PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 12554700-2 2003 In MG and EAMG, we detected serum AChE-R accumulation. eamg 10-14 acetylcholinesterase Rattus norvegicus 34-38 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 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 77-81 interferon gamma Mus musculus 28-37 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 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 complement component (3b/4b) receptor 1-like Mus musculus 32-36 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 92-96 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 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 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 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 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 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 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 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 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 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 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 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 7520837-3 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 7520837-3 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 7520837-3 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 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 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 7520837-6 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 7520837-6 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 7520837-6 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 182896-12 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 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 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 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 182896-11 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 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 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 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 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 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 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 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 91-95 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 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 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 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 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 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 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