Journal
CLINICAL IMMUNOLOGY
Volume 229, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2021.108775
Keywords
IL-10; Tonsil; Inflammation; Ras; B cell
Categories
Funding
- National Nature and Science Foundation of China [32090052, 81870706, 31570932, U1801286, 31000713, 31700805]
- Guangdong Provincial Key Laboratory of Regional Immunity and Diseases [2019B030301009]
- Funding of Medical and Health Technology Project of Guangzhou [20171A010042]
- Shenzhen Nanshan District Oversea Research Personnel Initiative Group Fund [LHTD20180007]
- Shenzhen science, technology and innovation committee [KQTD20170331145453160, KQJSCX20180328095619081]
- Longgang District Scientific Research Funds [LGKCYLWS2020046]
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This study investigated the role of Ras activation in down regulating IL-10 expression in tonsillar B cells, finding that B cells from tonsillar tissues with recurrent inflammation showed higher Ras activation, lower IL-10 expression, and higher Bcl2L12 expression than peripheral B cells. Bcl2L12 interacted with Ras activation to inhibit IL-10 expression in tonsillar B cells, which could be restored with inhibition of Bcl2L12.
The pathogenesis of recurrent tonsillitis is to be further investigated. B cell-derived interleukin (IL)-10 plays a critical role in immune regulation. Ras activation plays an important role in cancer and many immune disorders. This study aims to investigate the role of Ras activation in down regulating IL-10 expression in tonsillar B cells. Surgically removed tonsil tissues were collected from patients with recurrent acute tonsillar inflammation; B cells were isolated from the tonsillar tissues by flow cytometry sorting to be analyzed by the Ras-specific enzymelinked immunosorbent assay and pertinent immunological approaches. We found that, compared to peripheral B cells (pBC), B cells isolated from the tonsillar tissues with recurrent inflammation (tBC) showed higher Ras activation, lower IL-10 expression and higher Bcl2L12 expression. Bcl2L12 formed a complex with GAP (GTPase activating protein) to prevent Ras from deactivating. The Ras activation triggered the MAPK/Sp1 pathway to promote the Bcl2L12 expression in B cells. Bcl2L12 prevented the IL-10 expression in tBCs, that was counteracted by inhibition of Ras or the Ras signal transduction pathway. In conclusion, Bcl2L12 interacts with Ras activation to compromise immune tolerance in the tonsils by inhibiting the IL-10 expression in tBCs. Inhibition of Bcl2L12 can restore the IL-10 expression in tBCs.
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