Project description:We have shown that, in acute models of vaccination, the antimicrobial peptide cathelicidin potentiates Th17 cell differentiation. TO examine this in long-term, chronic inflammation, here we studied T cells in the mouse model of Multiple Sclerosis. We examined T cells from wildtype mice and those lacking cathelicidin.
Project description:We have shown that cathelicidin amplifies Th17 differentiation. To determine the mechanism through which this host defence peptide acts, we performed multiplex gene expression analysis (NanoString) to identify the effects of mouse cathelicidin (mCRAMP) on murine CD4+ T cells cultured under Th17-driving conditions.
Project description:Through this comparative proteomic study of equine CD4+ cells 376 membrane proteins could be identified. Several proteins showed changed abundance in horses affected by a spontaneous autoimmune disease (equine recurrent uveitis, ERU). Findings provide novel knowledge about changes in the CD4+ immune cell membrane proteome in a spontaneously and naturally occurring autoimmune disease in horses. The data is highly relevant for veterinary medicine and has proven translational quality for autoimmune uveitis in man.
Project description:Analysis of undifferentiated keratinocytes or differentiated keratinocytes stimulated with or without human cathelicidin antimicrobial peptide (CAMP) LL37. Results provide insight into the biological effects of CAMP on human keratinocytes. NHEKs were divided into two groups; low calcium (0.05 mM) and high calcium condition (1.6 mM). Then keratinocytes were stimulated with human cathelicidin antimicrobial peptide LL37 at 0, 2.56, and 7.68 M-NM-<M for 12 h to 24 h.
Project description:Analysis of undifferentiated keratinocytes or differentiated keratinocytes stimulated with or without human cathelicidin antimicrobial peptide (CAMP) LL37. Results provide insight into the biological effects of CAMP on human keratinocytes.
Project description:The mechanisms behind survival of autoimmune CD4 T cells during chronic stimulation are unclear. Examining early time-points during T cell priming showed that activation of autoimmune CD4 T cells in the absence of infectious signals allowed maintenance of TCF1 expression, albeit at reduced levels. Tcf7 locus was epigenetically modified in circulating autoimmune CD4 T cells, suggesting a pre-programmed de novo methylation of the locus in early stages of autoimmune CD4 T cell differentiation which mirrored the epigenetic profile of recently recruited CD4 CD62L+ T cells in the tissue. Collectively, the data presented here show that the unique environment during autoimmune CD4 T cell priming allows T cells to finetune TCF1 expression to maintain long-term survival and function.
Project description:The mechanisms behind survival of autoimmune CD4 T cells during chronic stimulation are unclear. Examining early time-points during T cell priming showed that activation of autoimmune CD4 T cells in the absence of infectious signals allowed maintenance of TCF1 expression, albeit at reduced levels. Tcf7 locus was epigenetically modified in circulating autoimmune CD4 T cells, suggesting a pre-programmed de novo methylation of the locus in early stages of autoimmune CD4 T cell differentiation which mirrored the epigenetic profile of recently recruited CD4 CD62L+ T cells in the tissue. Collectively, the data presented here show that the unique environment during autoimmune CD4 T cell priming allows T cells to finetune TCF1 expression to maintain long-term survival and function.
Project description:miRNA expression profiling of CD4+ T cells comparing naïve mice and experimental autoimmune uveitis (EAU) mice. EAU was induced by immunization of retinal antigen (IRBP1-20) in complete Freund’s adjuvant (CFA). CD4+ T cells were isolated and purified from the spleen and draining lymph nodes 13 days after immunization.