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Persistence and Function of Central and Effector Memory CD4⁺ T Cells following Infection with a Gastrointestinal Helminth¹

Colby Zaph^*, Kathryn A. Rook^*, Michael Goldschmidt^*, Markus Mohrs, Phillip Scott^* and David Artis^2,*

^* Department of Pathobiology, University of Pennsylvania, Philadelphia, PA 19104; and Trudeau Institute, Saranac Lake, NY 12983

Immunity in the gastrointestinal tract is important for resistance to many pathogens, but the memory T cells that mediate such immunity are poorly characterized. In this study, we show that following sterile cure of a primary infection with the gastrointestinal parasite Trichuris muris, memory CD4⁺ T cells persist in the draining mesenteric lymph node and protect mice against reinfection. The memory CD4⁺ T cells that developed were a heterogeneous population, consisting of both CD62L^high central memory T cells (T_CM) and CD62L^low effector memory T cells (T_EM) that were competent to produce the Th type 2 effector cytokine, IL-4. Unlike memory T cells that develop following exposure to several other pathogens, both CD4⁺ T_CM and T_EM populations persisted in the absence of chronic infection, and, critically, both populations were able to transfer protective immunity to naive recipients. CD62L^highCD4⁺ T_CM were not apparent early after infection, but emerged following clearance of primary infection, suggesting that they may be derived from CD4⁺ T_EM. Consistent with this theory, transfer of CD62L^lowCD4⁺ T_EM into naive recipients resulted in the development of a population of protective CD62L^highCD4⁺ T_CM. Taken together, these studies show that distinct subsets of memory CD4⁺ T cells develop after infection with Trichuris, persist in the GALT, and mediate protective immunity to rechallenge.

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