PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 150-154 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 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 276-280 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 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 182896-12 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 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 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 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 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 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