HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Birdsall, H. H. Articles by Rossen, R. D. Search for Related Content PubMed PubMed Citation Articles by Birdsall, H. H. Articles by Rossen, R. D.

Monocytes Stimulated by 110-kDa Fibronectin Fragments Suppress Proliferation of Anti-CD3-Activated T Cells¹

Holly H. Birdsall^2,*,,, Wendy J. Porter^*,, JoAnn Trial^*, and Roger D. Rossen^*,,

^* Research Center for AIDS and HIV Infections, Immunology Research Laboratory at the Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX 77030; and Department of Otorhinolaryngology, Department of Immunology, and Department of Medicine at Baylor College of Medicine, Houston, TX 77030

One hundred ten to 120-kDa fragments of fibronectin (FNf), generated by proteases released in the course of tissue injury and inflammation, stimulate monocytes to produce proinflammatory cytokines, promote mononuclear leukocytes (MNL) transendothelial migration, up-regulate monocyte CD11b and CD86 expression, and induce monocyte-derived dendritic cell differentiation. To investigate whether the proinflammatory consequences of FNf are offset by responses that can suppress proliferation of activated T lymphocytes, we investigated the effect of FNf-treated MNL on autologous T lymphocytes induced to proliferate by substrate-immobilized anti-CD3. FNf-stimulated MNL suppressed anti-CD3-induced T cell proliferation through both contact-dependent and contact-independent mechanisms. Contact-independent suppression was mediated, at least in part, by IL-10 and TGF- released by the FNf-stimulated MNL. After 24–48 h exposure to FNf, activated T cells and monocytes formed clusters displaying CD25, CD14, CD3, and CD4 that were not dissociable by chelation of divalent cations. Killing monocytes with L-leucine methyl ester abolished these T cell-monocyte clusters and the ability of the FNf-stimulated MNL to suppress anti-CD3 induced T cell proliferation. Thus, in addition to activating MNL and causing them to migrate to sites of injury, FNf appears to induce suppressor monocytes.

This article has been cited by other articles:

				B. Marom, M. A. Rahat, N. Lahat, L. Weiss-Cerem, A. Kinarty, and H. Bitterman Native and fragmented fibronectin oppositely modulate monocyte secretion of MMP-9 J. Leukoc. Biol., June 1, 2007; 81(6): 1466 - 1476. [Abstract] [Full Text] [PDF]