| Literature DB >> 25670392 |
Yalei Liu1, Mingming Liu2, Yang Zhang3, Chenxue Qu4, Guizhi Lu5, Youyuan Huang6, Hong Zhang7, Nan Yu8, Shanshan Yuan9, Ying Gao10, Yanming Gao11, Xiaohui Guo12.
Abstract
The pathophysiological mechanism underlying Hashimoto's thyroiditis (HT) is still unclear. Thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) are diagnostic hallmarks of HT. These IgG antibodies regulate the balance of immunologic tolerance and autoimmunity via Fcγ receptors (FcγRs). The aim of our study was to investigate the role of FcγRs in the pathogenesis of HT. The percentage of peripheral blood mononuclear cells (PBMCs) from HT patients bearing FcγRII was significantly lower than that seen in healthy donors, and the mean fluorescence intensity (MFI) value of FcγRII on PBMCs from HT patients was significantly higher. The percentage of PBMCs positive for FcγRIII also was significantly higher in HT patients, and the percentage of B cells bearing FcγRIIB in HT patients was significantly lower than that seen in healthy donors. Our study therefore provides evidence for FcγRs, especially FcγRIIB, being involved in the pathogenesis of HT.Entities:
Keywords: B cells; FcγRIIB; FcγRs; Hashimoto’s thyroiditis
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Year: 2015 PMID: 25670392 DOI: 10.1016/j.cellimm.2015.01.016
Source DB: PubMed Journal: Cell Immunol ISSN: 0008-8749 Impact factor: 4.868