Project description:We inflicted TBI to wildetype (wt) mice in order to establish whether the anti-inflammatory agent cyclophosphamide can be used therapeutically. Cyclophosphamide was found to regulate distinct inflammatory cells such as activated microglia separate from invading phagocytes and dendritic cells. Cyclophosphamide postinjury selectively reduces antigen-presenting dendritic cells. Findings show feasibility of drug development to interfere with brain inflammation.
Project description:Batf3 regulates key CD8alpha DC-specific genes. WT and KO cells were isolated from pooled spleens of C57BL/6 genetic background mice, that were either untreated, or injected with recombinant murine IL-12 in pyrogen-free saline at 2.5 ug/mL. Mice were injected i.p. with 0.5 ug of IL-12 once and sorted after 3 days. CD8alpha+ dendritic cells were sorted as B220- NK1.1- CD172a- CD11c+ MHCII+ CD24+ DEC205+ CD8alpha+ cells.
Project description:We inflicted TBI to wildetype (wt) mice in order to establish whether the anti-inflammatory agent cyclophosphamide can be used therapeutically. Cyclophosphamide was found to regulate distinct inflammatory cells such as activated microglia separate from invading phagocytes and dendritic cells. Cyclophosphamide postinjury selectively reduces antigen-presenting dendritic cells. Findings show feasibility of drug development to interfere with brain inflammation. TBI was carried out in injured wt B6 mice for postinjury treatment with cyclophospamide i.p. using saline as a control substance for comparison with injured but untreated mice. Total RNA was prepared from injured cerebral neocortex after three days. RNA samples were also from uninjured wt mice as reference for hybridization on Affymetrix microarrays.
Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
Project description:CD69 is a transmembrane protein expressed on the surface of activated leukocyte. The ligand for CD69 and the intracellular signaling pathway of this molecule are yet unknown. It is widely used as a marker of activated lymphocyte, but its function in immune system is not known. We used micro-array to define genes whose expression is regulated by activation antigene CD69. CD4 T cells were isolated from the spleen of wt B6 and CD69-deficient B6 mice and in vitro activated with anti-CD3/anti-CD28 coated beads. On one groupe of wt B6 cells, CD69 was activated using a anti-CD69 and secoundary antibody. RNA extraction and hybridization on Affymetrix microarrays was performed for wt B6, CD69-activated wt B6 and CD69-deficient B6 CD4 T cells.
