Disease relevance of Ccl27

• Molecular cloning of a novel CC chemokine, interleukin-11 receptor alpha-locus chemokine (ILC), which is located on chromosome 9p13 and a potential homologue of a CC chemokine encoded by molluscum contagiosum virus [1].
• CCL27 is a critical factor for the development of atopic dermatitis in the keratin-14 IL-4 transgenic mouse model [2].
• Human melanoma cells frequently express CC chemokine receptor (CCR)10, a receptor whose ligand (CCL27) is constitutively produced by keratinocytes [3].
• We conclude that CTACK and CCR4 can both support homing of T cells to skin, and that either one or the other is required for lymphocyte recruitment in cutaneous delayed type hypersensitivity [4].
• We generated recombinant adenovirus vectors with a fiber mutation, encoding mILC (Ad-RGD-mILC) and mFKN (Ad-RGD-mFKN) [5].

High impact information on Ccl27

• In vivo, intracutaneous CCL27 injection attracted lymphocytes and, conversely, neutralization of CCL27-CCR10 interactions impaired lymphocyte recruitment to the skin leading to the suppression of allergen-induced skin inflammation [6].
• Tumor necrosis factor-alpha and interleukin-1beta induced CCL27 production whereas the glucocorticosteroid clobetasol propionate suppressed it [6].
• In vivo, cutaneous injection of neutralizing antibodies to endogenous CCL27 blocked growth of CCR10-expressing melanoma cells [3].
• However, inhibition with anti-CTACK monoclonal antibody abrogates skin recruitment of CCR4-deficient T cells [4].
• Cutaneous T cell-attracting chemokine (CTACK; CCL27), expressed by skin keratinocytes, also attracts cutaneous memory T cells, and is hypothesized to assist in lymphocyte recruitment to skin as well [4].

Chemical compound and disease context of Ccl27

• TARC and RANTES, but not CTACK, are induced in two models of allergic contact dermatitis. Effects of cilomilast and diflorasone diacetate on T-cell-attracting chemokines [7].
• Chronic toxicity of biphenyl was characterized by increased incidences of urothelial desquamation in the renal pelvis in males and females and mineralization in the inner stripe of renal outer medulla in females, as well as changes in serum levels of BUN, ALP and some electrolytes in males and females [8].

Biological context of Ccl27

• Chemotaxis transmigration assay demonstrated that CCL27 promotes a greater degree of migration of T cells in diseased Tg mice [2].
• Because differences in ALP activity, bone-forming ability, cortical bone width, and osteoblastic activity were detected at birth, the different MAR/BFR phenotypes develop at very early life and even perhaps during embryogenesis [9].
• These data show that VIP, without affecting cell proliferation, can stimulate osteoblastic ALP biosynthesis and bone noduli formation by a mechanism mediated by cyclic AMP [10].
• Forskolin and choleratoxin stimulated ALP activity and cyclic AMP formation in a concentration-dependent manner, without affecting cell number [10].

Anatomical context of Ccl27

• Finally, CTACK selectively attracts CLA(+) memory T cells [11].
• CTACK is predominantly expressed in the skin and selectively attracts a tissue-specific subpopulation of memory lymphocytes [11].
• Specifically, CTACK message is found in the mouse epidermis and in human keratinocytes, and anti-CTACK mAbs predominantly stain the epithelium [11].
• To examine biological roles for PESKY we have overexpressed it in 3T3 cells [12].
• Using the murine embryonal stem cell system, we have identified a novel gene encoding a highly divergent member of the beta-chemokine family of proinflammatory mediators and have called this protein ESkine [13].

Associations of Ccl27 with chemical compounds

• Moreover, mutation of the tyrosines at the amino terminus of PSGL-1 to phenylalanine abolished the binding, further supporting the role of sulfated tyrosines in the CCL27-PSGL-1 interaction [14].
• In contrast, PTH/dexamethasone-treated cells formed Alcian blue-positive nodules but remained negative for alizarin red staining and ALP activity [15].
• BMP-2/insulin-treated cells became refractile without forming cartilaginous nodules and reached terminal differentiation, became positive for alizarin red staining, and developed considerable ALP activity [15].
• The highly proliferating bone marrow cells were negative for ALP and OCN, suggesting that they could represent early osteoblast precursors [16].
• The cyclic AMP phosphodiesterase inhibitors ZK 62 711 (10(-4) M) and isobutyl-methylxanthine (10(-4) M) stimulated ALP activity and synergistically potentiated the effect of VIP [10].

Other interactions of Ccl27

• In this study, we found that esDC express CCR7 and CCR10 (the receptor of CCL27) upon the LIGHT stimulation [17].
• LIGHT also upregulates CCL27, but not CCL19 and CCL21 expression in esDC [17].
• CONCLUSIONS: TARC and RANTES, but not CTACK, are involved in these two models of allergic contact dermatitis [7].
• In this study, we examined antitumor activity of a mouse CC chemokine ILC/CCL27 and a mouse CX(3)C chemokine fractalkine/CX(3)CL1 in vivo [5].

Analytical, diagnostic and therapeutic context of Ccl27

• Both human and mouse CTACK are detected only in skin by Southern and Northern blot analyses [11].
• In the present study, we investigated the role of CCL27, a T cell skin-homing chemokine known to be elevated in sera of human AD patients, in disease development in our animal model of AD [2].
• CCL27 transcripts are most abundantly expressed in the retina, as judged by in situ hybridization [18].
• METHODS: Conventional RT-PCR, 5' RACE, and dideoxy DNA sequencing were used to examine the sequences of CCL27 related RNAs in the eye [18].
• During the 8 days following viral infection we have compared ALP activity in serum and liver homogenates with ALP cytological localization in liver tissue (light and electron microscopy) [19].

References