Title:Mechanism by which Regulatory Rheumatoid Factor Prevents Experimental Autoimmune Encephalomyelitis
Volume: 18
Issue: 6
Author(s): Elena Stolyarova*, Liubov Beduleva, Igor Menshikov, Alexandr Snigiryev and Tatyana Khramova
Affiliation:
- Department of Immunology and Cell Biology, Institute of Natural Sciences, Udmurt State University, Izhevsk,Russian Federation
Keywords:
Experimental autoimmune encephalomyelitis, controlled contraction of lymphocyte expansion, activated CD4+
lymphocytes, CD4+CD95+ lymphocytes, regulatory rheumatoid factor, complement-dependent lysis.
Abstract: Background: One mechanism that underlies protection from autoimmunity and avoidance
of uncontrolled inflammation is the controlled contraction of lymphocyte expansion during the immune
response. We identified regulatory rheumatoid factor (regRF), the production of which is associated
with resistance to and remission of experimental autoimmune diseases. RegRF is anti-idiotypic
antibodies to lymphocyte receptors against autoimmune disease-inducing antigens; at the same time, it
is specific to epitopes in the hinge Fc fragments of IgG.
Objective: The aim of this study is to test the hypothesis that regRF prevents autoimmunity by limiting
the expansion of lymphocytes.
Methods: To test this hypothesis, we used a model of experimental autoimmune encephalitis.
Results: We found that in the lymph nodes that drain the injection site in rats producing regRF in response
to immunization with myelin basic protein (MBP) the proportion of CD4+lymphocytes was
lower than in rats in which MBP-immunization did not induce higher regRF levels. RegRF-containing
plasma obtained from MBP-immunized rats induces complement-dependent killing of MBP-activated
lymphocytes. Activated MBP-specific lymphocytes are not sensitive to the regRF-containing plasma of
intact rats.
Conclusion: The regRF produced during the immune response is a specific control factor for the expansion
of antigen-activated CD4+lymphocytes.
