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GIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA
A Journal on Dermatology and Sexually Transmitted Diseases
Official Journal of the Italian Society of Dermatology and Sexually Transmitted Diseases
Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,014
Giornale Italiano di Dermatologia e Venereologia 2003 February;138(1):9-17
Chemokines and T-lymphocyte recruitment in allergic contact dermatitis
Ottaviani C., Sebastiani S., Albanesi C., Girolomoni G., Cavani A.
Istituto Dermopatico dell’Immacolata, IRCCS, Roma
Allergic contact dermatitis (ACD) is a frequent immune-mediated pathology of the skin. The expression of ACD depends on a coordinated series of events that leads to the accumulation, upon contact with the sensibilising substance, of hapten-specific lymphocytes responsible for the cutaneous damage. T-lymphocyte migration to the peripheral tissues is controlled by resident cells that release numerous substances with chemotactic activity called chemokines. These chemokines are actively synthesised by keratinocytes, fibroblasts, mastocytes, cutaneous dendritic cells and endothelial cells as a response to signals of danger from the outside or as a consequence of cellular activation promoted by cytokines of lymphocyte origin such as IFN-g and TNF-a. The type and the quantity of chemokines released into the cutaneous micro-environment in the course of inflammatory processes strongly condition the characteristics of leukocyte infiltrate. It is in fact well demonstrated that various T-cell populations express a repertory of receptors for very well defined chemokines which makes them selectively responsive only to certain chemotactic stimuli. The chemokines CCL2/MCP-1, CCL5/RANTES, CXCL10/ IP-10, CCL17/TARC and CCL22/MDC are among the main protagonists of lymphocyte recruitment in the acute phase of ACD. The chemokine CCL1/I-309, produced by keratinocytes and by the infiltrate cells, appears later and prevalently attracts regulatory lymphocytes, proving also to be involved in the immune response extinction mechanisms.