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Downregulation of CD94/NKG2A Inhibitory Receptor on Decreased γδ T Cells in Patients with Systemic Lupus Erythematosus
Author(s) -
Wang L.,
Kang N.,
Zhou J.,
Guo Y.,
Zhang X.,
Cui L.,
Ba D.,
He W.
Publication year - 2012
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2012.02705.x
Subject(s) - downregulation and upregulation , antigen , immunology , cd69 , pathogenesis , immune system , receptor , systemic lupus erythematosus , stimulation , t cell , medicine , biology , il 2 receptor , disease , endocrinology , gene , biochemistry
γδ T cells are characterized by recognizing conserved endogenous and stress‐induced antigens without antigen presentation. It has been show that γδ T cells play an important role in anti‐tumour/microbe responses, but their function in autoimmune diseases is yet not clear. Here, we reported the quantity and phenotype of peripheral blood γδ T cells from systemic lupus erythematosus (SLE). Both the percentages of γδ T cells in peripheral blood and among CD3 + T cells of patients with SLE were significantly decreased, regardless of disease activity. However, activating marker CD69 and HLA‐DR was upregulated, while inhibiting receptor CD94/NKG2A was downregulated in γδ T cells of patients with SLE. The expression of CD69 is negatively correlated with the quantity of γδ T cells. Moreover, the expression of CD94/NKG2A remained low even with antigen stimulation on those γδ T cells. Our results suggested that the low expression level of CD94/NKG2A upon γδ T cell activation might lead to the over‐activation of γδ T cells in patients with SLE. These findings will be useful in elucidating the roles of γδ T cells in SLE pathogenesis.