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  • Title: CD40L is necessary for the priming of effector cells for lymphocytic and granulomatous experimental autoimmune thyroiditis.
    Author: Peterson KE, Braley-Mullen H.
    Journal: J Autoimmun; 1999 Feb; 12(1):1-12. PubMed ID: 10028017.
    Abstract:
    The interaction of CD40 on antigen presenting cells (APC) with CD40L on mouse thyroglobulin (MTg)-specific T cells may deliver an essential signal for the development of CD4(+) experimental autoimmune thyroiditis (EAT) effector cells and anti-MTg producing B cells. To determine the requirement for CD40-CD40L interactions in G-EAT, donor mice were injected with an anti-CD40L monoclonal antibody (mAb) on days -1, 0, and +1 relative to immunization with MTg and adjuvant. Recipients of spleen cells from MTg-primed donor mice injected with anti-CD40L did not develop EAT, while spleen cells from similarly immunized hamster Ig-treated donors transferred severe G-EAT. Although the decreased EAT severity was accompanied by increased IL-4 mRNA expression by CD4(+) T cells from anti-CD40L-treated donors, the increased IL-4 was not necessary for suppression of EAT, since anti-CD40L treatment prevented EAT in IL-4-deficient mice. Addition of MTg-primed B cells during in vitro activation of spleen cells from anti-CD40L-treated donors did not induce EAT in recipients, suggesting that anti-CD40L suppresses EAT by preventing the sensitization of EAT effector cells. Addition of anti-CD40L during in vitro activation of MTg-primed spleen cells or treatment of recipients with anti-CD40L had no effect on EAT severity, indicating that CD40-CD40L interactions are not required after EAT effector cells are primed to MTg.
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