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burgdorferi from the United States induced higher levels of several mediators associated with innate immune responses, including IL-1[beta], IL-8, IL-10, TNF, and CCL3, than did B.
Similarly, the expression of 18 cytokine genes (IL-7, IL-10, TNFAIP8, SPP2, TNFAIP3, IFNB, CCL19, TNFAIP8L1, IL-16, CNTF, CXCL13, TNFAIP8L3, TNFSF13B, IL-34, TGFB1, TNFAIP2, CCL3, and ADIPOQ) and 39 cytokine receptor genes (CXCR7, CSF2RA, IL-1RL1, I-L1R2, IL-17RA, IFNAR1, IL-18RAP, IL-31RA, IL-9R, IL-18R1, IL-20RB, IL-21R, IL-2RG, IL-20RA, IL-4I1, LILRB1, TLR1, IL-17REL, LILRB5, TGFBR1, TLR6, TNFRSF13B, XCR1, TLR7, TNFRSF13C, TLR15 etc.
We further demonstrated that the inhibition of CCL3 production by rolipram was mediated by inhibition of PDE4B and activation of the PKA signal pathway in mouse peritoneal macrophages.
CCL3, CCL4 and CCL5 produced by Th1 cells favor differentiation of CD4T-cell into Th1-type, activate macrophages in synergism with IFN-[gamma], acting like cytokines of type
tuberculosis, las celulas epiteliales juegan un papel importante ya que son capaces de producir CXCL8 (IL-8) y CCL2 no asi CCL3, CCL4, o CCL5.
THSG reduces intima-media thickness in the aortic arch of SHRs, increases the vascular diastolic rate in response to acetylcholine, and reduces remodeling and fibrosis-related mRNA expression, such as that of genes ACTA2, CCL3, COL1A2, COL3A1, TIMP1 WISP2, IGFBP1, ECE1, KLF5, MYL1 BMP4, FN1, and the plasminogen activator inhibitor-1 (PAI-1).
Oligonucleotide primers were as follows: CCL3, 5′-CCAAGTCTTCTCAGCGCCAT-3′ and 5′-TCCGGCTGTAGGAGAAGCAG-3′; GAPDH, 5′-GGAGCGAGACCCCACTAACA-3′ and 5′-ACATACTCAGCACCGGCCTC-3′.
Addition of GPE + PR inhibited the expression of most of the abovementioned genes including 1L1[beta], ILla, IL6, IL8, C3 and CCL3.
In order to better understand the early events on the host-parasite interactions, in this paper, we evaluated the production of proinflammatory (IFN-[gamma], IL-12p70, CCL3, CCL4, CCL5, CXCL10) and of anti-inflammatory (IL-10, IL-13) cytokines, chemokines and chemokine receptors taking advantage of the in vitro priming system using peripheral blood mononuclear cells (PBMCs) from healthy individuals stimulated by live promastigotes of L.
We also evaluated chemokine genes that have shown altered expression in septic patients: IL8 (interleukin 8), CXCL10 [chemokine (C-X-C motif) ligand 10], PF4 (platelet factor 4), CCL3 [chemokine (C-C motif) ligand 3], and CXCL1 [chemokine (C-X-C motif) ligand 1 (melanoma growth stimulating activity, alpha)].
In-vitro secretion of the chemokines CCL3 and CCL4 produced by CLL cells was inhibited by CAL-101.
The inflammatory signaling pathways regulate protein phosphorylation and cellular transcriptional events, thereby increasing the adipocyte production of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-[alpha]), interleukin (IL) 6, IL-1[beta], leptin, resistin, and chemokines such as MCP-1, CC-chemokine ligand 2 (CCL2), CCL3, and CXC-chemokine ligand 8.
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