CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperatively

Trends Immunol. 2005 Apr;26(4):180-5. doi: 10.1016/j.it.2005.02.005.

Abstract

IgG1 functions to neutralize and clear foreign antigens, such as extracellular bacteria. Therefore, it is important to understand the multiple mechanisms by which the level of IgG1) is regulated to maintain immune system and host homeostasis. Recent data show that the level of IgG1 produced by a B cell is increased following CD86 and beta2-adrenergic receptor (beta2AR) stimulation, through increased expression of the transcription factor Oct-2 and its coactivator OCA-B (Oct coactivator from B cells), respectively. This finding suggests that signaling pathways that are activated by an immunoreceptor (CD86) and a neuroreceptor (beta2AR) converge to regulate the IgG1 response.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Antigens, CD / metabolism*
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism*
  • B7-2 Antigen
  • Humans
  • Immunoglobulin G / biosynthesis
  • Membrane Glycoproteins / metabolism*
  • Mice
  • Models, Immunological
  • Neuroimmunomodulation
  • Receptors, Adrenergic, beta-2 / metabolism*
  • Signal Transduction

Substances

  • Antigens, CD
  • B7-2 Antigen
  • CD86 protein, human
  • Cd86 protein, mouse
  • Immunoglobulin G
  • Membrane Glycoproteins
  • Receptors, Adrenergic, beta-2