially required for induction of EAMG.	eamg	66-70	CD28 antigen	Mus musculus	6-10
9842901-7	1998	Thus, CD28 and CD40L are differentially required for induction of EAMG.	eamg	66-70	CD40 ligand	Mus musculus	15-20
9726835-6	1998	Taken together, these data demonstrate that resistance of the AChR protein to antibody-mediated degradation is the primary mechanism that accounts for the resistance to passive transfer EAMG in aged rats.	eamg	186-190	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	62-66
9670855-5	1998	In contrast, combined treatment with CTLA4Ig plus DAB389IL2 strikingly inhibited AChR antibody levels, and completely prevented EAMG.	eamg	128-132	cytotoxic T-lymphocyte-associated protein 4	Rattus norvegicus	37-42
9528890-1	1998	Nasal administration of microg doses of acetylcholine receptor (AChR) is effective in preventing the development of B cell-mediated EAMG in the Lewis rat, a model for human MG.	eamg	132-136	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	40-62
9528890-1	1998	Nasal administration of microg doses of acetylcholine receptor (AChR) is effective in preventing the development of B cell-mediated EAMG in the Lewis rat, a model for human MG.	eamg	132-136	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	64-68
9528890-3	1998	Ten-fold higher amounts of AChR given nasally (600 microg/rat) were required to ameliorate the manifestations of EAMG compared with the amounts necessary for prevention of EAMG.	eamg	113-117	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	27-31
9528890-7	1998	Collectively, these data indicate that nasal administration of AChR in ongoing EAMG induced selective suppression of Th1 functions, i.e. IFN-gamma and IgG2b production, but no influence on Th2 cell functions.	eamg	79-83	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	63-67
9528890-8	1998	The impaired Th1 functions may result in the production of less myasthenic anti-AChR antibodies and contribute to the amelioration of EAMG severity in rats treated with AChR 600 microg/rat by the nasal route.	eamg	134-138	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	169-173
9182902-6	1997	Since IFN-gamma, IL-4 and IL-10 promote the development of EAMG, the low expression of these cytokines might contribute to EAMG resistance in young Lewis rats.	eamg	59-63	interleukin 4	Rattus norvegicus	17-21
9182902-6	1997	Since IFN-gamma, IL-4 and IL-10 promote the development of EAMG, the low expression of these cytokines might contribute to EAMG resistance in young Lewis rats.	eamg	59-63	interleukin 10	Rattus norvegicus	26-31
9010275-6	1997	These results suggest that resistance against EAMG in aged rats is due to resistance of the AChR against antibody-mediated degradation, or to mechanisms able to compensate for AChR loss.	eamg	46-50	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	92-96
9140360-6	1997	Results from studies of time kinetics of cytokines imply that IFN-gamma is more agile at the onset of EAMG, probably being one of the initiating factors in the induction of the disease, and IL-4 may be mainly responsible for disease progression and persistance.	eamg	102-106	interferon gamma	Homo sapiens	62-71
9010275-6	1997	These results suggest that resistance against EAMG in aged rats is due to resistance of the AChR against antibody-mediated degradation, or to mechanisms able to compensate for AChR loss.	eamg	46-50	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	176-180
8610979-8	1996	Oral administration of AChR after immunization resulted in inhibition of the clinical manifestation of EAMG, concomitant with a paradoxical enhancement of the AChR-antibody responses.	eamg	103-107	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	23-27
8683141-7	1996	EAMG induced by immunization with purified native Torpedo AChR was also inhibited by TCM 240, but not a control mAb.	eamg	0-4	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	58-62
8760788-5	1996	Clinical EAMG was nearly completely prevented in CD4-8-, CD4-/-, and CD8-/- mice.	eamg	9-13	CD4 antigen	Mus musculus	49-52
