Folia Biologica
Journal of Cellular and Molecular Biology, Charles University 

The ability of the host to detect invasion by a pathogenic intruder and to activate the defence mechanism to eliminate the infection is essential for survival. The host defence system against the invading pathogen is composed from the innate and adaptive immunity. While the adaptive response is based on the recognition of antigen-specific lymphocytes and their clonal selection, the innate immune response is not pathogen-specific and provides rapid response that is not long-lasting; however, this response is essential for the generation of the adaptive immunity. An innate immune response has developed as a rapid and regulated defence mechanism in which the recognition of an invading pathogenic organism can occur upon binding to specific viral receptors, where many of these are signalling molecules or Toll-like receptors (TLRs) that can recognize the conserved patterns of proteins, lipoproteins, dsRNA, or unmethylated CpG DNA (Kopp and Medzhitov, 1999; Akira et al., 2001; Underhill and Ozinsky, 2002). While originally discovered by their ability to recognize bacterial and parasite invasion, it has been shown recently that mammalian TLRs can also recognize the patterns on the surface of virions such as the respiratory syncial virusencoded F fusion protein (Kurt-Jones et al., 2000) and viral RNA or DNA. Altogether, the broad array of cellular responses to invading pathogens can include phagocytosis, induction of inflammatory cytokines, chemokines and costimulatory molecules. Among the inflammatory cytokines, type I interferons (IFNs) play a unique role in the antiviral innate immune response, since they have not only the ability to directly inhibit viral replication, but also induce differentiation of dendritic cells, activation of natural killer (NK) cells and macrophages. However, aberrant expression of IFNα genes has been shown to be associated with several chronic viral infections and autoimmune diseases (Neighbor et al., 1981; Preble et al., 1982; Rhodes-Feuillette et al., 1983; Arvin and Miller, 1984; Fitzgerald-Bocarsly et al., 1991; Kunzi et al., 1995). There is also accumulating evidence that inappropriate or deregulated expression of chemokines or their receptors can play a role in the autoimmune response (Karpus et al., 1995) and rheumatoid arthritis (Nanki et al., 2000). Thus, the identification of factors that regulate the inducible and timely expression of these inflammatory proteins is of primary importance.

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