To determine the susceptibility and clinical significance of the NLRP3 inflammasome in ITP, we examined the SNPs of three NLRP3 inflammasome components and two inflammatory cytokines, including NLRP3 (rs35829419), CARD8 (rs2043211), NF-[kappa]B-94ins/del ATTG, IL-18 (rs1946518), and IL-1[beta] (rs16944).
The genotyping of NLRP3 (rs35829419), IL-1[beta] (rs16944), IL-18 (rs1946518), or CARD8 (rs2043211) in all subjects was performed using a standard TaqMan[R] allelic discrimination assay (Applied Biosystems, USA).
Meanwhile, a truncating polymorphism (rs2043211) can produce a nonfunctional CARD8 and induce an amplification of the inflammatory process, or even evolve into cancer .
There was no significant difference in the polymorphic distribution of IL-1[beta] (rs16944) ([chi square] = 0.879, P = 0.644), IL-18 (rs1946518) ([chi square] = 0.226, P = 0.893), CARD8 (rs2043211) ([chi square] = 4.672, P = 0.097), and NF-[kappa]B-94 ins/del ATTG ([chi square] = 2.489, P = 0.288) between the patients and controls.
and NLRP1 undergo autoproteolytic processing through a ZU5-like domain," PLoS ONE, vol.
Evidence of interaction of CARD8 rs2043211 with NALP3 rs35829419 in Crohn's disease.
Combined polymorphisms in genes encoding the inflammasome components NALP3and CARD8 confer susceptibility to Crohn's disease in Swedish men.
Consistent with 15 nM LBH589 being a sublethal concentration based on the absence of morphological cell apoptotic features, no detectable loss of cell number, and similar proportion of early apoptotic cells to DMSO control following 48 hours culture, our gene expression data demonstrated increased expression of antiapoptotic genes (BIRC3, BCL2L2, and CFLAR) and decreased expression of proapoptotic genes (CASP3, BCL2L11, CARD8
, CASP6, BNIP1, BCLAF1, CASP2, and APAF1) following LBH589 treatment (Figure 3).