The Journal of Experimental Medicine
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Published online 18 September 2000.
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© The Rockefeller University Press, 0022-1007/2000/9/907/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 6, September 18, 2000 907-912

Brief Definitive Report

Thiol-Mediated Redox Regulation of Intestinal Lamina Propria T Lymphocytes

Bernd Sidoa, Jutta Braunsteinb, Raoul Breitkreutzc, Christian Herfartha, and Stefan C. Meuerb

a Department of Surgery, University of Heidelberg, 69120 Heidelberg, Germany
b Institute of Immunology, University of Heidelberg, 69120 Heidelberg, Germany
c German Cancer Research Center, 69120 Heidelberg, Germany
Institute of Immunology, University of Heidelberg, Im Neuenheimer Feld 305, 69120 Heidelberg, Germany.49-6221-56-599049-6221-56-4000

Intestinal lamina propria T lymphocytes (LP-Ts) have a markedly low proliferative potential both in vivo and in vitro. Here, we have identified that the capacity of antigen-presenting cells to release cysteine upon receptor–ligand interactions represents a critical parameter for proliferation of LP-Ts. The availability of cysteine is limiting for the intracellular production of glutathione, which in turn is essential for cell cycle progression. When cysteine is provided either directly or by addition of the reducing agent 2-mercaptoethanol to cystine-containing culture medium, proliferation of LP-T is fully restored. Importantly, coculture with peripheral blood monocytes that easily take up cystine, reduce cystine, and secrete cysteine also restores reactivity of LP-Ts to T cell receptor/CD3 stimulation. In marked contrast, lamina propria macrophages lack this capacity to elaborate cysteine, and thereby secure physiological unresponsiveness to antigen exposure in the intestinal microenvironment. The well-documented local recruitment of blood monocytes in inflammatory bowel disease (IBD) may thus represent an important parameter underlying hyperresponsiveness of T cells, an essential component of the pathogenesis of IBD.

Key Words: macrophage • monocyte • inflammatory bowel disease • cysteine • glutathione

© 2000 The Rockefeller University Press


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