Kelch-like protein 14 promotes B-1a but suppresses B-1b cell developmentстатья из журнала
Аннотация: B-1 cells are innate-like B-cell population and produce natural antibodies that contribute to the first line of host defense. There are two subsets of B-1 cells: B-1a and B-1b. B-1a cells are the main producer of poly-reactive and autoreactive natural IgM antibodies, whereas B-1b cells can respond specifically to T-cell-independent antigens. Despite the functional significance of B-1a and B-1b cells, little information is available about what regulates the development of these two subsets. We found that Kelch-like protein 14 (KLHL14) was expressed at high levels in B cells but only at low levels in a few non-lymphoid tissues. Although mice lacking KLHL14 died right after birth, the heterozygotes developed normally with no gross abnormalities by appearance. B-cell development in the bone marrow and maturation and activation in the spleen were not affected in the heterozygous mice. However, the number of peritoneal B-1a cells was significantly reduced while B-1b cells were increased in Klhl14 heterozygous mice compared with wild-type (WT) mice. Consistently, Rag1-/- mice reconstituted with Klhl14-/- fetal liver cells had a more severe reduction of B-1a and an increase of B-1b cells in the peritoneal cavity. KLHL14 did not affect the turnover or apoptosis of B-1a and B-1b cells in vivo. Moreover, Klhl14-/- fetal liver contained a similar proportion and absolute numbers of the B-1 progenitor cells as did WT fetal liver. These results suggest that KLHL14 promotes B-1a development in mice.
Год издания: 2018
Авторы: Shuyin Li, Jun Liu, Min Qing, Tomokatsu Ikawa, Shoya Yasuda, Yang Yang, Yan-Qing Wang, Takeshi Tsubata, Yaofeng Zhao, Ji‐Yang Wang
Издательство: Oxford University Press
Источник: International Immunology
Ключевые слова: Proteoglycans and glycosaminoglycans research, Polysaccharides and Plant Cell Walls, Glycosylation and Glycoproteins Research
Другие ссылки: International Immunology (PDF)
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PubMed (HTML)
International Immunology (HTML)
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Открытый доступ: closed
Том: 30
Выпуск: 7
Страницы: 311–318