| First Author | Riese J | Year | 2022 |
| Journal | Front Immunol | Volume | 13 |
| Pages | 1053490 | PubMed ID | 36532028 |
| Mgi Jnum | J:332206 | Mgi Id | MGI:7411779 |
| Doi | 10.3389/fimmu.2022.1053490 | Citation | Riese J, et al. (2022) S1PR(4) deficiency results in reduced germinal center formation but only marginally affects antibody production. Front Immunol 13:1053490 |
| abstractText | INTRODUCTION: Splenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR(4)). Little is known about the functional relevance of S1PR(4) expression on those cells. METHODS: In this study, S1PR(4)-deficient mice were used to study the role of S1PR(4)-mediated S1P signaling in B cell motility in vitro and for the maintenance of the splenic architecture under steady state conditions as well as in polymicrobial abdominal sepsis in vivo. Finally, the impact of S1PR(4) deficiency on antibody production after immunization with T cell dependent antigens was assessed. RESULTS: Loss of S1PR(4) resulted in minor alterations of the splenic architecture concerning the presence of B cell follicles. After sepsis induction, the germinal center response was severely impaired in S1PR(4)-deficient animals. Splenic B cells showed reduced motility in the absence of S1PR(4). However, titres of specific antibodies showed only minor reductions in S1PR(4)-deficient animals. DISCUSSION: These observations suggest that S1P signaling mediated by S1PR(4) modifies chemokine-induced splenic B cell chemotaxis, thus modulating splenic microarchitecture, GC formation and T-cell dependent antibody production. |
