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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Low level exposure to inorganic mercury interferes with B cell receptor signaling in transitional type 1 B cells.

Authors: Gill, R; McCabe Jr, M J; Rosenspire, A J

Published In Toxicol Appl Pharmacol, (2017 Sep 01)

Abstract: Mercury (Hg) has been implicated as a factor contributing to autoimmune disease in animal models and humans. However the mechanism by which this occurs has remained elusive. Since the discovery of B cells it has been appreciated by immunologists that during the normal course of B cell development, some immature B cells must be generated that produce immunoglobulin reactive to self-antigens (auto-antibodies). However in the course of normal development, the vast majority of immature auto-reactive B cells are prevented from maturing by processes collectively known as tolerance. Autoimmune disease arises when these mechanisms of tolerance are disrupted. In the B cell compartment, it is firmly established that tolerance depends in part upon negative selection of self-reactive immature (transitional type 1) B cells. In these cells negative selection depends upon signals generated by the B Cell Receptor (BCR), in the sense that those T1 B cells who's BCRs most strongly bind to, and so generate the strongest signals to self-antigens are neutralized. In this report we have utilized multicolor phosphoflow cytometry to show that in immature T1 B cells Hg attenuates signal generation by the BCR through mechanisms that may involve Lyn, a key tyrosine kinase in the BCR signal transduction pathway. We suggest that exposure to low, environmentally relevant levels of Hg, disrupts tolerance by interfering with BCR signaling in immature B cells, potentially leading to the appearance of mature auto-reactive B cells which have the ability to contribute to auto-immune disease.

PubMed ID: 28668464 Exiting the NIEHS site

MeSH Terms: Animals; B-Lymphocytes/drug effects; B-Lymphocytes/metabolism*; Cell Line; Cell Membrane/drug effects; Cell Membrane/metabolism; Female; Immunoglobulins/metabolism; Immunohistochemistry; Lymphocytes/drug effects; MAP Kinase Signaling System/drug effects; Mercury Compounds/toxicity*; Mice; Mice, Inbred BALB C; Receptors, Antigen, B-Cell/drug effects*; Receptors, Antigen, B-Cell/metabolism*; Signal Transduction/drug effects*; Spleen/cytology

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