The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/7/53/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 1, July 1, 1999 53-64

Original Article

Anergy and Cytokine-Mediated Suppression as Distinct Superantigen-Induced Tolerance Mechanisms in Vivo

Carla Millera, Jack A. Ragheba, and Ronald H. Schwartza

a From the Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-0420

Recombinant-activating gene 2 (RAG-2–/–) T cell receptor–transgenic mice repeatedly injected with the superantigen staphylococcal enterotoxin A entered a tolerant state in which splenic CD4+ T cells produced little interleukin (IL)-2, interferon {gamma}, or IL-4. This state resulted from a combination of both clonal anergy and cytokine-mediated immunosuppression. The anergy persisted for at least 3 wk and could be distinguished from the suppression by a decrease in IL-2 production per cell, a block in the activation of early response kinases, and a failure to be reversed with anti–transforming growth factor (TGF)-β. Full suppression lasted for only 1 wk and involved both IL-10 and TGF-β, but required additional unknown molecules for optimal effect. These experiments show that complex in vivo interactions of multiple peripheral tolerance mechanisms can now be dissected at both the cellular and molecular levels.

Key Words: CD4+ T cell receptor transgenic cells • early response kinase activation • interleukin 2 • interleukin 10 • transforming growth factor β

1used in this paper: AP, alkaline phosphatase; CT, threshold cycle number; ERK, early response kinase; E/R, 50% EHAA plus 50% RPMI 1640; 6-FAM, 6-carboxyfluorescein; MAP, mitogen-activated protein; PCC, pigeon cytochrome c; RAG-2–/–, recombinant activating gene 2 knockout; RT, reverse transcriptase; SEA, staphylococcal enterotoxin A

© 1999 The Rockefeller University Press


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