8760788-5	1996	Clinical EAMG was nearly completely prevented in CD4-8-, CD4-/-, and CD8-/- mice.	eamg	9-13	CD4 antigen	Mus musculus	57-60
9099937-4	1996	Nasal tolerance to EAMG was accompanied by decreased numbers of AChR-reactive IFN-gamma and IL-4 mRNA-expressing cells, and strong up-regulation of TGF-beta mRNA-positive cells in lymphoid organs compared with non-tolerized EAMG control rats.	eamg	19-23	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	64-68
9099937-4	1996	Nasal tolerance to EAMG was accompanied by decreased numbers of AChR-reactive IFN-gamma and IL-4 mRNA-expressing cells, and strong up-regulation of TGF-beta mRNA-positive cells in lymphoid organs compared with non-tolerized EAMG control rats.	eamg	19-23	interferon gamma	Rattus norvegicus	78-87
9099937-4	1996	Nasal tolerance to EAMG was accompanied by decreased numbers of AChR-reactive IFN-gamma and IL-4 mRNA-expressing cells, and strong up-regulation of TGF-beta mRNA-positive cells in lymphoid organs compared with non-tolerized EAMG control rats.	eamg	19-23	interleukin 4	Rattus norvegicus	92-96
9099937-4	1996	Nasal tolerance to EAMG was accompanied by decreased numbers of AChR-reactive IFN-gamma and IL-4 mRNA-expressing cells, and strong up-regulation of TGF-beta mRNA-positive cells in lymphoid organs compared with non-tolerized EAMG control rats.	eamg	19-23	transforming growth factor alpha	Rattus norvegicus	148-156
9099937-6	1996	The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG, and that TGF-beta plays an important role in tolerance induction to EAMG.	eamg	97-101	interferon gamma	Rattus norvegicus	25-34
9099937-6	1996	The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG, and that TGF-beta plays an important role in tolerance induction to EAMG.	eamg	97-101	interleukin 4	Rattus norvegicus	39-43
9099937-6	1996	The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG, and that TGF-beta plays an important role in tolerance induction to EAMG.	eamg	171-175	transforming growth factor alpha	Rattus norvegicus	112-120
8610980-5	1996	The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG and that TGF-beta plays an important role in tolerance induction to EAMG.	eamg	97-101	interferon gamma	Rattus norvegicus	25-34
8610980-5	1996	The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG and that TGF-beta plays an important role in tolerance induction to EAMG.	eamg	97-101	interleukin 4	Rattus norvegicus	39-43
8610980-5	1996	The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG and that TGF-beta plays an important role in tolerance induction to EAMG.	eamg	170-174	transforming growth factor alpha	Rattus norvegicus	111-119
7829669-9	1994	Furthermore, the in vitro proliferative response of lymph node cells to Torpedo AChR and the purified protein derivative of Mycobacterium tuberculosis was significantly lower in the linomide-treated EAMG rats than in the controls.	eamg	199-203	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	80-84
7774622-5	1995	We suggest that CD8+ T cells are involved in the induction and persistance of EAMG by directly or indirectly affecting AChR-reactive T cells and anti-AChR IgG antibody-secreting cells.	eamg	78-82	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	119-123
7774622-5	1995	We suggest that CD8+ T cells are involved in the induction and persistance of EAMG by directly or indirectly affecting AChR-reactive T cells and anti-AChR IgG antibody-secreting cells.	eamg	78-82	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	150-154
7963585-3	1994	Despite MHC class I and CD8+ cell deficiency, beta 2-m-/- mice developed EAMG.	eamg	73-77	alpha-2-macroglobulin	Mus musculus	46-54
7963585-4	1994	Moreover, the incidence of EAMG in the beta 2-m-/- mice was higher than that of beta 2-m+/- heterozygous mice with normal class I expression and frequency of CD8+ cells.	eamg	27-31	alpha-2-macroglobulin	Mus musculus	39-47
7585970-2	1995	Therefore, it should be possible to design specific immunotherapeutic approaches to treat EAMG (and human MG) by interfering with AChR-specific helper T cells.	eamg	90-94	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	130-134
