Publikationsdatenbank

Inflammation in vivo is Modulated by GPR83 Isoform-4 but not GPR83 Isoform-1 Expression in Regulatory T Cells (2010)

Art

Zeitschriftenartikel / wissenschaftlicher Beitrag

Autoren

Hansen, W

Westendorf, A M

Toepfer, T

Mauel, S

Geffers, R

Gruber, A D

Buer, J

Quelle

Genes and immunity

Bandzählung: 11

Heftzählung: 4

Seiten: 357 – 361

ISSN: 1466-4879

Sprache

Englisch

Verweise

DOI: 10.1038/gene.2010.5

Pubmed: 20200545

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Most recently, we have described the G-protein coupled receptor 83 (GPR83), which is highly expressed by CD4(+)CD25(+) regulatory T cells (Tregs) to be involved in the induction of CD4(+)Foxp3(+) Tregs in the course of an ongoing immune response. Four GPR83 isoforms have been described. Here, we have shown that GPR83 isoform-4, which differs from GPR83 isoform-1 by 20 additional aminoacids in the second cytoplasmatic loop, is predominantly expressed by Tregs. Interestingly, GPR83 isoform-4 but not GPR83 isoform-1 retrovirally transduced T cells were able to interfere with inflammatory responses in vivo. Re-analysis of GPR83 transduced T cells revealed that this in vivo acquisition of suppressive activity was associated with the induction of Treg-associated molecules including Foxp3 in GPR83 isoform-4 but not GPR83 isoform-1 transduced CD4(+) T cells under inflammatory conditions. Our results suggest that the 20 additional aminoacids within GPR83 isoform-4 are involved in Treg induction during inflammatory immune responses.