title: PD-1/PD-L1 expression on CD(4+) T cells and myeloid DCs correlates with the immune pathogenesis of atrial fibrillation.
abstract: Although immuno-inflammatory response contributes to pathogenesis of AF, molecular and cellular mechanism in this process remains poorly understood. Recently, increasing evidence suggests that Programmed death-1 (PD-1)/PD-1 ligand (PD-L) pathway may be a potential pathway participating in AF pathogenesis. In this study, we detected the PD-1 and PD-L1, 2 expression on peripheral blood function cells by flow cytometry in 91 atrial fibrillation (AF) patients and 35 healthy volunteers. The expression of PD-1 on CD(4+) T cells and PD-L1 on myeloid dendritic cells (mDCs) in AF patients is significantly down-regulated compared with healthy volunteers. In addition, the extent of PD-1/PD-L1 down-regulation is closely related with AF burden. More importantly, Allogeneic mixed leukocyte reactions (MLR) shows that the mDCs PD-L1 down-regulation is associated with increased T cell (CD(4+) and CD(8+)) proliferation, increased type 1 effector cytokines (IL-2 and IFN-γ) secretion, and decreased type 2 effector cytokine (IL-10) secretion. Then, PD-L1 up-regulation by the stimulation of IFN-α can significantly convert this representation. Collectively, our report suggest that T(CD(4+))/mDCs-associated PD-1/PD-L1 pathway plays a key role in AF immune regulation. PD-1/PD-L1 down-regulation in AF patients promotes T cells function and may contribute to AF pathogenesis.
authors: Department of Cardiology of Tangdu Hospital, Fourth Military Medical University, Xi'an, China.|Department of Cardiology of PLA 161 Hospital, Wuhan, China.
authors: Li
authors: L
authors: Liu
authors: Department of Cardiology of Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
authors: Qiangsun
authors: Q
authors: Zheng
authors: Department of Cardiology of Tangdu Hospital, Fourth Military Medical University, Xi'an, China.
authors: Jun
authors: J
authors: Lee
authors: Department of Cardiology of PLA 161 Hospital, Wuhan, China.
authors: Zhiqiang
authors: Z
authors: Ma
authors: Department of Cardiology of PLA 161 Hospital, Wuhan, China.
authors: Qiming
authors: Q
authors: Zhu
authors: Department of Cardiology of PLA 161 Hospital, Wuhan, China.
authors: Zhiquan
authors: Z
authors: Wang
mesh_terms: D000368:Aged; D001281:Atrial Fibrillation / Q000276:immunology* / Q000378:metabolism; D060890:B7-H1 Antigen / Q000276:immunology* / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D049109:Cell Proliferation; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000276:immunology* / Q000378:metabolism; D015536:Down-Regulation / Q000276:immunology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology / Q000378:metabolism; D016753:Interleukin-10 / Q000276:immunology / Q000378:metabolism; D007376:Interleukin-2 / Q000276:immunology / Q000378:metabolism; D007959:Lymphocyte Culture Test, Mixed; D008297:Male; D008875:Middle Aged; D022423:Myeloid Cells / Q000276:immunology* / Q000378:metabolism; D061026:Programmed Cell Death 1 Receptor / Q000276:immunology* / Q000378:metabolism
chemical_list: D060890:B7-H1 Antigen; C423236:CD274 protein, human; D007376:Interleukin-2; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor; D016753:Interleukin-10; D007371:Interferon-gamma
keywords: Programmed death-1; atrial fibrillation; myloid dendritic cell; programmed death-ligand 1