7751658-7	1995	Because of the immunomodulating effects of IFN-alpha and its effect on the MHC class II expression, we tested the therapeutic efficacy of IFN-alpha on EAMG induced by immunization with acetylcholine receptor (AChR) in CFA.	eamg	151-155	interferon alpha 1	Homo sapiens	138-147
7520837-5	1994	Oral tolerance to EAMG was characterized by suppression of the levels of MNC expressing IFN-gamma and IL-4, but augmentation of cells expressing TGF-beta.	eamg	18-22	transforming growth factor alpha	Rattus norvegicus	145-153
7520837-6	1994	The results suggest that IFN-gamma, IL-4, and TGF-beta are involved in the development of EAMG, and that TGF-beta is important in the induction of oral tolerance to EAMG.	eamg	90-94	interferon gamma	Rattus norvegicus	25-34
7520837-3	1994	Upon in vivo recognition of AChR, popliteal, inguinal, and mesenteric lymph nodes, spleen and thymus of rats with EAMG contained higher levels of IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells compared to CFA-injected control rats, implicating the involvement in EAMG of AChR-reactive Th1 and Th2 cells in parallel.	eamg	114-118	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	28-32
7520837-6	1994	The results suggest that IFN-gamma, IL-4, and TGF-beta are involved in the development of EAMG, and that TGF-beta is important in the induction of oral tolerance to EAMG.	eamg	90-94	interleukin 4	Rattus norvegicus	36-40
7520837-3	1994	Upon in vivo recognition of AChR, popliteal, inguinal, and mesenteric lymph nodes, spleen and thymus of rats with EAMG contained higher levels of IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells compared to CFA-injected control rats, implicating the involvement in EAMG of AChR-reactive Th1 and Th2 cells in parallel.	eamg	114-118	interferon gamma	Rattus norvegicus	146-155
7520837-6	1994	The results suggest that IFN-gamma, IL-4, and TGF-beta are involved in the development of EAMG, and that TGF-beta is important in the induction of oral tolerance to EAMG.	eamg	90-94	transforming growth factor alpha	Rattus norvegicus	46-54
7520837-3	1994	Upon in vivo recognition of AChR, popliteal, inguinal, and mesenteric lymph nodes, spleen and thymus of rats with EAMG contained higher levels of IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells compared to CFA-injected control rats, implicating the involvement in EAMG of AChR-reactive Th1 and Th2 cells in parallel.	eamg	114-118	interleukin 4	Rattus norvegicus	157-161
7520837-6	1994	The results suggest that IFN-gamma, IL-4, and TGF-beta are involved in the development of EAMG, and that TGF-beta is important in the induction of oral tolerance to EAMG.	eamg	165-169	transforming growth factor alpha	Rattus norvegicus	105-113
8258147-5	1993	We conclude that oral administration of AChR, in addition to preventing clinical signs of EAMG and suppressing AChR-specific B cell responses, also counteracts the development of AChR-reactive IFN-gamma-secreting cells in certain lymphoid organs.	eamg	90-94	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	40-44
7520837-3	1994	Upon in vivo recognition of AChR, popliteal, inguinal, and mesenteric lymph nodes, spleen and thymus of rats with EAMG contained higher levels of IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells compared to CFA-injected control rats, implicating the involvement in EAMG of AChR-reactive Th1 and Th2 cells in parallel.	eamg	114-118	transforming growth factor alpha	Rattus norvegicus	167-175
7520837-3	1994	Upon in vivo recognition of AChR, popliteal, inguinal, and mesenteric lymph nodes, spleen and thymus of rats with EAMG contained higher levels of IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells compared to CFA-injected control rats, implicating the involvement in EAMG of AChR-reactive Th1 and Th2 cells in parallel.	eamg	114-118	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	276-280
7520837-5	1994	Oral tolerance to EAMG was characterized by suppression of the levels of MNC expressing IFN-gamma and IL-4, but augmentation of cells expressing TGF-beta.	eamg	18-22	interferon gamma	Rattus norvegicus	88-97
