Abstract
In Mycobacterium bovis Bacille Calmette-Guerin (BCG)-infected wild-type mice, there was a large expansion of an activated (CD44(hi)) splenic CD4 T cell population followed by a rapid contraction of this population to normal numbers. Contraction of the activated CD4 T cell population in wild-type mice was associated with increased apoptosis of activated CD4 T cells. In BCG- infected interferon (IFN)-γ knockout (KO) mice, the activated CD4 T cell population did not undergo apoptosis. These mice accumulated large numbers of CD4+CD44(hi) T cells that were responsive to mycobacterial antigens. Addition of IFN-γ to cultured splenocytes from BCG-infected IFN-γ KO mice induced apoptosis of activated CD4 T cells. IFN-γ-mediated apoptosis was abolished by depleting adherent cells or Mac-1+ spleen cells or by inhibiting nitric oxide synthase. Thus, IFN-γ is essential to a regulatory mechanism that eliminates activated CD4 T cells and maintains CD4 T cell homeostasis during an immune response.
Original language | English (US) |
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Pages (from-to) | 117-122 |
Number of pages | 6 |
Journal | Journal of Experimental Medicine |
Volume | 192 |
Issue number | 1 |
DOIs | |
State | Published - Jul 3 2000 |
Externally published | Yes |
Keywords
- Cell death
- Homeostasis
- Knockout mice
- Nitric oxide
- T lymphocytes
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology