title: Downregulation of CD94/NKG2A inhibitory receptor on decreased γδ T cells in patients with systemic lupus erythematosus.
abstract: 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.
authors.affiliation: Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: N
authors.initials: N
authors.lastname: Kang
authors.forename: J
authors.initials: J
authors.lastname: Zhou
authors.forename: Y
authors.initials: Y
authors.lastname: Guo
authors.forename: X
authors.initials: X
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Cui
authors.forename: D
authors.initials: D
authors.lastname: Ba
authors.forename: W
authors.initials: W
authors.lastname: He
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D015536:Down-Regulation; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D037181:Lectins, C-Type / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology*; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D010641:Phenotype; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000172:deficiency / Q000276:immunology*; D018709:Statistics, Nonparametric; D055815:Young Adult; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D037181:Lectins, C-Type; D055654:NK Cell Lectin-Like Receptor Subfamily C; D016692:Receptors, Antigen, T-Cell, gamma-delta; D000099192:CD69 Antigens