Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4
Qiuyan Chen1, A Catharine Ross
1Department of Nutritional Sciences, The Pennsylvania State University, 126-S Henderson Building, University Park, PA 16802, USA.
Retinoic acid (RA) increases antibody production in vivo but its role in B-cell activation is unclear. In a model of purified mouse splenic B cells stimulated by CD40 coreceptor (as a surrogate of T cell co-stimulation), IL-4, a principal Th-2 cytokine, and ligation of the B-cell antigen receptor, CD40 engagement or IL-4 alone induced B-cell activation indicated by increased Ig gamma1 germline transcripts, cell proliferation, and surface (s)IgG1 expression, while triple stimulation with the combination of anti-CD40/IL-4/anti-mu synergized to heighten B-cell activation. Although RA was growth inhibitory for anti-CD40-activated B cells, RA increased the proportion of B cells that had more differentiated phenotypes, such as expression of higher level of activation-induced deaminase, Blimp-1, CD138/syndecan-1 and sIgG1. Overall, RA can promote B-cell maturation at the population level by increasing the number of sIgG1 and CD138 expressing cells, which may be related to the potentiation of humoral immunity in vivo.
Retinoic acid (RA) increases antibody production in vivo but its role in B-cell activation is unclear. In a model of purified mouse splenic B cells stimulated by CD40 coreceptor (as a surrogate of T cell co-stimulation), IL-4, a principal Th-2 cytokine, and ligation of the B-cell antigen receptor, CD40 engagement or IL-4 alone induced B-cell activation indicated by increased Ig gamma1 germline transcripts, cell proliferation, and surface (s)IgG1 expression, while triple stimulation with the combination of anti-CD40/IL-4/anti-mu synergized to heighten B-cell activation. Although RA was growth inhibitory for anti-CD40-activated B cells, RA increased the proportion of B cells that had more differentiated phenotypes, such as expression of higher level of activation-induced deaminase, Blimp-1, CD138/syndecan-1 and sIgG1. Overall, RA can promote B-cell maturation at the population level by increasing the number of sIgG1 and CD138 expressing cells, which may be related to the potentiation of humoral immunity in vivo.
