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Failure to Suppress the Expansion of the Activated CD4 T Cell Population in Interferon –deficient Mice Leads to Exacerbation of Experimental Autoimmune Encephalomyelitis

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.

Mice deficient in interferon (IFN)- or IFN- receptor develop progressive and fatal experimental autoimmune encephalomyelitis (EAE). We demonstrate that CD4 T cells lacking IFN- production were required to passively transfer EAE, indicating that they were disease-mediating cells in IFN- knockout (KO) mice. IFN- KO mice accumulated 10–16-fold more activated CD4 T cells (CD4⁺CD44^hi) than wild-type mice in the central nervous system during EAE. CD4⁺CD44^hi T cells in the spleen and central nervous system of IFN- KO mice during EAE showed markedly increased in vivo proliferation and significantly decreased ex vivo apoptosis compared with those of wild-type mice. IFN- KO CD4⁺CD44^hi T cells proliferated extensively to antigen restimulation in vitro and accumulated larger numbers of live CD4⁺ CD44^hi T cells. IFN- completely suppressed proliferation and significantly induced apoptosis of CD4⁺CD44^hi 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- 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

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