Role of PIR-B in Autoimmune Glomerulonephritis
PIR-B, an inhibitory receptor expressed on murine B cells and myeloid cells, regulates humoral and cellular immune responses via its constitutive binding to the ligand, MHC class I molecules, on the same cells (cis) or on different cells (trans). Although it has been speculated that PIR-B is importa...
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doaj-2b4720aaf139415ca4c5102d2308de8d2020-11-24T21:24:18ZengHindawi LimitedJournal of Biomedicine and Biotechnology1110-72431110-72512011-01-01201110.1155/2011/275302275302Role of PIR-B in Autoimmune GlomerulonephritisToshiyuki Takai0Akira Nakamura1Shota Endo2Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo, Sendai 980-8575, JapanDepartment of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo, Sendai 980-8575, JapanDepartment of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo, Sendai 980-8575, JapanPIR-B, an inhibitory receptor expressed on murine B cells and myeloid cells, regulates humoral and cellular immune responses via its constitutive binding to the ligand, MHC class I molecules, on the same cells (cis) or on different cells (trans). Although it has been speculated that PIR-B is important for maintaining peripheral tolerance, PIR-B single deficiency does not cause overt autoimmune diseases. Recently, however, the combination of its deficiency with the Fas lpr mutation was found to result in augmented production of autoantibodies such as IgG rheumatoid factor and anti-DNA IgG, leading to glomerulonephritis in mice. Although the precise molecular mechanism for the overall scenario is unclear, PIR-B was found to suppress TLR9-mediated production of naturally autoreactive antibodies by innate B cells or B-1 cells by inhibiting the activation of Bruton's tyrosine kinase. Thus, PIR-B is an important regulator of innate immunity mediated by TLR9 in B-1 cells, which can otherwise provoke autoimmunity when overactivated.http://dx.doi.org/10.1155/2011/275302 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Toshiyuki Takai Akira Nakamura Shota Endo |
spellingShingle |
Toshiyuki Takai Akira Nakamura Shota Endo Role of PIR-B in Autoimmune Glomerulonephritis Journal of Biomedicine and Biotechnology |
author_facet |
Toshiyuki Takai Akira Nakamura Shota Endo |
author_sort |
Toshiyuki Takai |
title |
Role of PIR-B in Autoimmune Glomerulonephritis |
title_short |
Role of PIR-B in Autoimmune Glomerulonephritis |
title_full |
Role of PIR-B in Autoimmune Glomerulonephritis |
title_fullStr |
Role of PIR-B in Autoimmune Glomerulonephritis |
title_full_unstemmed |
Role of PIR-B in Autoimmune Glomerulonephritis |
title_sort |
role of pir-b in autoimmune glomerulonephritis |
publisher |
Hindawi Limited |
series |
Journal of Biomedicine and Biotechnology |
issn |
1110-7243 1110-7251 |
publishDate |
2011-01-01 |
description |
PIR-B, an inhibitory receptor expressed on murine B cells and myeloid cells, regulates humoral and cellular immune responses via its constitutive binding to the ligand, MHC class I molecules, on the same cells (cis) or on different cells (trans). Although it has been speculated that PIR-B is important for maintaining peripheral tolerance, PIR-B single deficiency does not cause overt autoimmune diseases. Recently, however, the combination of its deficiency with the Fas lpr mutation was found to result in augmented production of autoantibodies such as IgG rheumatoid factor and anti-DNA IgG, leading to glomerulonephritis in mice. Although the precise molecular mechanism for the overall scenario is unclear, PIR-B was found to suppress TLR9-mediated production of naturally autoreactive antibodies by innate B cells or B-1 cells by inhibiting the activation of Bruton's tyrosine kinase. Thus, PIR-B is an important regulator of innate immunity mediated by TLR9 in B-1 cells, which can otherwise provoke autoimmunity when overactivated. |
url |
http://dx.doi.org/10.1155/2011/275302 |
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AT toshiyukitakai roleofpirbinautoimmuneglomerulonephritis AT akiranakamura roleofpirbinautoimmuneglomerulonephritis AT shotaendo roleofpirbinautoimmuneglomerulonephritis |
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1725989152018661376 |