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*Substance via MeSH
Medline Plus Health Information
*Immunization
The Journal of Immunology, 2003, 170: 236-242.
Copyright © 2003 by The American Association of Immunologists

Efficient Induction of Primary and Secondary T Cell-Dependent Immune Responses In Vivo in the Absence of Functional IL-2 and IL-15 Receptors1

Aixin Yu*, Jiehao Zhou{dagger}, Norman Marten{dagger}, Cornelia C. Bergmann{dagger},{ddagger}, Michele Mammolenti*, Robert B. Levy* and Thomas R. Malek2,*

* Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, FL 33101; and Departments of {dagger} Pathology and {ddagger} Neurology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033

IL-2 and IL-15 are thought to be important cytokines for T cell-dependent immune responses. Mice deficient in IL-2, IL-2R{alpha}, and IL-2R{beta} are each characterized by a rapid lethal autoimmune lymphoproliferative disorder that complicates their use in studies aimed at investigating the role of these cytokines and receptors for immune responses in vivo. We have previously characterized a novel transgenic (Tg) mouse on the IL-2R{beta}-/- genetic background (Tg-/- mice) that lacks autoimmune disease but still contains peripheral T cells that are nonresponsive to IL-2 and IL-15. In the present study, these mice were used to investigate the extent by which IL-2 and IL-15 are essential for T cell immunity in vivo. Tg-/- mice generated near normal primary and secondary Ab responses to OVA, readily mounted first and second set allogeneic skin graft rejection responses, and developed primary and recall CD8 T cell responses to vaccinia virus. However, Tg-/- mice generated a slightly lower level of IgG2a Abs to OVA, exhibited a somewhat delayed first set skin graft rejection response with lower allo-specific CTL, and developed a significantly lower number of IFN-{gamma}-producing vaccinia-specific CD8+ T cells. Thus, although T effector function is somewhat impaired, T cell immunity is largely functional in the absence of IL-2- and IL-15-induced signaling through IL-2R{beta}.




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