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Aspergillus fumigatus primes dendritic cells to stimulate IL‐17 production from CD4+ T cells
Author(s) -
Fei Mingjian,
Oriss Timothy,
Steele Chad,
Kolls Jay,
Ray Prabir,
Ray Anuradha
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.674.15
Subject(s) - aspergillus fumigatus , immune system , immunology , acquired immune system , tlr2 , allergic bronchopulmonary aspergillosis , biology , microbiology and biotechnology , t cell , dendritic cell , aspergillus , innate immune system , antibody , immunoglobulin e
Aspergillus fumigatus (A. fumigatus) is a fungus that induces allergic airways diseases in immunocompromised patients, and in patients with cystic fibrosis or severe asthma. Host defense against this fungus depends on both innate and adaptive immunity. DCs have been shown to transport conidia or hyphae from the airway to the lung draining lymph node and initiate T cell responses. Fungus‐induced Th2 response has been associated with allergic bronchopulmonary aspergillosis while Th1 response favors resistance to the pathogen. We have initiated studies to understand adaptive immune responses against A. fumigatus. We have found that resting conidia are not able to induce activation of bone marrow derived‐DCs, while swollen conidia efficiently promote DC maturation. In order to investigate how Aspergillus‐programmed DCs prime T cell responses, we cocultured fungus‐exposed DCs with CD4+ T cells in the presence or absence of TCR activation by specific antigen or anti‐CD3 antibody. Even without TCR signaling, similar to DCs exposed to the dectin‐1 agonist curdlan, Aspergillus‐conditioned DCs induced IL‐17 from T cells, which was not elicited by control DCs that were not exposed to any stimuli. Collectively, our observations show the ability of Aspergillus to prime DCs for IL‐17 production from CD4+ T cells, which is increasingly being associated with allergic diseases. Funded by: HL84932 and HL 77430 (to A.R.)