Disease relevance of Ccl17

• The specific Ab against TARC attenuated OVA-induced airway eosinophilia and diminished the degree of airway hyperresponsiveness with a concomitant decrease in Th2 cytokine levels [1].
• RESULTS: RANTES and TARC were elevated in both models of allergic contact dermatitis 24 h after challenge, whereas CTACK remained unchanged [2].
• The beneficial effect of corticosteroids in bronchial asthma is due in part to their direct inhibitory effects on TARC production [3].

High impact information on Ccl17

• The thymus and activation-regulated chemokine (TARC/CCL17) is produced by DCs and facilitates the attraction of activated T cells [4].
• Cells expressing the CCR4 ligand TARC (thymus- and activation-regulated chemokine) were detected within infiltrated islets from prediabetic mice [5].
• Inactivation of the peroxisomal ABCD2 transporter in the mouse leads to late-onset ataxia involving mitochondria, Golgi and endoplasmic reticulum damage [6].
• Our results for the first time indicate that TARC is a pivotal chemokine for the development of Th2-dominated experimental allergen-induced asthma with eosinophilia and AHR [1].
• Serial Analysis of Gene Expression in Progressing and Regressing Mouse Tumors Implicates the Involvement of RANTES and TARC in Antitumor Immune Responses [7].

Biological context of Ccl17

• These expression profiles indicate that tissue specificity of Scya17 is precisely regulated by two independent mechanisms, one by transcription from its own promoter and the other from the promoter of Scyd1 followed by tissue-specific alternative splicing [8].
• Analysis of the genomic organization of the two genes revealed that Scyd1 and Scya17, encoding TARC, are tightly linked on chromosome 8 and that fracTARC is generated by alternative splicing of the two genes [8].

Anatomical context of Ccl17

• On the other hand, Scya17 and the fracTARC gene are reciprocally expressed in thymus, brain, lung, and kidney and are never expressed in the same tissue [8].
• The main pathological feature in abcd2-/- mice is a late-onset cerebellar and sensory ataxia, with loss of cerebellar Purkinje cells and dorsal root ganglia cell degeneration, correlating with accumulation of VLCFAs in the latter cellular population [6].
• In addition, the induced migration of mouse eosinophils by TARC, MIP-1beta, and KC suggests that unidentified receptor-ligand interactions contribute to eosinophil recruitment [9].
• RESULTS: TARC was expressed mainly in the bronchial epithelial cells [3].
• Thymus and activation-regulated chemokine (TARC/CCL17) produced by mouse epidermal Langerhans cells is upregulated by TNF-alpha and IL-4 and downregulated by IFN-gamma [10].

Associations of Ccl17 with chemical compounds

• CONCLUSIONS: The corticosteroid dexamethasone inhibits TARC production in a murine model of allergic asthma in vivo [3].
• TARC was reduced by diflorasone diacetate in the DNCB model but was highly induced in the TDI model; in contrast, TARC was not influenced by cilomilast [2].

Regulatory relationships of Ccl17

• TARC production by murine LC was upregulated by TNF-alpha and IL-4 and downregulated by IFN-gamma, dose-dependently [10].

Other interactions of Ccl17

• Fractalkine shares signal sequence with TARC: gene structures and expression profiles of two chemokine genes [8].
• Th2 cytokine microenvironments in skin may increase TARC production by mature LC, providing attraction of Th2 cells in skin [10].
• CONCLUSIONS: TARC and RANTES, but not CTACK, are involved in these two models of allergic contact dermatitis [2].

Analytical, diagnostic and therapeutic context of Ccl17

• Dexamethasone also decreased TARC production in the bronchoalveolar lavage fluid and decreased expression of TARC mRNA and TARC protein in lung tissue [3].
• RT-PCR was performed using fresh and cultured LC to evaluate TARC mRNA levels [10].
• ELISA was carried out using supernatant of cultured LC to calculate secreted TARC protein levels [10].

References