cAMP accumulation in T-cells inhibits anti-CD3 monoclonal antibody-induced actin polymerization

J Neuroimmunol. 1995 Jan;56(1):107-12. doi: 10.1016/0165-5728(94)00142-b.

Abstract

The results presented in this report offer a novel explanation for how stimulation of the beta-adrenergic receptor (beta AR) inhibits the ability of T cells to proliferate after interaction with immobilized anti-CD3 monoclonal antibody (mAb). Accordingly, T cells binding to immobilized anti-CD3 mAb but not anti-CD4 mAb undergo time-dependent F-actin assembly with concomitant formation of pseudopodia. This process is completely inhibited in the presence of isoproterenol (ISO) indicating that stimulation of the beta AR on T cells interferes with the biochemical processes responsible for the assembly of actin. To confirm these observations, we quantitated the formation of F-actin in T cells stimulated with immobilized anti-CD3 mAb in the presence of cAMP elevating agents. The results show that stimulation of the beta AR on T-cells, as well as the addition of forskolin or dibutyryl cAMP, abrogates the formation of F-actin.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Actins / antagonists & inhibitors*
  • Actins / metabolism
  • Antibodies, Monoclonal / immunology*
  • Bucladesine / pharmacology
  • CD3 Complex / immunology*
  • Colforsin / pharmacology
  • Cyclic AMP / metabolism*
  • Humans
  • Isoproterenol / pharmacology
  • Receptors, Adrenergic, beta / physiology
  • T-Lymphocytes / metabolism*
  • T-Lymphocytes / physiology

Substances

  • Actins
  • Antibodies, Monoclonal
  • CD3 Complex
  • Receptors, Adrenergic, beta
  • Colforsin
  • Bucladesine
  • Cyclic AMP
  • Isoproterenol