Journal
CELLULAR IMMUNOLOGY
Volume 216, Issue 1-2, Pages 65-72Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/S0008-8749(02)00510-5
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Funding
- NIAID NIH HHS [AI-41922, AI-40488] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI041922, R01AI040488] Funding Source: NIH RePORTER
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To confirm the primary role of CD4 T cells in pulmonary tuberculosis, mice with a disruption of their CD4 gene (CD4 KO) were exposed to an aerosol of Mycobacterium tuberculosis and survival, cellular responses in the lung and granuloma development followed. CD8 and NK cells from the lungs of infected CD4 KO mice expressed IFN-gamma and were recruited in numbers similar to those seen in the C57BL/6 mice; recruitment correlated with initial control of bacteria. The major defect in mice lacking CD4 was the significant reduction in total cellular recruitment into the lungs. CD4 KO mice did not generate the typical mononuclear granulomatous lesions, instead the cellular influx was macrophage in character and was localized as perivascular cuffing. Early control of M. tuberculosis growth is therefore independent of CD4+ cells but such cells are required to ensure recruitment of mononuclear cells to the lung and thus ensure long-term survival. (C) 2002 Elsevier Science (USA). All rights reserved.
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