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Activated T Lymphocytes Regulate Hyaluronan Binding to Monocyte CD44 Via Production of IL-2 and IFN-¹

Department of Medicine, Division of Rheumatology, Allergy and Clinical Immunology, Department of Immunology, and Duke University Arthritis Center, Duke University Medical Center, Durham, NC 27710

Interactions of the cell surface proteoglycan CD44 with the extracellular matrix glycosaminoglycan hyaluronan (HA) are important during inflammatory immune responses. Our previous studies indicated that monocyte HA binding could be induced by TNF-. Moreover, monocyte HA binding could be markedly up-regulated by culturing PBMC with anti-CD3 (TCR complex) mAbs. The present study was undertaken to identify soluble factors and/or cell surface molecules of activated T lymphocytes that might regulate HA binding to monocytes. Abs to IL-1, IL-1, IL-2, IL-3, IL-10, IL-15, GM-CSF, IFN-, and TNF- were tested for their effects on anti-CD3 mAb-, Con A-, and PMA/ionomycin-mediated monocyte HA binding in PBMC cultures. Anti-TNF-, anti-IL-2, and anti-IFN- Abs, when added together to PBMC cultures, completely blocked Con A- and partially blocked anti-CD3- and PMA/ionomycin-induced monocyte HA binding. Furthermore, when added together to PBMC cultures, IL-2 and TNF- induced high levels of monocyte HA binding. Likewise, IFN- augmented TNF--induced monocyte HA binding. To investigate the role of T cell-monocyte direct contact in induction of monocyte HA binding, we studied PMA/ionomycin-activated, paraformaldehyde-fixed CD4⁺ T cells in these assays. Fixed, PMA/ionomycin-activated CD4⁺ T lymphocytes induced monocyte HA binding, but direct T cell-monocyte contact was not required. Moreover, anti-IFN- and anti-TNF- Abs blocked fixed PMA/ionomycin-activated CD4⁺ T cell-induced monocyte HA binding. Taken together, these studies indicate roles for soluble T lymphocyte-derived factor(s), such as IL-2 and IFN-, and a role for monocyte-derived TNF- in Con A-, TCR complex-, and PMA/ionomycin-induced HA binding to monocyte CD44.

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