Subversion of B lymphocyte signaling by infectious agents

Abstract

Infectious agents and their hosts interact in a complex manner, involving not only superficially apparent mechanisms, but also the signaling machinery that governs host cells responses. Thus, signaling events, surface molecule expression, and transcriptional control may be affected in various cell types, with profound consequences for the function of individual cells and organ systems. Studies of the biochemistry of cell signaling and cell invasion by infectious agents have begun to detail the interplay between elements of infectious organisms and the host at the molecular level. Consequently, the resulting interferences with lymphocyte signaling may disturb the function of the immune system. In B cells, alterations of immune receptor signaling has implications for human diseases. By affecting the mechanisms of the host's immune defense, this may not only lead to inadequate elimination of an infectious agent, but also to autoimmunity or neoplasia.

Spotlight on the role of hormonal factors in the emergence of autoreactive B-lymphocytes

“…In a genetically susceptible individual, exposure to environmental factors, such as UV irradiation, diet, infectious agents, a stress response, drugs or pollutants, may initiate an autoimmune process [8,259,260]. Hormones may act in conjunction with these factors, and it is reasonable to postulate that environmental estrogens may also modulate the immune system [62].…”

Down-modulation of the antigen receptor by a superantigen for human B cells

“…In B cells, for example, mounting evidence indicates that infectious agents can subvert the cellular transduction machinery [25]. However, the impact of SAgs on the human B cell repertoire in vivo has been difficult to test and the role of SAg proteins in pathogenicity and virulence is not understood.…”

DNA Methylation Alterations in Systemic Lupus Erythematosus

“…Also, transgenic introduction of Epstein-Barr nuclear antigen 1 (EBNA-1) into mouse models induces the production of anti-Sm antibodies [29]. The sequence homology between microorganism and self-components can induce crosslinked reactions [30]. Also, LMP2A can subsert signalling pathways [31].…”