Innate Immune Activation and CD4+ T Cell Priming during Respiratory Fungal Infection.
Rivera, Amariliz 1; Ro, Grace 1; Van Epps, Heather L. 1,2; Simpson, Tyler 1; Leiner, Ingrid 1; Sant'Angelo, Derek B. 1; Pamer, Eric G. 1,*
[Article] Immunity. 25(4):665-675, October 2006.

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: Aspergillus fumigatus is a mold that causes a spectrum of diseases, including lethal lung infections in immunocompromised humans and allergic asthma in atopic individuals. T helper 1 (Th1) CD4 T cells protect against invasive A. fumigatus infections whereas Th2 CD4 T cells exacerbate asthma upon inhalation of A. fumigatus spores. Herein, we demonstrate that A. fumigatus-specific T cells were rapidly primed in lymph nodes draining the lung and fully differentiated into interferon-[gamma] (IFN-[gamma])-producing Th1 CD4 T cells upon arrival in the airways. T-bet induction in A. fumigatus-specific CD4 T cells was enhanced by MyD88-mediated signals in draining lymph nodes, but T cell proliferation, trafficking, and Th1 differentiation in the airways were Toll-like receptor (TLR) and MyD88 independent. Our studies demonstrate that CD4 T cell differentiation during respiratory fungal infection occurs incrementally, with TLR-mediated signals in the lymph node enhancing the potential for IFN-[gamma] production whereas MyD88-independent signals promote Th1 differentiation in the lung.

(C) 2006Elsevier, Inc.