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IL-2 is a cytokine with multiple and even divergent functions; it has been described as a key cytokine for in vitro T cell proliferation but is also essential for down-regulating T cell responses by inducing activation-induced cell death as well as regulatory T cells. The in vivo analysis of IL-2 function in regulating specific T cell responses has been hampered by the fact that mice deficient in IL-2 or its receptors develop lymphoproliferative diseases and/or autoimmunity. Here we generated chimeric mice harboring both IL-2R-competent and IL-2R-deficient T cells and assessed CD8+ T cell induction, function and maintenance after acute or persistent viral infections. Induction and maintenance of CD8+ T cells were relatively independent of IL-2R signaling during acute/resolved viral infection. In marked contrast, IL-2 was crucial for secondary expansion of memory CD8+ T cells and for the maintenance of virus-specific CD8+ T cells during persistent viral infections. Thus, depending on the chronicity of antigen exposure, IL-2R signaling is either essential or largely dispensable for induction and maintenance of virus-specific CD8+ T cell responses.

Original publication




Journal article


Eur J Immunol

Publication Date





1502 - 1512


Adoptive Transfer, Animals, Antigens, Viral, Bone Marrow Transplantation, CD8-Positive T-Lymphocytes, Chronic Disease, Epitopes, T-Lymphocyte, Glycoproteins, Interferon-gamma, Interleukin-2, Interleukin-2 Receptor alpha Subunit, Interleukin-7 Receptor alpha Subunit, L-Selectin, Lymphocyte Activation, Lymphocytic choriomeningitis virus, Lysosome-Associated Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Peptide Fragments, Receptors, Antigen, T-Cell, Receptors, Interleukin-2, Signal Transduction, Tumor Necrosis Factor-alpha, Viral Proteins, Virus Diseases