Costimulatory molecule expression on leukocytes from mice with experimental autoimmune encephalomyelitis treated with IFN-beta.

Interferon-beta (IFN-beta) is of benefit in the treatment of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), but the mechanisms by which it exerts this beneficial effect remain uncertain. The present data demonstrate that IFN-beta therapy impairs the proliferative response to concanavalin A (ConA) and myelin basic protein (MBP), decreases expression of the CD80 molecule on leukocytes of treated mice, and may thereby impede the Th1 cell activation-promoting anergy in EAE. Moreover, IFN-beta therapy increases expression of the CTLA4 molecule, which induces a counterregulatory Th2 response.

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.

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.

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.

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.