Browsing by Subject "γδ T cell"

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    γδ T cells in Skin Inflammation
    (Begell House, 2022) Zhang, Wenwu; Pajulas, Abigail; Kaplan, Mark H.; Microbiology and Immunology, School of Medicine
    Gamma delta (γδ) T cells are a subset of T lymphocytes that express T cell receptor γ and δ chains and display structural and functional heterogeneity. γδ T cells are typically of low abundance in the body and account for 1–5% of the blood lymphocytes and peripheral lymphoid tissues. As a bridge between innate and adaptive immunity, γδ T cells are uniquely poised to rapidly respond to stimulation and can regulate immune responses in peripheral tissues. The dendritic epidermal T cells (DETCs) in the skin epidermis can secrete growth factors to regulate skin homeostasis and re-epithelization and release inflammatory factors to mediate wound healing during skin inflammatory responses. Dermal γδ T cells can regulate the inflammatory process by producing IL-17 and other cytokines or chemokines. Here, we offer a review of the immune functions of γδ T cells, intending to understand their role in regulating skin barrier integrity and skin wound healing, which may be crucial for the development of novel therapeutics in skin diseases like atopic dermatitis and psoriasis.
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    γδ T cells suppress Plasmodium falciparum blood stage infection by direct killing and phagocytosis
    (Springer Nature, 2021) Junqueira, Caroline; Polidoro, Rafael; Castro, Guilherme; Absalon, Sabrina; Liang, Zhitao; Santara, Sumit Sen; Crespo, Ângela; Pereira, Dhelio B.; Gazzinelli, Ricardo T.; Dvorin, Jeffrey D.; Lieberman, Judy; Pharmacology and Toxicology, School of Medicine
    Activated Vγδ9Vδ2 (γδ2) T lymphocytes that sense parasite-produced phosphoantigens are expanded in Plasmodium falciparum-infected patients. Although previous studies suggested that γδ2 T cells help control erythrocytic malaria, whether γδ2 T cells recognize infected red blood cells (iRBCs) was uncertain. Here we show that iRBCs stained for the phosphoantigen sensor, butyrophilin 3A1 (BTN3A1). γδ2 T cells formed immune synapses and lysed iRBCs in a contact, phosphoantigen, BTN3A1 and degranulation-dependent manner, killing intracellular parasites. Granulysin released into the synapse lysed iRBCs and delivered death-inducing granzymes to the parasite. All intra-erythrocytic parasites were susceptible, but schizonts were most sensitive. A second protective γδ2 T cell mechanism was identified. In the presence of patient serum, γδ2 T cells phagocytosed and degraded opsonized iRBCs in a CD16-dependent manner, decreasing parasite multiplication. Thus, γδ2 T cells have two ways to control blood stage malaria – γδT cell antigen receptor (TCR)-mediated degranulation and phagocytosis of antibody-coated iRBCs.