An article published this year in “Scientific Reports” using one of our products, “Caspase3”, by our customers from Department of Cellular Biology and Immunology, IPBLN-CSIC, Granada, Spain in the analysis of howCD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism. Congrats and Thanks.
Summay:
In this study,
we investigated the role of CD38 in a pristane-induced murine model of lupus.
CD38-deficient (Cd38−/−) but not ART2-deficient (Art2−/−) mice developed less severe lupus compared to wild type (WT)
mice, and their protective phenotype consisted of (i) decreased
IFN-I-stimulated gene expression, (ii) decreased numbers of peritoneal CCR2hiLy6Chi inflammatory
monocytes, TNF-α-producing Ly6G+ neutrophils and Ly6Clo monocytes /macrophages, (iii) decreased production of
anti-single-stranded DNA and anti-nRNP autoantibodies, and (iv) ameliorated
glomerulonephritis. Cd38−/− pristane-elicited peritoneal exudate cells had
defective CCL2 and TNF-α secretion
following TLR7 stimulation. However, Tnf-α and Cxcl12 gene
expression in Cd38−/− bone marrow (BM) cells was intact, suggesting a
CD38-independent TLR7/TNF-α/CXCL12 axis in
the BM. Chemotactic responses of Cd38−/− Ly6Chi monocytes and Ly6G+ neutrophils were not impaired. However, Cd38−/− Ly6Chi monocytes and Ly6Clomonocytes/macrophages had defective apoptosis-mediated cell
death. Importantly, mice lacking the cation channel TRPM2 (Trpm2−/−) exhibited very
similar protection, with decreased numbers of PECs, and apoptotic Ly6Chi monocytes and
Ly6Clo monocytes/macrophages compared to WT mice. These
findings reveal a new role for CD38 in promoting aberrant inflammation and
lupus-like autoimmunity via an apoptosis-driven mechanism. Furthermore, given
the implications of CD38 in the activation of TRPM2, our data suggest that CD38
modulation of pristane-induced apoptosis is TRPM2-dependent.
Reference:
Product link:
PURE - anti Human
Anti Active Caspase-3
No comments:
Post a Comment