KC (a), CCL3 (b), CCL5
(c), IL-17 (d), TNF[alpha] (e), IFN-[gamma] (f), CCL2 (g), and IP-10 (h) were found to be significantly downregulated in anti-IL-21 mAb-treated mice.
For example, GM-CSF and CCL5
are potent chemoattractants and stimulators of eosinophil proliferation [14-16].
Twenty-six SNPs covering 12 chemokine genes (CCL2, CCL5
, CCL16, CCL17, CCL21, CCL22, CCL24, CXCL8, CXCL9, CXCL10, CXCL12, and CXCL16) were genotyped successfully and all SNPs of controls met the Hardy-Weinberg equilibrium.
Upon topical irritant exposure, MUTZ-3 LC migrate in a CCL5
dependent manner into the dermis where they undergo an IL-10 dependent phenotypic change to a macrophage-like cell within the dermal compartment (Kosten et al., 2015b).
To evaluate the expression of different genes under homeostatic conditions and upon 6h of LPS exposure, real-time RT-PCR was performed for CCL4, CCL5
, CCL11, IL-8, IL-1[beta], IL-6, and epidermal growth factor (EGF).
Furthermore, it has been documented that an assembly of circulating chemokines CCL2, CCL5
, and CXCL8 play an important role in mast cell activation and generation of histamine and serotonin .
The cells produced significant amount of IL-6, CCL2, TNF-[alpha], and CCL5
upon LPS stimulation (Figure 6(c)).
We have also shown that histamine enhances IL-1[beta]-induced granulocyte-macrophage colony stimulating factor (GM-CSF) release but strongly inhibits CCL5
(RANTES) release by ASM cells from people with and without asthma .
Examples of these mediators include CCL5
(Chemokine [C-C motif] ligand 5), which promotes invasive behavior (103), TNF-[alpha], and, to a minor extent, IL-1[beta], which induces effects such as E-cadherin repression, reduced [beta]-catenin in the plasma membrane, vimentin expression, actin cytoskeleton reorganization, and increased adherence to substrate (104).
A commonly used anti-endometriosis herb preparation (Channel Flow) consisting of nine individual Chinese medical herbs was found to have direct effects on cell proliferation, apoptosis, and CCL5
production in endometriotic stromal cells (Wieser et al., 2009).
Natural ligands for CCR5 are CCL3 (MIP-1a), CCL4, (MIP-1b), CCL5
(RANTES) [1, 2, 7].
With further investigation, they concluded that morphine induces production of the protein CCL5
, which they discovered is released by astrocytes, a type of brain cell.