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Keratinocytes costimulate naive human t cells via CD2: a potential target to prevent the development of proinflammatory th1 cells in the skin

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Cellular & Molecular Immunology 2020年第4期17卷 380-394页

作者： Christian Orlik Daniel Deibel Johanna Küblbeck Emre Balta Sabina Ganskih Jüri Habicht Beate Niesler Jutta Schröder-Braunstein Knut Schäkel Guido Wabnitz Yvonne Samstag Institute of Immunology Section Molecular ImmunologyHeidelberg UniversityIm Neuenheimer Feld 30569120 HeidelbergGermany Institute of human Genetics Department of Human Molecular Geneticsand nCounter Core FacilityHeidelberg UniversityIm Neuenheimer Feld 36669120 HeidelbergGermany Department of Dermatology Heidelberg UniversityIm Neuenheimer Feld 44069120 HeidelbergGermany

the interplay between keratinocytes and immune cells,especially t cells,plays an important role in the pathogenesis of chronic inflammatory skin *** psoriasis,keratinocytes attract t cells by releasing chemokines,while skin-infiltrating selfreactive t cells secrete proinflammatory cytokines,e.g.,IFN γand IL-17A,that cause epidermal ***,in chronic graftversus-host disease,allogenic IFN γ-producing th1/tc1 and IL-17-producing th17/tc17 cells are recruited by keratinocyte-derived chemokines and accumulate in the ***,whether keratinocytes act as nonprofessional antigen-presenting cells to directly activate naive human t cells in the epidermis remains ***,we demonstrate that under proinflammatory conditions,primary human keratinocytes indeed activate naive human t *** activation required cell contact and costimulatory signaling via CD58/CD2 and CD54/*** t cells costimulated by keratinocytes selectively differentiated into th1 and th17 *** particular,keratinocyte-initiated th1 differentiation was dependent on costimulation through CD58/*** latter molecule initiated StAt1 signaling and IFN γproduction in t *** of t cells by keratinocytes resulting in th1 and th17 differentiation represents a new explanation for the local enrichment of th1 and th17 cells in the skin of patients with a chronic inflammatory skin ***,local interference with t cell–keratinocyte interactions may represent a novel strategy for the treatment of th1 and th17 cell-driven skin diseases.

关键词： keratinocytes inflammatory skin diseases psoriasis human t cells costimulation CD2 LFA-1 nonprofessional antigenpresenting cells th1 cells th17 cells

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Acacetin blocks Kv1.3 channels and inhibits human t cell activation

Acacetin blocks Kv1.3 channels and inhibits human T cell act...

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中国生理学会第24届全国会员代表大会暨生理学学术大会

作者：赵宁董倩付晓幸杜丽丽程翔杜以梅廖玉华华中科技大学同济医学院附属协和医院心内科/离子通道研究室

Backgrounds/Aims:Acacetin,a natural flavonoid compound,has been proven to exert anti-inflammatory and immunomodulatory ***1.3 channels,highly expressed in human t cells,are attractive therapeutic targets to treat inflammatory and immunological *** present study was designed to characterize the inhibition of Kv1.3 channels by Acacetin in human t cells and examine its role in t cell ***:Whole-cell patch-clamp was applied to record the Kv1.3 and KCa currents in human t cells;Western blot was used to detect Kv1.3 expression as well as NFAt1 and NF-κB activity;Fluo-4,CCK-8 and an ELISA kit were used to measure Ca2+influx,proliferation,and IL-2 secretion,***:Acacetin decreased the Kv1.3 current,accelerated the decay rate and negatively shifted thesteady-state inactivation curves in a concentration-dependent *** IC50 values at+40 m V for peak and the current at end of pulse were 21.09±2.75 and 3.63±0.25μmol/L,*** with Acacetin for 24 h significantly inhibited Kv1.3 protein ***,paralleling Kv1.3inhibition,Acacetin also inhibited Ca2+influx,the Ca2+-activated transcription factors NFAt1,NF-κB p65/p50 activity,and proliferation as well as IL-2 *** interfering RNA against Kv1.3 reduced the inhibitory effect of Acacetin on IL-2 ***:Acacetin blocks the Kv1.3 channel and inhibits human t cell *** action most likely contributes to its immunomodulatory and anti-inflammatory actions.

关键词： Acacetin Kv1.3 potassium channel chemical blockade immunomodulatory human t cells

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