Disease relevance of CCL27

• Because of the skin-associated expression pattern of CCL27, we focused on the expression of CCL27 and CCR10 in normal skin compared with inflammatory and autoimmune skin diseases [1].
• Increased serum cutaneous T cell-attracting chemokine (CCL27) levels in patients with atopic dermatitis and psoriasis vulgaris [2].
• CCL27 is continuously expressed by keratinocytes, but highly upregulated in inflammatory skin diseases such as atopic dermatitis and psoriasis [3].
• The cutaneous T cell-attracting chemokine (CTACK/CCL27) was found highly elevated in onchocerciasis patients compared to infection-free European controls (P = 0.0004) and it did not change following ivermectin or placebo to 1 year post-therapy [4].
• The presence of these cells is most likely an allergen-mediated effect, as increased levels of CCL27 and CCR10 could not be detected 21 days after initiating an irritant contact dermatitis reaction [5].

High impact information on CCL27

• Antitumor effect by interleukin-11 receptor alpha-locus chemokine/CCL27, introduced into tumor cells through a recombinant adenovirus vector [6].
• Collectively, ILC/CCL27 may be a good candidate molecule for cancer gene therapy [6].
• The aim of this study was to prospectively evaluate the usefulness of the Italian Liver Cirrhosis Project (ILCP) classification of esophageal varices, together with the gastric features of portal hypertension, in predicting the first upper gastrointestinal bleeding in cirrhosis [7].
• METHODS: Patients with knee arthritis (not due to gout, osteoarthritis, or septic arthritis) were randomized over 3 treatment arms: ALC, ALP, and JAC [8].
• Moreover, we showed that UVB irradiation induces the release of CCL27 (cutaneous T cell-attracting chemokine) from epidermal compartments into dermal compartments and up-regulates the expression of a distinct set of chemokines in keratinocytes [9].

Chemical compound and disease context of CCL27

• Expression of vascular endothelial growth factor, apoptosis inhibitors (survivin and p16) and CCL27 in alopecia areata before and after diphencyprone treatment: an immunohistochemical study [10].
• Alendronate-treated women with at least a 30% reduction in bone ALP had a lower risk of non-spine (RH = 0.72; CI: 0.55, 0.92) and hip fractures (RH = 0.26; CI: 0.08, 0.83) relative to those with reductions <30% [11].
• The Spanish Lung Cancer Group (SLCG) compared the GC regimen with an etoposide plus cisplatin combination (EP), the Hoosier Oncology Group (HOG) compared it with single-agent cisplatin, and the Italian Lung Cancer Project (ILCP) compared it with a mitomycin plus ifosfamide plus cisplatin combination (MIC) [12].
• Cases were analyzed for local failure (LF) with respect to histology (invasive ductal (IDC), IDC with associated DCIS (IDC/DCIS), invasive lobular (ILC)), age, tumor size, total excision volume, reexcision, total dose, tamoxifen therapy, and chemotherapy [13].
• As expected, the decrease of both bone formation markers (bone ALP and PINP) was delayed compared to that of bone resorption and significant (p < 0.05-0.01) only after 2 months of treatment in the estrogen-treated group compared to the placebo group [14].

Biological context of CCL27

• CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27 [15].
• Strangely, CCL27 can also be produced as a non-secreted form, as a result of alternative splicing [16].
• Chemotaxis transmigration assay demonstrated that CCL27 promotes a greater degree of migration of T cells in diseased Tg mice [17].
• Furthermore, increased BMDK migration caused by CTACK/CCL27 significantly accelerated the wound-healing process without any influence over either angiogenesis or keratinocyte proliferation [18].
• Here, we used mutagenesis, kinetic analysis, and computer modeling to identify the residues important for the binding of known ALP inhibitors to the TNALP active site [19].

Anatomical context of CCL27

• CCL27 is constitutively produced by keratinocytes but can also be induced upon stimulation with TNF-alpha and IL-1beta [1].
• Both CCL27 and CCL28 are ligands for CCR10 and attract CCR10(+) lymphocytes [15].
• The recently discovered CC chemokine ligand 27 (CCL27), through interaction with its cognate receptor, CC chemokine receptor 10 (CCR10), appears to be involved in attracting a subset of memory T cells to the skin during some cutaneous inflammatory responses [16].
• Basic fibroblast growth factor, hepatocyte growth factor, interleukin-8, and CCL27 each slightly increased migration [20].
• CC chemokine ligand 27 (CCL27) was expressed in the epidermis and endothelium of both infected and uninfected skin [21].

Associations of CCL27 with chemical compounds

• In conclusion, local CCL27-mediated retention of CCR10+ CD4+ T cells in sites previously challenged by ACD could be responsible for phenomena such as local skin memory observed in retest reactions and flare-up reactions in which the presence of persisting T cells results in an accelerated inflammatory response upon renewed allergen challenge [5].
• Intracellular Ca(2+) chelator BAPTA/AM or cyclic adenosine monophosphate (cAMP)-dependent protein kinase inhibitor H-89 partially blocked the inhibitory effects of PGE(2) on CCL27 production and NF-kappaB activity, and the addition of both completely abrogated the inhibition [22].
• Prostaglandin E(2) suppresses CCL27 production through EP2 and EP3 receptors in human keratinocytes [22].
• Furthermore, in 7 patients with AD, serum TARC and CTACK levels were studied after the start of systemic cyclosporin A treatment [23].
• Biochemical parameters (serum albumin, bilirubin, ALP, AST and ALT), lipid peroxides, hydroxyproline, as well as histological changes in liver tissues were analyzed [24].

Regulatory relationships of CCL27

• OBJECTIVE: We examined the in vitro effects of IL-17 on TNF-alpha-induced CCL27 production in human keratinocytes [25].

Other interactions of CCL27

• In contrast to CTACK, however, MEC also supports migration through CCR3 [26].
• Stimulation of L1.2/hGPR2 transfectants with hESkine induced their migration and resulted in intracellular calcium mobilization [27].
• CTACK/CCL27 is pivotal in mediating the migration of lymphocytes into the skin, through the binding to the chemokine receptor CCR10 [3].
• Keratinocytes in these lesions excessively produce chemokines, CCL27, CCL2, or CCL5 which trigger inflammatory infiltrates [28].
• Suppressive effects of antimycotics on tumor necrosis factor-alpha-induced CCL27, CCL2, and CCL5 production in human keratinocytes [28].

Analytical, diagnostic and therapeutic context of CCL27

• METHODS: Keratinocytes were incubated with TNF-alpha in the presence or absence of PGE(2) . CCL27 secretion and mRNA level were analyzed by means of ELISA and RT-PCR, respectively [22].
• CCL27 secretion and mRNA levels were analyzed by means of ELISA and RT-PCR, respectively [25].
• Aim of this study was to investigate using immunohistochemistry techniques the interrelation between T immunoreactive cells and the expression of CCR10 and its ligand CCL27 in 59 cutaneous melanocytic lesions [29].
• 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 [17].
• OBJECTIVE: To compare the efficacy of arthroscopic lavage plus administration of corticosteroids (ALC), arthroscopic lavage plus administration of placebo (ALP), and joint aspiration plus administration of corticosteroids (JAC) in knee arthritis, and to evaluate whether clinical or histologic characteristics determine outcome [8].

References