The Journal of Experimental Medicine
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Published online 3 July 2000.
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© The Rockefeller University Press, 0022-1007/2000/7/117/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 1, July 3, 2000 117-122

Brief Definitive Reports

Interferon {gamma} Eliminates Responding Cd4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated Cd4 T Cells

Dyana K. Daltona, Laura Haynesa, Cong-Qiu Chua, Susan L. Swaina, and Susan Wittmera

a From The Trudeau Institute, Saranac Lake, New York 12983
The Trudeau Institute, 100 Algonquin Ave., P.O. Box 59, Saranac Lake, NY 12983.518-891-5126518-891-3080 ext. 168

ddalton{at}trudeauinstitute.org

In Mycobacterium bovis Bacille Calmette-Guérin (BCG)-infected wild-type mice, there was a large expansion of an activated (CD44hi) 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)-{gamma} knockout (KO) mice, the activated CD4 T cell population did not undergo apoptosis. These mice accumulated large numbers of CD4+CD44hi T cells that were responsive to mycobacterial antigens. Addition of IFN-{gamma} to cultured splenocytes from BCG-infected IFN-{gamma} KO mice induced apoptosis of activated CD4 T cells. IFN-{gamma}–mediated apoptosis was abolished by depleting adherent cells or Mac-1+ spleen cells or by inhibiting nitric oxide synthase. Thus, IFN-{gamma} is essential to a regulatory mechanism that eliminates activated CD4 T cells and maintains CD4 T cell homeostasis during an immune response.

Key Words: T lymphocytes • homeostasis • cell death • knockout mice • nitric oxide

© 2000 The Rockefeller University Press


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