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  • Title: High-dose cyclophosphamide inhibits anterior chamber-associated immune deviation (ACAID) and the production of extracellular antigen-specific T cell proteins induced by trinitrophenylated (TNP) spleen cells.
    Author: Wang Y, O'Rourke J, Cone RE.
    Journal: Cell Immunol; 1995 Oct 15; 165(2):284-8. PubMed ID: 7553893.
    Abstract:
    Injection of antigen into the anterior chamber (AC) of the eye induces the production of IgM and IgG1 antibodies and potentiates the appearance in serum of extracellular antigen-specific T cell proteins (TABM) that are specific for the AC-injected antigen. In contrast, delayed-type hypersensitivity (DTH) to the injected antigen is suppressed. This manifestation of anterior chamber-associated immune deviation (ACAID) is believed to be a key part of the basis of the immune privilege of the eye. Because cyclophosphamide (CY) exerts selective effects on immunoregulatory T cells and macrophages, we sought to determine its effects on the appearance in serum of TNP-specific TABM in mice following intracameral injection with TNP murine spleen cells followed by epicutaneous sensitization and challenge with picrylchloride. Injection of 200 mg/kg CY 2 days before AC injection of TNP spleen cells, sensitization, and challenge prevented the suppression of DTH and the production of TNP-specific TABM. The production of TNP-specific immunoglobulins was not affected. Injection of a low dose of 20 mg/kg CY enhanced DTH 100-300% in control animals, but did not prevent either ACAID or the production of TABM. These results provide further evidence that serum TABM may be a serologic indicator of T lymphocyte activity in ACAID and that ACAID is mediated by cells sensitive to high-dose CY.
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