Heat-stressed CD4+ T lymphocytes: Differential modulations of adhesiveness to extracellular matrix glycoproteins, proliferative responses and tumour necrosis factor-α secretion

R. Hershkoviz, R. Alon, Y. A. Mekori, D. Gilat, L. Cahalon, A. Miller, O. Lider

Research output: Contribution to journalArticlepeer-review

Abstract

Although cells of the immune system often function under feverish conditions, the effects of elevated temperatures on T cells have not been fully elucidated. Herein, the effects of a 1-hr exposure to 41° of CD4+ human T cell were studied. Heat-shock treatment of activated CD4+ T cells reduced their adhesion to fibronectin and laminin, the major adhesive glycoproteins of the extracellular matrix (ECM) by 25-40%. This decrease was partially due to a minor decrease in the surface expression of β1 integrins, which specifically interact with fibronectin and laminin. In contrast, the capacities of heat-stressed T cells to proliferate and to secrete tumour necrosis factor-α (TNF-α) were increased upon cell activation. In vivo, heat-treated antigen-primed murine T cells, injected directly into the antigen challenging site, induced a more severe delayed-type hypersensitivity (DTH) response than those not exposed to elevated temperatures. In contrast, the same heat-treated cells inoculated intravenously did not induce DTH, suggesting that these cells were impaired with respect to penetration of blood vessel walls. Thus, the effects of heat shock on key cellular functions are expressed in different manners: T-cell-ECM adhesiveness and subsequent extravasation are impaired, whereas their abilities to proliferate and to secrete TNF-α are augmented.

Original languageEnglish
Pages (from-to)241-247
Number of pages7
JournalImmunology
Volume79
Issue number2
StatePublished - 1993
Externally publishedYes

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