S1PR2 links germinal center confinement and growth regulation.

Immunol Rev

Department of Microbiology and Immunology, Howard Hughes Medical Institute, University of California, San Francisco, CA 94143-0414, USA.

Published: May 2012

Germinal centers (GCs) are sites of rapid B-cell proliferation and somatic mutation. These ovoid structures develop within the center of follicles and grow to a stereotypic size. The cell migration and interaction dynamics underlying GC B-cell selection events are currently under intense scrutiny. In recent study, we identified a role for a migration inhibitory receptor, S1PR2, in promoting GC B-cell confinement to GCs. S1PR2 also dampens Akt activation and deficiency in S1PR2 or components of its signaling pathway result in a loss of growth control in chronically stimulated mucosal GCs. Herein, we detail present understanding of S1PR2 and S1P biology as it pertains to GC B cells and place this information in the context of a current model of GC function.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3335345PMC
http://dx.doi.org/10.1111/j.1600-065X.2012.01114.xDOI Listing

Publication Analysis

Top Keywords

s1pr2
5
s1pr2 links
4
links germinal
4
germinal center
4
center confinement
4
confinement growth
4
growth regulation
4
regulation germinal
4
germinal centers
4
centers gcs
4

Similar Publications

Blocking the Sphingosine-1-Phosphate Receptor 2 (S1P) Reduces the Severity of Collagen-Induced Arthritis in DBA-1J Mice.

Int J Mol Sci

December 2024

Department of Biomedical and Pharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul 02446, Republic of Korea.

The amount of sphingosine 1-phosphate (S1P) found in the synovial tissue of individuals with rheumatoid arthritis is five times greater than that in those with osteoarthritis. Our study aims to determine whether inhibiting S1P can mitigate collagen-induced rheumatoid arthritis (CIA) by using an S1P antagonist, JTE-013, alongside DBA-1J wild-type (WT) and knock-out (KO) mice. CIA causes increases in arthritis scores, foot swelling, synovial hyperplasia, pannus formation, proteoglycan depletion, cartilage damage, and bone erosion, but these effects are markedly reduced when JTE-013 is administered to WT mice.

View Article and Find Full Text PDF

Background: The aim of our study was to determine the role of sphingolipids, which control proliferation and apoptosis, in the placenta of pregnant women with pregnancy-associated breast cancer (PABC) after chemotherapy compared with healthy patients.

Methods: We analyzed (by the PCR method) the gene expression of key sphingolipid metabolism enzymes (sphingomyelinases (SMPD1 and SMPD3), acid ceramidase (ASAH1), ceramide synthases (CERS 1-6), sphingosine kinase1 (SPHK1), sphingosine-1-phosphate lyase 1 (SGPL1), and sphingosine-1-phosphate receptors (S1PR1, S1PR2, and S1PR3)) and the content of subspecies of ceramides, sphingosine, and sphingosine-1-phosphate in seven patients with PABC after chemotherapy and eight healthy pregnant women as a control group.

Results: We found a significant increase in the expression of genes of acid ceramidase (ASAH1), sphingosine-1-phosphate lyase 1 (SGPL1), sphingosine kinase (SPHK1), and ceramide synthases (CERS 1-3, 5, 6) in the samples of patients with PABC during their treatment with cytostatic chemotherapy.

View Article and Find Full Text PDF

Objectives: The disruption of blood-brain barrier (BBB) is associated with poor outcomes of TBI patients. Sphingosine-1-phosphate receptor 2 (S1pr2), a member of the G protein-coupled receptor family, is involved in endothelial activation and the regulation of vascular integrity. We hypothesized that the inhibition of S1pr2 may alleviate BBB disruption and explored potential underlying molecular mechanisms.

View Article and Find Full Text PDF

Lipopolysaccharide (LPS) mediated caspases-4 (humans) and caspase-11 (rodent) (caspase-4/11) signaling can cause maturation of inflammatory cytokine IL-1β and cellular pyroptosis in the macrophages through guanylate-binding proteins (GBPs). However, how caspase-4/11s bind with GBPs together to activate caspase-4/11 by LPS remains elusive. We here found that BA derivatives from gut microbiota can regulate sensitivity of macrophages to LPS and Gram-negative bacteria through .

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!