Article: article from journal or magazin.
Mice transgenic for a soluble form of murine cytotoxic T lymphocyte antigen 4 are refractory to murine acquired immune deficiency sydrome development.
Interactions between B and CD4+ T cells are central to the pathogenesis of retrovirus-induced murine acquired immune deficiency virus (MAIDS). Prompted by previous work showing that treatment with cytotoxic T lymphocyte antigen 4 immunoglobulin (CTLA4Ig) partly inhibited the disease, we studied the course of infection in mice deficient for CD28-B7 interactions (mCTLA4-Hgamma1 transgenic mice). Despite a relative viral load identical to that of non-transgenic mice, the transgenic mice did not develop any of the major MAIDS symptoms (i.e. lymphoproliferation and immune anergy). The mCTLA4-Hgamma1 did not however, completely inhibit B-cell activation as indicated by a slight hypergammaglobulinaemia and microscopic blastic transformation. Absence of MAIDS in transgenic mice was associated with much lower levels of both interleukin-4 and interferon-gamma transcripts following viral infection. These results support the theory that the CD28/B7 costimulatory pathway is a critical determinant to MAIDS development.
Animals, Antigens, CD, Antigens, Differentiation/genetics, Cell Division, Cytokines/genetics, Flow Cytometry, Gene Expression, Immunoconjugates, Immunoglobulin G/blood, Interferon-gamma/genetics, Interleukin-12/genetics, Interleukin-13/genetics, Interleukin-15/genetics, Interleukin-4/genetics, Interleukin-5/genetics, Interleukin-6/genetics, Interleukin-9/genetics, Lymphocytes, Mice, Mice, Transgenic, Murine Acquired Immunodeficiency Syndrome/genetics, Murine Acquired Immunodeficiency Syndrome/immunology, RNA, Messenger/analysis, Reverse Transcriptase Polymerase Chain Reaction, Spleen/immunology, Tumor Necrosis Factor-alpha/genetics
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