Lymphocyte proliferation induced by pertussis toxin utilizes a pathway parallel to transforming growth factor-beta-sensitive growth.
Pertussis toxin (PTX) has been shown to potentiate autoimmunity in experimental autoimmune disease. The exact mechanism of this effect has not been determined; however, the modification of G proteins by ADP-ribosylation has been suggested. Here it is demonstrated that this modification may contribute to autoimmunity by the abrogation of transforming growth factor-beta (TGF-beta) growth-inhibitory signals. Anti-TGF-beta demonstrated the same effect on lymphocytes as high concentrations of PTX in vitro.
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D000246:Adenosine Diphosphate Ribose / Q000276:immunology; D000818:Animals; D015551:Autoimmunity / Q000276:immunology; D002478:Cells, Cultured; D007376:Interleukin-2 / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D037342:Pertussis Toxin; D018125:Receptors, Transforming Growth Factor beta / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors*; D010566:Virulence Factors, Bordetella / Q000494:pharmacology*
D007376:Interleukin-2; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D010566:Virulence Factors, Bordetella; D000246:Adenosine Diphosphate Ribose; D037342:Pertussis Toxin