Passive transfer of experimental autoimmune myasthenia by lymph node cells in inbred guinea pigs.

Tarrab-Hazdi, R; Aharonov, Aharon; Abramsky, Oded; Yaar, Israel; Fuchs, Sara

doi:10.1084/jem.142.3.785

Cited by 49 publications

(9 citation statements)

References 7 publications

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“…However, in acute and passive EAMG, a widespread invasion of macrophages occurs at the endplate [49,53,95]. In acute EAMG, macrophages bear cytophilic antibodies specifically directed against AChR [ 108], and passive transfer of lymph node cells from EAMG animals can induce the disease in recipient animals [90,138]. In cultures of rat skeletal muscle cells, an application ofmacrophages from EAMG rats produces cytotoxic effects in 24 to 72 hours [139].…”

Section: Cell-mediated Immunity At Endplatesmentioning

confidence: 99%

Immunopathologic events at the endplate in myasthenia gravis

Ashizawa

Appel

1985

Springer Semin Immunopathol

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Section: Cell-mediated Immunity At Endplatesmentioning

confidence: 99%

Immunopathologic events at the endplate in myasthenia gravis

Ashizawa

Appel

1985

Springer Semin Immunopathol

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“…In 1973 it was shown that immunization of rabbits with the acetylcholine receptor resulted in the development of a disease almost identical to myasthenia gravis (14,24). This disorder can be transferred with lymphocytes (36), whereas a single transfer of antibodies directed to ace tylcholine receptor only induces a transient disease ( 19).…”

Section: Introductionmentioning

confidence: 99%

Role of Virus for the Induction of Myasthenia gravis

Cm¹,

Hammarström²,

Berg³

1978

Eur Neurol

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Virus has been suggested as an etiological agent in myasthenia gravis. In this investigation 36 patients with the clinical diagnosis of myasthenia gravis were tested for antibodies against ornithosis, mycoplasma pneumoniae and 16 viral antigens. Rabbits with experimentally induced autoimmune myasthenia gravis were similarly tested. There was no overall correlation to any microorganism, which might have suggested the involvement of a viral infection in the pathogenesis of the disease. Neither was there any difference in incidence of antibodies in female patients carrying the HLA B8 antigen, an antigen which is associated with myasthenia gravis, as compared to HLA B8 negative individuals.

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mentioning

confidence: 99%

“…Peripheral T lymphocytes of EAMG-affected animals can be prestimulated in vitro by AcChoR (4,5). AcChoR-specific T lymphocytes from EAMG rats have been shown to be involved in immune responses against AcChoR and in the development of EAMG (5,6). T cells from MG patients proliferate in vitro in the presence of AcChoR (7)(8)(9) and the analysis of T-cell subsets in myasthenics has shown, in several patients, a defect in peripheral T-suppressor cell number (10,11) or an impairment of T-cell suppressor functions (10)(11)(12)(13).…”

mentioning

confidence: 99%

Acetylcholine receptor-specific suppressive T-cell factor from a retrovirally transformed T-cell line.

Sinigaglia¹,

Gotti²,

Castagnoli³

et al. 1984

Proc. Natl. Acad. Sci. U.S.A.

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In both experimental and human myasthenia gravis an impairment in the immune regulation leads to an increased synthesis of antibodies against the nicotinic acetylcholine receptor (AcChoR). The present work reports the establishment of an AcChoR-specific suppressive T-cell line obtained by viral transformation of AcChoR-enriched murine T lymphocytes. Enriched T cells from Torpedo AcChoR-primed mice, prestimulated in vitro with antigen, were infected with radiation leukemia viruses and injected intravenously in congeneic recipient mice. Six months later lymphomas were observed in 20% of the injected mice and two of them, of donor origin, were established as permanent continuous cell lines in vitro. One of these lines, named LA41, expresses Thy-1.2, Lyt-2, and I.Jb surface markers. Culture supernatants of LA41 cells suppress the antigen-specific in vitro proliferation of Torpedo AcChoR-primed lymphocytes. This suppression is antigen-specific since the response induced by fetal calf AcChoR and by other antigens is not affected by addition of LA41 culture supernatant in the proliferative assay. LA41 culture supernatant injected in vivo at the time of antigen-priming suppresses also significantly the production of anti-AcChoR antibodies but not the synthesis of antibodies against other antigens-i.e., fetal calf AcChoR or a-bungarotoxin. These data show that LA41 cells constitutively produce Torpedo AcChoR-specific suppressor factor.

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Passive transfer of experimental autoimmune myasthenia by lymph node cells in inbred guinea pigs.

Cited by 49 publications

References 7 publications

Immunopathologic events at the endplate in myasthenia gravis

Immunopathologic events at the endplate in myasthenia gravis

Role of Virus for the Induction of Myasthenia gravis

Acetylcholine receptor-specific suppressive T-cell factor from a retrovirally transformed T-cell line.

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