S1PR deficiency results in reduced germinal center formation but only marginally affects antibody production.

INTRODUCTION

Splenic B cells exhibit a high expression of the G protein-coupled sphingosine-1-phosphate (S1P) receptor type 4 (S1PR). Little is known about the functional relevance of S1PR expression on those cells.

METHODS

In this study, S1PR-deficient mice were used to study the role of S1PR-mediated S1P signaling in B cell motility and for the maintenance of the splenic architecture under steady state conditions as well as in polymicrobial abdominal sepsis . Finally, the impact of S1PR deficiency on antibody production after immunization with T cell dependent antigens was assessed.

RESULTS

Loss of S1PR 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-deficient animals. Splenic B cells showed reduced motility in the absence of S1PR. However, titres of specific antibodies showed only minor reductions in S1PR-deficient animals.

DISCUSSION

These observations suggest that S1P signaling mediated by S1PR modifies chemokine-induced splenic B cell chemotaxis, thus modulating splenic microarchitecture, GC formation and T-cell dependent antibody production.