CCR10

CCR10

A gene on chromosome 17q21.1-q21.3 that encodes a member of the chemokine receptor family, which is similar to G protein-coupled receptors. CCR10 is the receptor for CCL27, the binding of which results in T cell-mediated skin inflammation.
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In addition, cytokine-cytokine receptor interaction signaling pathways were predicted to have strong relationships with the target genes, such as CCL23 ( ENST00000591423 ) , CCR10 ( NM_016602 ), and TNFRSF6B (NM_003823) .
Apart from CXCR4, isolated MSCs also expressed CCR1, CCR4, CCR7, CCR10, CXCR5, and CXCR6 [55].
TI-Treg cells express a variety of chemokine receptors, including CCR4, CCR5, CCR6, CCR7, CCR10, CXCR3, and CXCR4, and migrate efficiently in response to tumor-derived chemokines [23, 95, 96].
In addition, other cytokines and chemokine receptors, including IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, IL-13, IL-18, CCR3, CXCR3, CXCR4, and CCR10, have been found to be upregulated in the skin lesions, blister fluids, PBMC, or plasma of drug hypersensitivity patients and to participate in the immune regulation of drug hypersensitivity [131, 138, 142, 143, 152-154].
In inflamed skin, activated T cells express high levels of CCR10, whose engagement with CCL27, which is produced by keratinocytes and is highly displayed on inflamed venules in the skin, is critical for T cell recruitment to the skin.
Unpublished microarray data obtained on OE-MSCs indicate that CCR10 is the most highly expressed C-C chemokine receptors (CCR) in these cells.
Yang et al., "Role of CCR10 and CCL27 in skin resident T cell development and homeostasis," The Journal of Immunology, vol.
Autocrine regulation of re-epithelialization after wounding by chemokine receptors CCR1, CCR10, CXCR1, CXCR2, and CXCR3.
This translocation creates NPM-ALK (Nucleophosphmin anaplastic lymphoma kinase) gene with transforming potential,7 while other mutations are also implicated like defective expression of TCR, CCR8, and CCR10.10 Unlike primary cutaneous CD30+ LCL, which may remain localized for prolonged periods, this systemic counterpart with secondary cutaneous involvement is an aggressive disease with rapid spread to other organs, including the skin.1,8,9 It is thus imperative that metastatic systemic LCL of worse prognosis be excluded as a cause of a CD30+ cutaneous nodule, and must not be overlooked in the evaluation of CD30+ LCLs.1,2
(24) Concurrent with antigen presentation, dendritic cells located in PPs induce gut-imprinting molecules (e.g., CC chemokine receptor [CCR]9, CCR10, [alpha]4[beta]7 integrin) on antigen-specific lymphocytes through the retinoic acid cascade for their subsequent migration to the effector tissues (e.g., intestinal lamina propria) (Fig.