7520837-5	1994	Oral tolerance to EAMG was characterized by suppression of the levels of MNC expressing IFN-gamma and IL-4, but augmentation of cells expressing TGF-beta.	eamg	18-22	interleukin 4	Rattus norvegicus	102-106
8041342-4	1994	Analysis of both EAMG and MG has revealed that the effector agents in this autoimmune disease are anti-AChR antibodies, whose production is regulated by anti-AChR CD4+ T cells.	eamg	17-21	CD4 molecule	Homo sapiens	163-166
8386206-10	1993	Age-related resistance in the EAMG model can provide more information about the factors that determine the severity of myasthenia gravis.	eamg	30-34	renin binding protein	Rattus norvegicus	0-3
1436658-5	1992	This in vitro autoradiographic method revealed a quantitative reduction of AChR at the motor end-plates in EAMG.	eamg	107-111	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	75-79
8505410-2	1993	The oral administration of Torpedo AChR to Lewis rats prior to immunization with Torpedo AChR and complete Freund"s adjuvant resulted in prevention or delay in the onset of EAMG.	eamg	173-177	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	35-39
8432621-1	1993	Treatment of Lewis rats with the beta 2-adrenergic agonist terbutaline suppressed clinical symptoms of acute passive transfer EAMG induced with monoclonal anti-acetylcholine receptor antibody and accelerated clinical recovery in affected animals.	eamg	126-130	UDP glucuronosyltransferase 1 family, polypeptide A7C	Rattus norvegicus	33-39
1516631-7	1992	These results (a) provide evidence that antigenic modulation of endplate AChR is sufficient to generate passive transfer of EAMG and (b) further support the pathogenic potential of the anti-MIR antibodies in MG.	eamg	124-128	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	73-77
7683442-8	1993	The AChR and subunit-reactive T cells could--via secretion of effector molecules including IFN-gamma--play an important role in the initiation and perpetuation of EAMG, and consequently also of human myasthenia gravis.	eamg	163-167	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	4-8
7683442-8	1993	The AChR and subunit-reactive T cells could--via secretion of effector molecules including IFN-gamma--play an important role in the initiation and perpetuation of EAMG, and consequently also of human myasthenia gravis.	eamg	163-167	interferon gamma	Homo sapiens	91-100
1312030-3	1992	Myogenin and MRF4 transcript levels were observed to be 3.1- and 2.6-fold higher in muscle of rats with EAMG than in controls, respectively.	eamg	104-108	myogenin	Rattus norvegicus	0-8
1951638-4	1991	EAMG was induced either actively by immunization with AChR, or transferred passively with monoclonal antibodies (mAb) binding to AChR.	eamg	0-4	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	54-58
1951638-4	1991	EAMG was induced either actively by immunization with AChR, or transferred passively with monoclonal antibodies (mAb) binding to AChR.	eamg	0-4	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	129-133
1988504-8	1991	These results suggest extensive sharing of idiotopes among anti-AChR mAb, which are also present in EAMG serum.	eamg	100-104	cholinergic receptor nicotinic alpha 2 subunit	Rattus norvegicus	64-68
34923373-6	2022	These results suggest that BBR might improve EAMG by rebalancing T cell subsets through targeting JAK-STAT pathway.	eamg	45-49	Janus kinase 1	Rattus norvegicus	98-101
34923373-6	2022	These results suggest that BBR might improve EAMG by rebalancing T cell subsets through targeting JAK-STAT pathway.	eamg	45-49	signal transducer and activator of transcription 1	Rattus norvegicus	102-106
34702288-10	2021	We found CD4+ T-cell differentiation was shifted from Treg cells towards Th1/Th17 in the DM+EAMG group compared to the EAMG group.	eamg	92-96	Cd4 molecule	Rattus norvegicus	9-12
34702288-10	2021	We found CD4+ T-cell differentiation was shifted from Treg cells towards Th1/Th17 in the DM+EAMG group compared to the EAMG group.	eamg	119-123	Cd4 molecule	Rattus norvegicus	9-12