Document Detail

Role of thrombospondin-1 in T cell response to ocular pigment epithelial cells.
MedLine Citation:
PMID:  17513749     Owner:  NLM     Status:  MEDLINE    
Ocular pigment epithelium (PE) cells promote the generation of T regulators (PE-induced Treg cells). Moreover, T cells exposed to PE acquire the capacity to suppress the activation of bystander T cells via TGFbeta. Membrane-bound TGFbeta on iris PE cells interacts with TGFbeta receptors on T cells, leading to the conversion of T cells to CD8(+) Treg cells via a cell contact-dependent mechanism. Conversely, soluble forms of TGFbeta produced by retinal PE cells can convert CD4(+) T cells into Treg cells in a manner that is independent of cell contact. In this study, we looked at the expression of immunoregulatory factors (TGFbeta, thrombospondins, CD59, IL-1 receptor antagonist, etc.) in PE cells as identified via an oligonucleotide microarray. Several thrombospondin-binding molecules were detected, and thus we focused subsequent analyses on thrombospondins. Via the conversion of latent TGFbeta to an active form that appears to be mediated by thrombospondin 1 (TSP-1), cultured iris PE and retinal PE cells induce a PE-induced Treg cell fate. After conversion, both ocular PE and PE-induced Treg cells express TSP-1. Regulatory T cell generation was amplified when the T cells also expressed TSP-1. In addition, PE-induced Treg cells significantly suppressed activation of bystander T cells via TSP-1. These results strongly suggest that the ability of ocular PE and PE-induced Treg cells to suppress bystander T cells depends on their capacity to produce TSP-1. Thus, intraocular TSP-1 produced by both ocular parenchymal cells and regulatory T cells is essential for immune regulation in the eye.
Yuri Futagami; Sunao Sugita; Jose Vega; Kazuhiro Ishida; Hiroshi Takase; Kazuichi Maruyama; Hiroyuki Aburatani; Manabu Mochizuki
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  178     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2007-05-21     Completed Date:  2007-07-12     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6994-7005     Citation Subset:  AIM; IM    
Department of Ophthalmology and Visual Science, Tokyo Medical and Dental University Graduate School of Medicine, Tokyo, Japan.
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MeSH Terms
Amino Acid Sequence
Bystander Effect / immunology
Cells, Cultured
Immunologic Factors / biosynthesis,  genetics,  physiology
Lymphocyte Activation / genetics,  immunology
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Transgenic
Molecular Sequence Data
Organ Specificity / genetics,  immunology
Pigment Epithelium of Eye / cytology,  immunology*,  metabolism*
T-Lymphocyte Subsets / immunology*,  metabolism*
T-Lymphocytes, Regulatory / cytology,  immunology,  metabolism
Thrombospondin 1 / biosynthesis,  deficiency,  genetics,  physiology*
Transforming Growth Factor beta / biosynthesis
Up-Regulation / genetics,  immunology
Grant Support
Reg. No./Substance:
0/Immunologic Factors; 0/Thrombospondin 1; 0/Transforming Growth Factor beta

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