Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 535, Issue -, Pages 99-105Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.11.126
Keywords
CEACAM1; B cells; BCR signaling; Spontaneous proliferation; Lymphoid tissues
Categories
Funding
- Japanese Ministry of Education, Culture, Sports, Science and Technology [22117508, 15K15288, 26221307, 16H05286, 20H03658, 20590737, 24590936, 18K07997]
- Practical Research Project for Rare/Intractable Diseases from the Japan Science and Technology Agency [16eK0109047h0003]
- Japan Agency for Medical Research and Development [16eK0109047h0003]
- Memorial Fund of Nihon Univ. Medical Alumni Association
- TMDU-MRI Collaboration Research Program
- Foundation for Advancement of International Science
- Abbott Japan Allergy Research Award
- Takeda Science Foundation
- Naoki Tsuchida Research Grant
- Japan Foundation for Applied Enzymology
- Grants-in-Aid for Scientific Research [20590737, 18K07997, 16H05286, 26221307, 24590936, 15K15288, 20H03658, 22117508] Funding Source: KAKEN
Ask authors/readers for more resources
Research suggests that CEACAM1 can regulate mature B cell activation mediated by BCR, playing an important role in immune responses.
Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) expressed in T cells may regulate immune responses in the gut. In addition to T cells, B cells are also an important population in the gutassociated lymphoid tissues that orchestrate mucosal homeostasis. However, the role of CEACAM1 in B cells has not been elucidated. We herein analyzed mature B cells to determine the functions of CEACAM1. Flow cytometry revealed high expression of CEACAM1 on B cells in secondary lymphoid tissues. Cytokine production induced by activation of B cell receptor (BCR) signaling was suppressed by CEACAM1 signaling in contrast to that associated with either Toll-like receptor 4 or CD40 signaling. Confocal microscopy revealed co-localization of CEACAM1 and BCR when activated with anti-Ig mu F(ab')(2) fragment. Overexpression of CEACAM1 in a murine B cell line, A20, resulted in reduced expressions of activation surface markers with decreased Ca2+ influx after BCR signal activation. Overexpression of CEACAM1 suppressed BCR signal cascade in A20 cells in association with decreased spontaneous proliferation. Our results suggest that CEACAM1 can regulate BCR-mediated mature B cell activation in lymphoid tissues. Therefore, further studies of this molecule may lead to greater insights into the mechanisms of immune responses within peripheral tissues and the potential treatment of inflammatory diseases. (C) 2020 The Authors. Published by Elsevier Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available