Retinoic acid promotes mouse splenic B cell surface IgG expression and maturation stimulated by CD40 and IL-4

Abstract

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 Igγ1 germline transcripts, cell proliferation, and surface (s)IgG1 expression, while triple stimulation with the combination of anti-CD40/IL-4/anti-μ 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.

Toll-Like Receptor 3 Ligand and Retinoic Acid Enhance Germinal Center Formation and Increase the Tetanus Toxoid Vaccine Response

“…Retinoic acid (RA), an active metabolite of vitamin A (ret-inol), is well known as a potent agent of cell differentiation, including for B cells (9,11,18,33,36) and other immunoregulatory cells. Vitamin A, RA, and related retinoids have been shown to be necessary for maintaining antigen-specific antibody responses (47).…”

Molecular mechanisms of reversing neural degeneration by retinoic acid, a major derivative of vitamin A

“…The B cell proliferation and activation by up regulating co-receptor molecules is aided by similar molecules (Ma et al, 2005). Further, immunological diversity is controlled by RAR-ATRA receptor molecules by up regulating proteins needed for phenomena such as class switching and somatic hyper mutation (Cattoretti et al, 2006) while RAR-ATRA also helps in B cell maturation (Chen and Ross, 2007). In addition, RA paracrine signaling mechanisms allow cellular cross talking among leukocytes to overcome infectious conditions (Guo et al, 2015).…”

“…Bone Morphogenic Proteins (BMP) which are under the Super family of Transforming Growth Factor β (TFG -β) are primarily responsible for carrying out molecular cross talking with other pathways which are essential for bone morphogenesis (Chen and Ross, 2007). Essential molecular communicating mechanism involves Smad1 protein and BMP proteins; which are prime molecules sustaining bone morphogenesis (Feng and Derynck, 2005;Wang et al, 2011).…”

“…Uncontrolled differentiation involves in disease and abnormal situations where RA come to the play. The RA is known to carry out a major function in regulating these effector molecules via suppressing Smad1 pathway, thereby causing bone morphogenesis (Chen and Ross, 2007). Retinoic acid also induces proliferation of osteoclasts from myeloid progenitor cells carrying out maintenance of osteoclasts till maturation (Greena et al, 2016).…”

Relationship between Immune Function and Serum Vitamin A in Japanese Black Beef Cattle

“…Previous studies have shown that retinoic acid (RA) can enhance direct action on B cell populations [9]. RA can enhance antibody responses by a direct effect upon B cells, and modulate cytokine receptors to extend to B cells [23].…”