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Nat Immunol ; 8(4): 369-77, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17351619

ABSTRACT

Interferon-gamma is key in limiting Mycobacterium tuberculosis infection. Here we show that vaccination triggered an accelerated interferon-gamma response by CD4(+) T cells in the lung during subsequent M. tuberculosis infection. Interleukin 23 (IL-23) was essential for the accelerated response, for early cessation of bacterial growth and for establishment of an IL-17-producing CD4(+) T cell population in the lung. The recall response of the IL-17-producing CD4(+) T cell population occurred concurrently with expression of the chemokines CXCL9, CXCL10 and CXCL11. Depletion of IL-17 during challenge reduced the chemokine expression and accumulation of CD4(+) T cells producing interferon-gamma in the lung. We propose that vaccination induces IL-17-producing CD4(+) T cells that populate the lung and, after challenge, trigger the production of chemokines that recruit CD4(+) T cells producing interferon-gamma, which ultimately restrict bacterial growth.


Subject(s)
CD4-Positive T-Lymphocytes/immunology , Interleukin-17/immunology , Interleukin-23/immunology , Mycobacterium tuberculosis/immunology , Tuberculosis Vaccines/immunology , Tuberculosis/immunology , Adjuvants, Immunologic/pharmacology , Animals , Antigens, Bacterial/immunology , Bacterial Proteins/immunology , Cytokines/immunology , Enzyme-Linked Immunosorbent Assay , Female , Flow Cytometry , Immunohistochemistry , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Mice, Transgenic
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