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Myasthenia gravis: steroid-induced effects on lymphocyte subpopulations in myasthenia gravis.

Lymphocyte subpopulations from patients with myasthenia gravis were evaluated during chronic steroid therapy. A marked lymphocytopenia (10-70%) was initially (day 3-21) noticed as well as a preferential depletion of thymus-derived cells which paralleled the clinical deterioration. Thus there was a relative increase in B cells, although their absolute number remained rather constant. These changes were reverted within 2-4 weeks in spite of continuous treatment. These findings are compatible with a release of myasthenic factors (anti-acetylcholine receptor antibodies?) during the initial steroid-induced cell damage, the long-term beneficial effects being due to loss or suppression of autoreactive helper t cells.

Adolescent↗

Differences in fine specificity of anti-acetylcholine receptor antibodies between subgroups of spontaneous myasthenia gravis of recent onset, and of penicillamine induced myasthenia.

The antigenic specificity of anti-acetylcholine receptor antibodies (anti-AChR) from 70 recent onset myasthenia gravis (MG) and nine penicillamine MG patients was determined by inhibition experiments using monoclonal antibodies (m.abs) raised against human AChR. Differences were found between individuals and between the three clinical subgroups of idiopathic MG distinguished by age of onset, thymic pathology and HLA associations. Penicillamine-induced MG anti-AChR differed from that in age-matched MG controls but was similar to that in young-onset cases. The variable and heterogeneous antigenic specificity in MG suggests that AChR itself rather than a cross-reacting epitope is the primary antigen. Differences in specificity between MG subgroups may reflect a diversity of triggering factors or of immunoglobulin genes.

Adolescent↗

Myasthenia gravis: studies on HL-A antigens and lymphocyte subpopulations in patients with myasthenia gravis.

Thirth-three patient with a clinical diagnosis of myasthenia gravis were tissue-typed for HL-A antigens. In agreement with earlier reports a significant increase in antigens HL-A1 and HL-A8 were found in this material. Two of the patients were treated with chronic thoracic duct drainage. Proportions of T and B lymphocytes in lymph and peripheral blood were estimated in these patients. In the lymph an initial decrease in the proportion of T cells occurred, which was accompanied by a subsequent increase in the proportion of B cells. Towards the end of the chronic drainage period this effect was reversed. A slightly different picture occurred in blood lymphocytes. Initially, there was an increase in both T and B cells, followed by a decrease in T-cells numbers in one patient, whereas in the second patient the proportion of T cells decreased from the onset of drainage while the proportion of B cells steadily increased. These studies showed that available markers for determination of T ANd B cells were useful for studies of lymphocyte subpopulations in blood and lymph. Lmyphocytes from the thoracic duct were also tested for their reactivity to various mitogens specific for either T or B cells. The B-cell mitogens which were used were dextran sulphate, lipopolysaccharide, purified protein derivative, as well as rabbit anti-human beta2-microglobulin serum. The T-cell mitogens investigated were concanavalin A and phytohaemagglutinin. No significant differences in the responsiveness of thoracic duct lymphocytes compared to normal peripheral blood lymphocytes were found.

Adult↗

Clonotypic analysis of anti-acetylcholine receptor antibodies from experimental autoimmune myasthenia gravis-sensitive Lewis rats and experimental autoimmune myasthenia gravis-resistant Wistar Furth rats.

A single immunization of Lewis rats with purified acetylcholine receptor (AChR) emulsified in adjuvant typically stimulates the production of oligoclonal AChR-reactive antibodies (as demonstrated by IEF) dominated by the IgG2a subclass, of moderate but clonotypically heterogeneous relative Ag-binding avidity, and capable of inducing symptoms of experimental autoimmune myasthenia gravis. Although similar immunization of Wistar Furth rats produces AChR-reactive antibodies with similar characteristics of clonotypic heterogeneity, avidity, and isotype expression, no detectable signs of AChR-dependent muscle impairment is observed. This contrasts the ability to induce impaired AChR function upon the passive transfer of pre-formed Lewis anti-AChR antibodies into naive Wistar Furth rats, suggesting that disease resistance in this model is not conferred at the level of the AChR itself. Moreover, if more aggressive immunization protocols are used (i.e., multiple injections of AChR), a transient breakthrough of AChR-dependent muscle dysfunction can be induced directly in the Wistar Furth strain indicating that the potential for the production of disease-causing antibodies does exist in the Wistar Furth repertoire. IEF analysis of Wistar Furth anti-AChR antibodies has revealed that hyperimmunization results in modified antibody clonotype expression that might explain changing expression of disease symptoms; however, explanations for the apparent "resistance" of Wistar Furth rats to disease induction are likely to be complex.

Animals↗

[Ocular manifestations of myasthenia. Apropos of 60 cases of myasthenia observed at the Dakar University Hospital Center].

The authors report 43 cases with ocular signs among 60 cases of myasthenia gravis encountered over a period of 23 years in the Ophthalmologic and Neurologic clinics of the University Teaching Hospital of Dakar. After analysis of the aetiological, clinical, evolutional and therapeutic features, they insist on the importance of the ocular symptoms that eventually can help to early diagnosis and treatment.

Adolescent↗