Research Papers: Immunology:
Deficient for endoplasmic reticulum calcium sensors Stim1 and Stim2 affects aberrant antibody affinity maturation in B cells
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Xuhua Mao1, Jianfeng Zhang2, Yue Han3, Chao Luan3, Yu Hu3, Zhimin Hao3, Min Chen3
1 Department of Clinical Laboratory, Yixing People’s Hospital, China
2 Department of Preventive Health Care, the Second Affiliated Hospital of Southeast University, China
3 Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Institute of Dermatology, Chinese Academy of Medical Sciences, China
Min Chen, email:
Keywords: B cells, calcium influx, Stim1, Stim2, antibody affinity, Immunology and Microbiology Section, Immune response, Immunity
Received: June 01, 2016 Accepted: August 13, 2016 Published: August 27, 2016
Antigen specific B cells undergo a process termed affinity maturation in the germinal centers of secondary lymphoid organs where B cells with high affinity receptors are selected to mature into antibody-producing cells or to the memory B cell pool. It is known that B cell antigen receptor (BCR) signaling plays pivotal role in this selection process. Calcium influx is an essential component of BCR signaling. The current report is to determine the effect of calcium influx on antibody affinity maturation. In our studies, mice deficient for both endoplasmic reticulum calciumsensor Stim1 and Stim2 was immunized with T-cell dependent and independent antigens. Antibody affinity was measured by ELISA. We demonstrated that Stim1 &Stim2 deficient B cells exhibit accelerated pace of affinity maturation compared to wild type controls while the overall antibody production was not dramatically impaired to T-independent antigen immunization. In conclusion, calcium influx plays an important role in antibody affinity maturation in humoral immune responses. The knowledge can be used in manipulate humoral immune response for the design of effective vaccines.
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