Modulation of the severity of experimental autoimmune encephalomyelitis by gammadelta T lymphocytes activated by mycobacterial antigens.

Immunity to mycobacterial antigens may contribute to the maintenance of self-tolerance. Exposure of the immune system to mycobacterial antigen might well stimulate the immune system to exert control over unwanted self-reactive clones. We demonstrated that in vivo administration of Mycobacterium tuberculosis, PPD, and PPD peptide (180-196) prior to immunization with Myelin Basic Protein (MBP) led to a moderate increase of gammadelta T cells, suppression of the immune response, and reduction in the severity of Experimental Autoimmune Encephalomyelitis. The immunosuppression observed is due, at least in part, to the production of Transforming growth factor-beta (TGFbeta) by the gammadelta T lymphocytes.

Pattern of cytokine secretion by peripheral blood cells of patients with multiple sclerosis in Brazil.

Autoimmune T cells play a key role as regulators and effectors of organ-specific autoimmune disease. In multiple sclerosis (MS), activated T cells specific for myelin components produce a plethora of inflammatory cytokines and mediators that contribute to myelin damage. The production of proinflammatory and regulatory cytokines by peripheral blood cells from patients with active and stable MS and healthy controls were examined. The results show that TNF alpha production was somewhat elevated in active MS with no significant increase in the level IFN gamma, whereas in the chronic phase the anti-inflammatory cytokines IL-10 and TGF beta increased, accompanied by a reduction in IFN gamma when stimulated by myelin basic protein. Multiple Sclerosis (2000) 6 293 - 299

Interferon beta modulates experimental autoimmune encephalomyelitis by altering the pattern of cytokine secretion.

The mechanism of action underlying the beneficial effect of IFNbeta in Multiple Sclerosis is poorly understood. Experimental Autoimmune Encephalomyelitis (EAE) is the experimental model for Multiple Sclerosis; therefore, we investigated the effects of recombinant mouse IFNbeta on the severity of EAE induced in SJL mice and on cytokine production by Th1 and Th2 lymphocytes. The results indicated that rmIFN beta reduced the disease activity with an I.P. dosage of 10,000 U/day every other day, and successfully treated EAE mice revealed reduced amounts of IFN gamma; no changes in the levels of IL4 were observed, although thera was a significant increase in IL10 and TGFbeta production. Beneficial effects on EAE are associated with inhibition of inflammatory cytokines and stimulation of anti-inflammatory cytokines.

Evidence for cross-reactivity between antigen derived from Trypanosoma cruzi and myelin basic protein in experimental Chagas disease.

Some autoimmune diseases are thought to arise after an infection. Infectious agents can initiate a chronic inflammatory response associated with autoimmune reactions. Chagas disease, caused by the intracellular parasite Trypanosoma cruzi, is an excellent model for autoimmune disease induced by an infection. The chronic disease is characterized by rich inflammatory infiltrate in myocardial and nervous tissues, with virtually no demonstrable parasites. We were able to demonstrate the presence of antibody to myelin basic protein (MBP) in the serum from T. cruzi chronically infected mice. Lymphocytes from mice immunized with T. cruzi-derived soluble extract antigen (TCSE) proliferate in response to MBP in vitro. Lymphocytes from animals immunized with MBP also were activated by TCSE in vitro. By studying the overlapping peptides from the MBP molecule, we were able to identify two regions responsible for the cross-reactivity.