Article abstract
Nature Immunology 8, 369 - 377 (2007)
Published online: 11 March 2007 | doi:10.1038/ni1449
IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge
Shabaana A Khader1, Guy K Bell1, John E Pearl1, Jeffrey J Fountain1, Javier Rangel-Moreno1, Garth E Cilley1, Fang Shen2, Sheri M Eaton1, Sarah L Gaffen2, Susan L Swain1, Richard M Locksley3, Laura Haynes1, Troy D Randall1 & Andrea M Cooper1
Abstract
Interferon-
is key in limiting Mycobacterium tuberculosis infection. Here we show that vaccination triggered an accelerated interferon- 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- 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-, which ultimately restrict bacterial growth.
- Trudeau Institute, Saranac Lake, New York 12983, USA.
- Department of Oral Biology, School of Dental Medicine, University at Buffalo, The State Univeristy of New York, Buffalo, New York 14214, USA.
- Howard Hughes Medical Institute, Department of Medicine and Microbiology & Immunology, University of California San Francisco, San Francisco, California 94143, USA.
Correspondence to: Andrea M Cooper1 e-mail: acooper@trudeauinstitute.org
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