Brief Definitive Reports

Interferon Eliminates Responding CD4 T Cells during Mycobacterial Infection by Inducing Apoptosis of Activated CD4 T Cells

Correspondence to: Dyana K. Dalton, The Trudeau Institute, 100 Algonquin Ave., P.O. Box 59, Saranac Lake, NY 12983. Tel:518-891-3080 ext. 168 Fax:518-891-5126 E-mail:ddalton{at}trudeauinstitute.org.

In Mycobacterium bovis Bacille Calmette-Guérin (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)- 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- to cultured splenocytes from BCG-infected IFN- KO mice induced apoptosis of activated CD4 T cells. IFN-–mediated apoptosis was abolished by depleting adherent cells or Mac-1⁺ spleen cells or by inhibiting nitric oxide synthase. Thus, IFN- 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

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