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Signal regulatory protein α regulates the homeostasis of T lymphocytes in the spleen.
Gunma University.
Gunma University.
Gunma University.
Gunma University.
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2011 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 187, no 1, 291-297 p.Article in journal (Refereed) Published
Abstract [en]

The molecular basis for formation of lymphoid follicle and its homeostasis in the secondary lymphoid organs remains unclear. Signal regulatory protein α (SIRPα), an Ig superfamily protein that is predominantly expressed in dendritic cells or macrophages, mediates cell-cell signaling by interacting with CD47, another Ig superfamily protein. In this study, we show that the size of the T cell zone as well as the number of CD4(+) T cells were markedly reduced in the spleen of mice bearing a mutant (MT) SIRPα that lacks the cytoplasmic region compared with those of wild-type mice. In addition, the expression of CCL19 and CCL21, as well as of IL-7, which are thought to be important for development or homeostasis of the T cell zone, was markedly decreased in the spleen of SIRPα MT mice. By the use of bone marrow chimera, we found that hematopoietic SIRPα is important for development of the T cell zone as well as the expression of CCL19 and CCL21 in the spleen. The expression of lymphotoxin and its receptor, lymphotoxin β receptor, as well as the in vivo response to lymphotoxin β receptor stimulation were also decreased in the spleen of SIRPα MT mice. CD47-deficient mice also manifested phenotypes similar to SIRPα MT mice. These data suggest that SIRPα as well as its ligand CD47 are thus essential for steady-state homeostasis of T cells in the spleen.

Place, publisher, year, edition, pages
American Association of Immunologists , 2011. Vol. 187, no 1, 291-297 p.
National Category
Immunology in the medical area
Identifiers
URN: urn:nbn:se:umu:diva-54529DOI: 10.4049/jimmunol.1100528PubMedID: 21632712OAI: oai:DiVA.org:umu-54529DiVA: diva2:524098
Available from: 2012-04-27 Created: 2012-04-27 Last updated: 2017-12-07Bibliographically approved

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CiteExportLink to record
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  • apa
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