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10.3109/08916934.2010.530627

http://scihub22266oqcxt.onion/10.3109/08916934.2010.530627
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C4465387!4465387!21231893
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suck abstract from ncbi


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pmid21231893      Autoimmunity 2011 ; 44 (3): 211-8
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  • SLAMF6-driven co-stimulation of human peripheral T cells is defective in SLE T cells #MMPMID21231893
  • Chatterjee M; Kis-Toth K; Thai TH; Terhorst C; Tsokos GC
  • Autoimmunity 2011[May]; 44 (3): 211-8 PMID21231893show ga
  • The CD28 co-stimulatory pathway is well established for T cell activation. However, there is evidence suggesting the existence of additional co-stimulatory pathways. Here we report that a member of the SLAM superfamily, SLAMF6, or CD352 plays an important role in T cell co-stimulation. Cross-linking of SLAMF6 with anti-CD3 primes human T cell to secrete Th1 cytokines. Among the T cell subsets, CD8+ and CD3+CD4?CD8? cells display the highest Th1 production responses. Engagement of SLAMF6 mobilizes the modulation of the same set of NF-?B-associated genes. Although the expression of SLAMF6 on the surface of T cells from patients with systemic lupus erythematosus (SLE) T cells is comparable to that on the normal T cells, engagement of SLAMF6 results in severely reduced Th1 and IL-2 cytokine production. Our results suggest the existence of an additional co-stimulatory pathway in human T cells, which is defective in SLE T cells.
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