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| 1 | Keratinocytes costimulate naive human T cells via CD2: a potential target to prevent the development of proinflammatory Th1 cells in the skin显示文摘The interplay between keratinocytes and immune cells,especially T cells,plays an important role in the pathogenesis of chronic inflammatory skin diseases.During 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 hyperplasia.Similarly,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 skin.However,whether keratinocytes act as nonprofessional antigen-presenting cells to directly activate naive human T cells in the epidermis remains unknown.Here,we demonstrate that under proinflammatory conditions,primary human keratinocytes indeed activate naive human T cells.This activation required cell contact and costimulatory signaling via CD58/CD2 and CD54/LFA-1.Naive T cells costimulated by keratinocytes selectively differentiated into Th1 and Th17 cells.In particular,keratinocyte-initiated Th1 differentiation was dependent on costimulation through CD58/CD2.The latter molecule initiated STAT1 signaling and IFN γproduction in T cells.Costimulation 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 disease.Consequently,local interference with T cell–keratinocyte interactions may represent a novel strategy for the treatment of Th1 and Th17 cell-driven skin diseases. | Christian Orlik Daniel Deibel Johanna Küblbeck Emre Balta Sabina Ganskih Jüri Habicht Beate Niesler Jutta Schröder-Braunstein Knut Schäkel Guido Wabnitz Yvonne Samstag | 2020 | Cellular & Molecular Immunology2020，17，4： | 4 |
| 2 | Functional analysis of bispecific antibody (EpCAMxCD3)-mediated T-lymphocyte and cancer cell interaction by single-cell force spectroscopy显示文摘 | Hoffmann S C Wabnitz G H Samstag Y | | 0，，09： | 1 |
| 3 | Actin cytoskeletal dynamics in T lymphocyte activation and migration显示文摘 | Samstag Y Eibert SM Klemke M | 2003 | J Leukoc Biol2003，73，1： | 1 |
| 4 | Dephosphorylation of serine 3 regulates nuclear translocation of cofilin显示文摘 | Nebl G Meuer S C Samstag Y | 1996 | J Biol Chem1996，271，26： | 1 |
| 5 | Ectopic expression of L - plastin in humantumor cells : diagnostic and therapeutic implications 显示文摘 | Samstag Y Klemke M | 2007 | Advancesin Enzyme Regulation2007，47，： | 1 |
| 6 | Ras initiates phosphatidyl-inositol-3-kinase(PI3K)/PKB mediated signalling pathways in untransformed human peripheral blood T lymphocytes显示文摘 | Samstag Y Nebl G | 2005 | Adv Enzyme Regul2005，45，9： | 1 |
| 7 | Ectopic expression of L - plastin in human tumor cells:Diagnostic and therapeutic implica- tions 显示文摘 | Samstag Y Klemke M | 2007 | Advances in Enzyme Regulation2007，47，4： | 1 |
| 8 | Dephosphorylation of serine 3 regulates nuclear translocation of cofilin显示文摘 | Nebl G Meuer S C Samstag Y | 1996 | J Biol Chem1996，271，26： | 1 |
| 9 | Dephesphorylation of sefine 3 regulates nuclear translocation of cofllin 显示文摘 | Nebl G Meue SC Samstag Y | 1996 | J Biol Chem1996，271，26： | 1 |
| 10 | Toxic shock syndrome toxin- 1-mediated toxicity inhibited by neutralizing antibodies late in the course of continual in vivo and in vitro exposure 显示文摘 | Stich N Model N Samstag A | 2014 | Toxins (Basel)2014，6，6： | 1 |
| 11 | Dephosphorylation of serine 3 regulates nuclear translocation of cofilin显示文摘 | Nebl G Meuer S C Samstag Y | 1996 | J Biol Chem1996，271，26： | 1 |
| 12 | Patient Risk Factors for Pressure Ulcers During Cardiac Surgery显示文摘 | Linda J. Lewicki Lorraine Mion Karen G. Splane Doris Samstag Michelle Secic | 1997 | AORN Journal1997，，5： | 1 |
| 13 | Bacterial carriage on the finger-nails of or nurses显示文摘 | Wynd CA Samstag DE Lapp AM | 1994 | AORN J1994，60，5： | 1 |
| 14 | JCB:细胞核内钙信号可改变T细胞应答,有助开发免疫抑制疗法显示文摘组成免疫系统的免疫细胞可以区分“自己”和“非己”的蛋白分子。比如,如果我们暴露于细菌或病毒等病原体,而这些病原体表面带有外来分子,机体就会做出免疫应答。相比之下,免疫细胞会对机体自身的分子产生耐受。 | Sara Monaco Beate Jahraus Yvonne Samstag Hilmar Bading | 2017 | 现代生物医学进展2017，17，8： | 0 |
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