IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge
Autor: | Susan L. Swain, Shabaana A. Khader, Sheri M. Eaton, Jeffrey J. Fountain, Richard M. Locksley, Laura Haynes, Guy K. Bell, Garth E Cilley, Troy D. Randall, Javier Rangel-Moreno, Fang Shen, Andrea M. Cooper, John E. Pearl, Sarah L. Gaffen |
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Rok vydání: | 2006 |
Předmět: |
CD4-Positive T-Lymphocytes
Male T cell Immunology Enzyme-Linked Immunosorbent Assay Mice Transgenic Interleukin-23 Mycobacterium tuberculosis Interleukin 21 Mice Adjuvants Immunologic Bacterial Proteins medicine Interleukin 23 Immunology and Allergy Animals Tuberculosis Tuberculosis Vaccines Mice Knockout Antigens Bacterial biology Cd4 t cell Interleukin-17 biology.organism_classification Flow Cytometry Virology Immunohistochemistry Vaccination Mice Inbred C57BL medicine.anatomical_structure Cytokines Female Interleukin 17 |
Zdroj: | Nature immunology. 8(4) |
ISSN: | 1529-2908 |
Popis: | 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. |
Databáze: | OpenAIRE |
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