Type II collagen oral tolerance; mechanism and role in collagen-induced arthritis and rheumatoid arthritis.

Oral tolerance means a diminished immune response to previously fed antigens. Repeated oral administrations of type II collagen (CII) induce oral tolerance and inhibit the development of collagen-induced arthritis (CIA). Dendritic cells (DCs) in the gut-associated lymphoid tissue (GALT) take up the CII and then present it to T cells to generate regulatory T cells (Tregs), which induce systemic immune tolerance to CII.

CTLA4-Ig modifies dendritic cells from mice with collagen-induced arthritis to increase the CD4+CD25+Foxp3+ regulatory T cell population.

Cytotoxic T lymphocyte antigen-4 (CTLA4) and IgG fusion protein, CTLA4-Ig, is a therapeutic agent used for rheumatoid arthritis. It binds B7 molecules on dendritic cells (DCs) and thereby blocks B7/CD28 costimulatory interaction and inhibits effective T cell proliferation. However, the effect of CTLA4-Ig on the regulatory T cell (Treg) is still not known.

Myelodysplastic syndrome with erythroid aplasia following pure red cell aplasia.

Myelodysplastic syndrome (MDS) with erythroid aplasia is a very rare disorder that has not been clearly defined. We experienced a case of pure red cell aplasia (PRCA), which evolved to MDS with erythroid aplasia. A 59-year-old male with transfusion-dependent PRCA was referred to our hospital for an evaluation of newly developed thrombocytopenia.

The MCP-1 promoter -2518 polymorphism in Behcet's disease: correlation between allele types, MCP-1 production and clinical symptoms among Korean patients.

Objective: To compare the G vs. A variation at the MCP-1 promoter -2518 position among normal Koreans and Behcet patients, and to investigate possible association of this polymorphism with disease pathogenesis.

Methods: The allele type of -2518 polymorphism was determined by restriction fragment length polymorphism of Pvu II.