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    Online Resource
    Online Resource
    The American Association of Immunologists ; 2012
    In:  The Journal of Immunology Vol. 188, No. 1_Supplement ( 2012-05-01), p. 55.5-55.5
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 55.5-55.5
    Abstract: CARD9 is a critical adaptor molecule signaling for NF-κB activation triggered via C-type lectin receptors (CLRs), which recognize carbohydrate structures of microbes. Cryptococcus neoformans, a yeast-like fungus is recognized by some CLRs, such as mannose receptor or DC-SIGN, whereas the role of CLRs or CARD9 in the host defense to this infection remains to be elucidated. In this study, we analyzed the role of CARD9 in the protective immune response to C. neoformans infection. C57BL/6 and CARD9KO mice were infected intratracheally with C. neoformans (B3501). The number of live microbes, histopathological findings and cytokine synthesis in lungs and the cytokine response of paratracheal lymph node (LN) cells upon antigenic re-stimulation were evaluated. CARD9KO mice were highly susceptible to infection with C. neoformans, as shown by increased number of live microbes in lungs compared to control, which was associated with less marked granulomatous response and remarkable multiplication of yeast cells in the alveolar spaces. Expression of RORγt and IL-17A mRNA and intracellular expression of IL-17A by T, NKT and γδ T cells were strongly attenuated in the lungs of CARD9KO mice. IL-17A production by the re-stimulated LN cells was mostly abrogated in these mice. By contrast, Th1-cytokine response was not much affected. These results suggest that CARD9 is a key molecule in the Th17 response to C. neoformans, which is associated with the host defense against this infection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
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