Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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

DOI

10.1002/eji.200637023

Type

Journal article

Journal

Eur J Immunol

Publication Date

06/2007

Volume

37

Pages

1502 - 1512

Keywords

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