Open AccessInduction ofMycobacterium tuberculosis-Specific Primary and Secondary T-Cell Responses in Interleukin-15-Deficient Mice
Author(s) -
Vanja Lazarevic,
David J. Yankura,
Sherrie J. Divito,
JoAnne L. Flynn
Publication year - 2005
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.73.5.2910-2922.2005
Subject(s) - biology , immunology , mycobacterium tuberculosis , cytotoxic t cell , cd8 , immune system , effector , interferon gamma , tuberculosis , t cell , cytokine , interleukin 2 , interleukin 4 , medicine , pathology , in vitro , biochemistry
Several studies have provided evidence that interleukin-15 (IL-15) can enhance protective immune responses against Mycobacterium tuberculosis infection. However, the effects of IL-15 deficiency on the functionality of M. tuberculosis-specific CD4 and CD8 T cells are unknown. In this study, we investigated the generation and maintenance of effector and memory T-cell responses following M. tuberculosis infection of IL-15(-/-) mice. IL-15(-/-) mice had slightly higher bacterial numbers during chronic infection, which were accompanied by an increase in gamma interferon (IFN-gamma)-producing CD4 and CD8 T cells. There was no evidence of increased apoptosis or a defect in proliferation of CD8 effector T cells following M. tuberculosis infection. The induction of cytotoxic and IFN-gamma CD8 T-cell responses was normal in the absence of IL-15 signaling. The infiltration of CD4 and CD8 T cells into the lungs of "immune" IL-15(-/-) mice was delayed in response to M. tuberculosis challenge. These findings demonstrate that efficient effector CD4 and CD8 T cells can be developed following M. tuberculosis infection in the absence of IL-15 but that recall T-cell responses may be impaired.