International Immunology Advance Access originally published online on March 15, 2006
International Immunology 2006 18(4):565-572; doi:10.1093/intimm/dxh398
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Quantitative assessment concerning the contribution of IL-2Rß for superantigen-mediated T cell responses in vivo
Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, PO Box 016960, Miami, FL 33101, USA
Present address: Division of Immunology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA
Correspondence to: T. Malek; E-mail: tmalek{at}med.miami.edu
IL-2- and IL-2R-deficient mice readily develop T cell-dependent immune responses in vivo, but the relevance of this finding is complicated by severe concurrent autoimmunity. Furthermore, the detection of such responses does not address whether under normal circumstances IL-2 dominates T cell immunity. In the present report, we investigated the extent IL-2-independent T cell growth is mediated by other cytokines in the IL-2 family and compared such responses to those generated by IL-2/IL-2R-sufficient T cells. T cell expansion and contraction to the superantigen staphylococcal enterotoxin A (SEA) by autoimmune-free IL-2Rß–/– CD4 and CD8 T cells were comparable to normal control mice, although their CD8+ T cells did not optimally develop into IFN
-producing effector cells. The proliferation by these IL-2Rß-deficient T cells in vivo was independent of IL-2, IL-4 and IL-15 and not blocked by mAbs to the common chain. However, in co-adoptive transfer experiments, wild-type T cells exhibited somewhat more extensive proliferation than IL-2Rß-deficient T cells to SEA and this difference was almost entirely accounted for by CD8+ T cells. Collectively, these data indicate that substantial T cell proliferation occurs in the absence of responsiveness to cytokines in the IL-2 family, although maximal T cell proliferation and development of IFN-producing effector CD8+ T cells depend upon IL-2Rß.
Keywords: cytokines, cytokine receptors, cell proliferation, superantigen, T cells
* These authors contributed equally to this work.
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