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Gallium arsenide augments antigen processing by peritoneal macrophages for CD4+ helper T cell stimulation.

作者信息

Hartmann C B, McCoy K L

机构信息

Department of Microbiology and Immunology, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298, USA.

出版信息

Toxicol Appl Pharmacol. 1996 Dec;141(2):365-72. doi: 10.1006/taap.1996.0301.

DOI:10.1006/taap.1996.0301
PMID:8975760
Abstract

Gallium arsenide (GaAs) suppresses numerous immunologic functions of leukocytes at distal locations from the exposure site. The effect of direct GaAs exposure on peritoneal cells was examined by i.p. administration of the chemical. No alteration in the frequency of various cell lineages, including macrophages, B cells, CD4+ and CD8+ T cells, and granulocytes, occurred within the peritoneal population from GaAs-exposed mice. The ability of macrophages to function as antigen-presenting cells (APC) by processing a panel of soluble protein antigens was investigated by the stimulation of antigen-specific helper T cell hybridomas to secrete interleukin-2. On a per cell basis, GaAs-exposed macrophages were more efficient than vehicle control cells in activating the T cells with all native antigens examined. GaAs exposure increased the expression of major histocompatibility complex class II molecules, which are recognized by these T cells, on the surface of macrophages. However, the level of T cell activation with peptide fragments of the antigens, which do not require processing, was not enhanced with GaAs-exposed cells as APC. In contrast, the capability of latex bead-exposed macrophages to function as APC was comparable to that of vehicle control cells, suggesting that GaAs modulatory effects were not merely due to phagocytosis of particles. These findings suggest that direct GaAs exposure augments antigen processing, but not presentation, by macrophages perhaps by activating the cells, which may contribute to the immunotoxicity and inflammatory reaction caused by respiratory exposure to GaAs.

摘要

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