The Journal of Experimental Medicine
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J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/01/31/12 $2.00
Volume 185 January 1997 31-42

T Helper Subset Differentiation in the Absence of Invariant Chain

By Daniel R. Brown,* Kevin Swier,* Naomi H. Moskowitz,* Marisa F. Naujokas,Dagger Richard M. Locksley,§ and Steven L. Reiner*

From the * Department of Medicine, Committee on Immunology, Gwen Knapp Center for Lupus & Immunology Research, and Dagger  Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, Illinois 60637; and § Departments of Medicine and Microbiology & Immunology, University of California, San Francisco, California 94143

The outcome of murine infection with Leishmania major is regulated by major histocompatibility complex class II-restricted T helper cells. Invariant chain-deficient (Ii -/-) mice have impaired ability to present major histocompatibility complex class II-restricted antigens, and reduced numbers of CD4+ T cells. Despite these deficits, C57BL/6 Ii -/- mice controlled L. major infection comparably to wild-type mice. As assessed by mRNA analysis and in vitro antigen restimulation for IFN-gamma , Ii -/- mice had normal induction of Th1 subset differentiation even though antigen-dependent proliferation of their lymph node cells was substantially compromised. In addition, BALB/c Ii -/- mice exhibited a progressive course of infection and Th2 effector cell development that were comparable to that seen in wild-type BALB/c mice. We wished to determine whether this unexpected efficiency of T helper subset induction despite inefficient T cell stimulation could be modeled in vitro. In the presence of rIL-12 or rIL-4 naive parasite-specific transgenic T cells could mature into IFN-gamma -or IL-4-secreting T helper cells, respectively, even when antigen presentation was suboptimal or antigen dose was submitogenic. These experiments demonstrate that activation of T helper cells to a threshold required for IL-2 production or proliferation is not required to achieve induction of disease-regulating T helper cell effector functions, and that pathogen-associated secondary activation signals may facilitate the full differentiation of T helper subsets during limiting presentation of antigenic peptides.


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