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1 timulating factor (G-CSF) and the ELR(+) CXC chemokine CXCL1.
2 inflammatory cytokines IL1beta, IL6, and the chemokine CXCL1.
3 opoietic tissue of the neutrophil-recruiting chemokine CXCL1.
4 t through seed-derived factors including the chemokine CXCL1.
5 on in response to both retinoic acid and the chemokine CXCL1.
6 bility through secreted products such as the chemokines CXCL1, 2, 3, and 8, through adhesion-dependen
7 ast, cathepsins specifically process ELR CXC chemokines CXCL1, -2, -3, -5, and -8 N-terminally to the
8 n-coupled receptor (GPCR) that binds the CXC chemokines, CXCL1-3 and CXCL5-8, and induces intracellul
9 lm infection led to significant increases in chemokine (CXCL1 and CCL2) and proinflammatory cytokine
11 ptor family, induced potent secretion of the chemokines CXCL1 and CCL2 as well as expression of induc
12 ated with marked astrocytic synthesis of the chemokines CXCL1 and CCL2 in response to both cytokine c
13 teria has higher levels of mRNA encoding the chemokines CXCL1 and CCL2 than does tissue isolated from
15 ts demonstrated diminished production of the chemokines CXCL1 and CXCL2 and delayed neutrophil and T
17 eased mRNA expression of neutrophil-specific chemokines CXCL1 and CXCL2 in the lungs of C57BL/6 and I
18 he melanoma growth and migration stimulatory chemokines CXCL1 and CXCL2 were significantly up-regulat
19 d T cells, whereas the neutrophil-attracting chemokines CXCL1 and CXCL2 were up-regulated in the CNS
20 -protein-coupled receptor CXCR2 (recognizing chemokines CXCL1 and CXCL2) as another arm feeding into
21 steoblasts constitutively expressed the ELR+ chemokines CXCL1 and CXCL2, and CXCL2 expression was ind
26 we found that expression of 2 PMN-attracting chemokines, Cxcl1 and Cxcl2, was rapidly and dramaticall
27 ogenous luminal restoration of IL-17-related chemokines, CXCL1 and CXCL5, improves host defenses agai
28 motactic chemokines KC (keratinocyte-derived chemokine) (CXCL1) and MIP-2 (macrophage inflammatory pr
29 es, TNF-alpha elicited marked release of the chemokine CXCL1, and the release was blocked by carbenox
31 nflammatory cytokines (sICAM-1 and IL-6) and chemokines (CXCL1, CCL1, CCL2 and CCL5) that are hallmar
32 ng showed many up-regulated genes, including chemokines (Cxcl1, Ccl7), cytokines (tumor necrosis fact
33 TNF-alpha, IL1-b, IFN-gamma, and IL-12), and chemokines (CXCL1, CXCL2, CCL2, CCL3, CCL4, and CXCL10).
34 tory molecules (CD80, CD86, CD40, and CD70), chemokines (CXCL1, CXCL2, CXCL3, CCL12, CCL17), as well
36 6, IL-23, IL-1beta, as well as IL-17 and the chemokines CXCL1, CXCL2, and CCL2, whereas similarly tre
37 d endothelial expression of the neutrophilic chemokines CXCL1, CXCL2, and CXCL5 and led to a function
39 d deficit in their capability to release the chemokines CXCL1, CXCL2, CCL3, and CCL4 and TNF-alpha in
41 F], interleukin-17 [IL-17], and IL-1beta) or chemokine (CXCL1, CXCL5, CXCL9, and CXCL10) induction.
42 gories: proangiogenic factors (MMP9, VEGFA), chemokines (CXCL1, CXCL5, IL8, CCL2), cytokines (IL1B, I
45 differentially elicited a further downstream chemokine (CXCL1/CXCL8) autocrine loop, with the two loo
46 were expressed at adult levels, whereas the chemokines CXCL1, CXCL9, and CCL2 remained at baseline l
47 onuclear cells (PMNs) through binding of the chemokines CXCL1 (CXCR1) and CXCL8 (CXCR1 and CXCR2).
48 al colony forming units, and by elevation of chemokine CXCL1, cytokine IL-6, and endogenous G-CSF pro
49 okines, as well as a prolonged half-life for chemokine CXCL1-encoding mRNA after treatment with IL-17
50 instead reduced secretion of the angiogenic chemokine CXCL1 from head and neck cancer cells in vitro
51 ncer Genome Atlas showed that the neutrophil chemokine CXCL1 gene was highly upregulated in colon tum
52 , HNP 1-3, elafin, and LL-37) and neutrophil chemokines (CXCL1/GRO-alpha, CXCL2/GRO-beta, CXCL5/ENA-7
53 and correspondingly had lower levels of the chemokine CXCL1 in bronchoalveolar lavage fluid and lung
56 previous studies have revealed that the CXC chemokine, CXCL1, is overexpressed in human malignant me
59 i) DC produced elevated levels of the murine chemokine CXCL1 (KC), interleukin 12p40, and RANTES in r
60 appin-2-treated PA01 up-regulated the murine chemokine CXCL1/KC after 2 hours with a corresponding in
61 cytes but with elevated levels of the ELR(+) chemokines (CXCL1/keratinocyte-derived chemokine and CXC
65 ow here that IL-17 enhanced the stability of chemokine CXCL1 mRNA and other mRNAs through a pathway t
69 r alpha (TNF-alpha), IL-10, and IL-6 and the chemokine CXCL1 were upregulated in cocultured HT-29 cel
70 and VCAM-1), and enhanced the release of CXC chemokine CXCL1 when incubated with primary cultures of
71 lso had higher levels of the proinflammatory chemokine CXCL1, which CD T cells produce, in the kidney
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