Journal
JOURNAL OF IMMUNOLOGY
Volume 170, Issue 1, Pages 236-242Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.170.1.236
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Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [R01RR011576] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL052461] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI040114, R01AI033314, R29AI033314, R56AI040114] Funding Source: NIH RePORTER
- NCRR NIH HHS [RR11576] Funding Source: Medline
- NHLBI NIH HHS [HL52461] Funding Source: Medline
- NIAID NIH HHS [AI40114, AI146689, AI33314] Funding Source: Medline
- NINDS NIH HHS [NS18146] Funding Source: Medline
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IL-2 and IL-15 are thought to be important cytokines for T cell-dependent immune responses. Mice deficient in IL-2, IL-Ralpha, and IL-2Rbeta 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-2Rbeta(-/-) 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-2Rbeta.
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