CXCR3型
CD8型
银屑病性关节炎
归巢(生物学)
免疫系统
免疫学
细胞毒性T细胞
T细胞
生物
滑液
CXCL10型
趋化因子受体
CXCL9型
关节炎
癌症研究
医学
趋化因子
病理
骨关节炎
体外
替代医学
生物化学
生态学
作者
Frank Penkava,Martín Del Castillo Velasco-Herrera,Matthew D. Young,Nicole Yager,Lilian Ngozi Nwosu,Arthur G. Pratt,Alicia Lledó Lara,Charlotte Guzzo,Asher Maroof,Lira Mamanova,Suzanne Cole,Mirjana Efremova,Davide Simone,Andrew Filer,Chrysothemis C. Brown,Andrew L. Croxford,John D. Isaacs,Sarah A. Teichmann,Paul Bowness,Sam Behjati,Hussein Al-Mossawi
标识
DOI:10.1038/s41467-020-18513-6
摘要
Psoriatic arthritis (PsA) is a debilitating immune-mediated inflammatory arthritis of unknown pathogenesis commonly affecting patients with skin psoriasis. Here we use complementary single-cell approaches to study leukocytes from PsA joints. Mass cytometry demonstrates a 3-fold expansion of memory CD8 T cells in the joints of PsA patients compared to peripheral blood. Meanwhile, droplet-based and plate-based single-cell RNA sequencing of paired T cell receptor alpha and beta chain sequences show pronounced CD8 T cell clonal expansions within the joints. Transcriptome analyses find these expanded synovial CD8 T cells to express cycling, activation, tissue-homing and tissue residency markers. T cell receptor sequence comparison between patients identifies clonal convergence. Finally, chemokine receptor CXCR3 is upregulated in the expanded synovial CD8 T cells, while two CXCR3 ligands, CXCL9 and CXCL10, are elevated in PsA synovial fluid. Our data thus provide a quantitative molecular insight into the cellular immune landscape of psoriatic arthritis.
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