CD36 has recently been shown to facilitate monocyte Toll-like receptor 2 (TLR2) recognition of lipoteichoic acid (LTA), much like CD14 in TLR4 recognition of lipopolysaccharide. We previously found that bovine gammadelta T cells express CD36 transcripts. Here, we tested whether bovine gammadelta T cells express CD36 protein and if so, whether it functions in a manner similar to the monocyte molecule. CD36 transcripts and internal and cell surface protein could be detected in resting, sorted gammadelta T cells. Phorbol 12-myristate 13-acetate (PMA)/ionomycin treatment increased CD36 transcript levels (detectable at 4 h) and protein expression (internal and cell surface). Increased surface antigen expression was detectable by 24 h and was maximal at 72 h following PMA/ionomycin stimulation. Anti-CD36 monoclonal antibody inhibited increased macrophage-inflammatory protein-1alpha gene expression in gammadelta T cells activated by LTA. In conclusion, gammadelta T cells express CD36, previously thought to be a myeloid and endothelial cell-restricted surface antigen, and it contributes to responses by these cells to microbial LTA.
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http://dx.doi.org/10.1189/jlb.1005616 | DOI Listing |
Exp Dermatol
January 2025
Department of Medicine and Division of Clinical Immunology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
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Medical School, University of Western Australia, Perth, WA, Australia.
Tissue-resident lymphocytes (TRLs) provide a front-line immunological defense mechanism uniquely placed to detect perturbations in tissue homeostasis. The heterogeneous TRL population spans the innate to adaptive immune continuum, with roles during normal physiology in homeostatic maintenance, tissue repair, pathogen detection, and rapid mounting of immune responses. TRLs are especially enriched in the liver, with every TRL subset represented, including liver-resident natural killer cells; tissue-resident memory B cells; conventional tissue-resident memory CD8, CD4, and regulatory T cells; and unconventional gamma-delta, natural killer, and mucosal-associated invariant T cells.
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Laboratory of Host Defenses, Department of Biological Sciences, KAIST, Daejeon 34141, Republic of Korea; KAIST Institute of Health Science and Technology, KAIST, Daejeon 34141, Republic of Korea. Electronic address:
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Laboratory of Inflammation Research, School of Life Science, Handong Global University, Pohang 37554, Republic of Korea.
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November 2024
Department of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, 6200 MD Maastricht, The Netherlands.
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