摘要：

Interferons ()s are involved in numerous immune interactions during and contribute to both induction and regulation of innate and adaptive antiviral mechanisms. play a pivotal rule in the outcome of a , as demonstrated by the impaired resistance against different in deficient for the receptors -2 and IFNGR. During , are involved in numerous immune interactions as inducers, regulators, and effectors of both innate and adaptive antiviral mechanisms. /beta is produced rapidly when viral factors, such as , CpG DNA, or dsRNA, interact with cellular pattern-recognition receptors (PRRs), such as receptors, toll-like receptors (), and cytosolic receptors. These -virus interactions signal downstream to activate factors needed to achieve expression from /beta genes. These include regulatory factor-3 (), , , c-/ATF-2, and NF-kappaB. In contrast, is induced by receptor-mediated stimulation or in response to early produced cytokines, including interleukin-2 (IL-12), , and /beta, or by stimulation through T cell receptors () or natural killer (NK) cell receptors. signal through receptors, activating mainly Jak-pathways but also other signal pathways. Cytokine and -induced expression uses distinct signal pathways involving such factors as NFAT, and NF-kappaB. This results in induction and activation of numerous intrinsic antiviral factors, such as -activated (), the 2-5A system, Mx proteins, and several apoptotic pathways. In addition, modulate distinct aspects of both innate and adaptive immunity. Thus, /beta and affect activities of macrophages, NK cells, dendritic cells (DC), and T cells by enhancing , cell trafficking, and and expression profiles, ultimately resulting in enhanced antiviral effector functions. This review focuses on the latest findings regarding induction and regulation of , primarily during the early phase of an antiviral . Both cellular and molecular aspects are discussed from the perspective of -virus interactions.

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