The Journal of Experimental Medicine
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Published online 3 July 2000.
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© The Rockefeller University Press, 0022-1007/2000/7/123/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 1, July 3, 2000 123-128

Brief Definitive Reports

Failure to Suppress the Expansion of the Activated Cd4 T Cell Population in Interferon {gamma}–Deficient Mice Leads to Exacerbation of Experimental Autoimmune Encephalomyelitis

Cong-Qiu Chua, Susan Wittmera, and Dyana K. Daltona

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

Mice deficient in interferon (IFN)-{gamma} or IFN-{gamma} receptor develop progressive and fatal experimental autoimmune encephalomyelitis (EAE). We demonstrate that CD4 T cells lacking IFN-{gamma} production were required to passively transfer EAE, indicating that they were disease-mediating cells in IFN-{gamma} knockout (KO) mice. IFN-{gamma} KO mice accumulated 10–16-fold more activated CD4 T cells (CD4+CD44hi) than wild-type mice in the central nervous system during EAE. CD4+CD44hi T cells in the spleen and central nervous system of IFN-{gamma} KO mice during EAE showed markedly increased in vivo proliferation and significantly decreased ex vivo apoptosis compared with those of wild-type mice. IFN-{gamma} KO CD4+CD44hi T cells proliferated extensively to antigen restimulation in vitro and accumulated larger numbers of live CD4+ CD44hi T cells. IFN-{gamma} completely suppressed proliferation and significantly induced apoptosis of CD4+CD44hi T cells responding to antigen and hence inhibited accumulation of live, activated CD4 T cells. We thus present novel in vivo and in vitro evidence that IFN-{gamma} may limit the extent of EAE by suppressing expansion of activated CD4 T cells.

Key Words: T lymphocytes • apoptosis • autoimmune diseases • animal disease models • knockout mice

© 2000 The Rockefeller University Press


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