Unaltered levels of transplant arteriosclerosis in the absence of the B cell homing chemokine receptor CXCR5.
Chemokine receptors and their ligands are crucial for lymphocyte trafficking under both homeostatic and inflammatory conditions. The chemokine receptor CXCR5 controls B cell migration and the organization of B cell follicles. The aim of this study was to investigate the impact of CXCR5 on the development of transplant arteriosclerosis. Fully MHC mismatched BALB/c (H2(d)) donor aortas were transplanted into C57BL/6-CXCR5(-/-) (H2(b)), C57BL/6-CXCR5(+/-) (H2(b)) or C57BL/6-CXCR5(+/+) (H2(b)) recipients. Grafts were analysed by morphometry and immunofluorescence and intra-graft cytokine mRNA production was analysed by RT-PCR. Transplant arteriosclerosis was evident in CXCR5+/+ and CXCR5+/- mice and only mildly reduced in CXCR5-/- recipients indicating that absence of CXCR5 had no substantial effect on the development of transplant arteriosclerosis. Analysis of the cellular infiltrate of aortic grafts implanted in CXCR5-/- recipients revealed no differences in the number of T-cells, macrophages and B cells as compared to controls. Intra-graft cytokine production showed no significant changes in Th1 (IL-12) and Th2 (IL-4) cytokines as well as in TGF-beta and iNOS production. These data suggest that lack of CXCR5 expression by recipient T- and B-cells has little effect on the development of transplant arteriosclerosis.
Ensminger
Stephan M
SM
Department of Cardiac Surgery, Friedrich-Alexander University Erlangen-Nuernberg, Germany. stephan.ensminger@uk-erlangen.de
Abele-Ohl
Silke
S
Ohl
Lars
L
Spriewald
Bernd M
BM
Ramsperger-Gleixner
Martina
M
Weyand
Michael
M
Förster
Reinhold
R
D000818:Animals; D001013:Aorta, Thoracic / Q000276:immunology / Q000378:metabolism / Q000473:pathology* / Q000637:transplantation*; D001161:Arteriosclerosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D006084:Graft Rejection; D007150:Immunohistochemistry; D018664:Interleukin-12 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008264:Macrophages / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D054380:Receptors, CXCR5 / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016201:Receptors, Lymphocyte Homing / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014184:Transplantation, Homologous
C513179:CXCR5 protein, mouse; D054380:Receptors, CXCR5; D016201:Receptors, Lymphocyte Homing; D016212:Transforming Growth Factor beta; D018664:Interleukin-12; D015847:Interleukin-4; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse