Suppression of antigen-specific Th2 cell-dependent IgM and IgG1 production following norepinephrine depletion in vivo.

摘要: The mechanism by which the Th2 cell-dependent Ab response is modulated sympathetic neurotransmitter norepinephrine (NE) was investigated. Our model system used severe combined immunodeficient ( scid ) mouse that depleted of NE with 6-hydroxydopamine before reconstitution a clone β 2 -adrenergic receptor (β2AR) neg KLH-specific cells and resting trinitrophenyl (TNP)-specific β2AR pos B enriched from spleens unimmunized mice. Following challenge TNP-keyhole limpet hemocyanin (KLH), production in these mice hapten-, carrier-, allotype-specific as well MHC restricted. Depletion resulted 50–75% suppression primary anti-TNP IgM compared NE-intact controls, while secondary returned to control levels. In contrast, both IgG1 responses were suppressed 85 40%, respectively. Using exposed either βAR- or αAR-selective antagonist, effect on shown be mediated βAR. addition, administration β2AR-selective agonist NE-depleted partially reversed depletion. Expression TNP-specific confirmed radioligand binding, immunofluorescence, cAMP analysis. Also, splenic histology comparable Ag exposure, follicle expansion germinal center formation after exposure. Taken together, results suggest stimulation expressed necessary for maintenance an optimal vivo.