Monocytes stimulated by 110-kDa fibronectin fragments suppress proliferation of anti-CD3-activated T cells

Holly H. Birdsall, Wendy J. Porter, Jo Ann Trial, Roger D. Rossen

Research output: Contribution to journalArticlepeer-review

10 Scopus citations

Abstract

One hundred ten to 120-kDa fragments of flbronectin (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 FN-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-β 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.

Original languageEnglish (US)
Pages (from-to)3347-3353
Number of pages7
JournalJournal of Immunology
Volume175
Issue number5
DOIs
StatePublished - Sep 1 2005

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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