Thrombospondin-1 Derived from APCs Regulates Their Capacity for Allosensitization

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Thrombospondin-1 Derived from APCs Regulates Their Capacity for Allosensitization

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Title: Thrombospondin-1 Derived from APCs Regulates Their Capacity for Allosensitization
Author: Saban, D. R.; Bock, F.; Chauhan, Sunil Kumar; Masli, S.; Dana, Reza

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Citation: Saban, D. R., F. Bock, S. K. Chauhan, S. Masli, and R. Dana. 2010. “Thrombospondin-1 Derived from APCs Regulates Their Capacity for Allosensitization.” The Journal of Immunology 185 (8) (September 15): 4691–4697. doi:10.4049/jimmunol.1001133.
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Abstract: Thrombospondin (TSP)-1 is a matricellular glycoprotein with immunoregulatory properties, which include inhibition of APC function. We show in transplantation that TSP-1 inhibits T cell allosensitization and consequently suppresses immune rejection. This was revealed by comparing wild-type (WT) versus TSP-1 null allografts in corneal transplantation, as the cornea is a rich source of TSP-1. Compared with only 50% of rejected WT allografts, nearly all TSP-1 null allografts succumbed to rejection. This effect was reflected by donor-derived APCs, which exhibited a distinctively greater capacity for allosensitization in transplanted hosts. Corroborated in MLRs, greater proliferation levels and robust IFN-γ (but not IL-10)–positive T cells resulted from stimulation by TSP-1 null APCs relative to WT ones. Moreover, enhanced expression of MHC class II and B7 maturation markers were detected on TSP-1 null APCs during inflammation. Increased expression of CCR7 was further matched by enhanced lymph node migration of TSP-1 null APCs posttransplantation. We therefore conclude that APC-derived TSP-1 suppresses their capacity to allosensitize T cells, and this regulation stems from their resistance to taking on a mature form. Future strategies targeting APCs for TSP-1 upregulation may thus be effective in promoting allograft survival.
Published Version: doi:10.4049/jimmunol.1001133
Other Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3090006/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:34787800
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