IntroductionThe magnitude and quality of innate immune response is essential for appropriate adaptive response. The activation of naive CD8 ϩ T cells, the main effector cells in the course of viral infections, their clonal expansion, development of effector cells, and maintenance and expansion of memory CD8 ϩ T cells after antigen reappearance are precisely regulated and dependent on an adequate context of costimulation and cytokine/chemokine environment, provided by cells responding to "first defense line" signals of innate immunity. [1][2][3][4] Mast cells (MCs), pivotal effector cells in immunoglobulin (Ig) E-associated disorders, have recently been recognized as important elements in innate immune defenses. 5 Strategically located at host/environment interfaces like the skin, airways, and gastrointestinal and urogenital tracts, 6,7 MCs are equipped with a large variety of receptors to detect signs of infections including Toll-like receptors (TLRs), CD48, and complement receptors. 8 MCs activated via these receptors secrete a large number of proinflammatory products including granule-associated preformed mediators (histamine, serotonin, proteases, proteoglycans), lipid mediators (leukotrienes B 4 and C 4 and prostaglandins), as well as cytokines, chemokines, and growth factors. 9 In contrast to the well-established crucial role of MCs in induction of host defense responses to bacteria and parasites, the function of MCs in antiviral immune responses remains to be characterized in detail. Recently, a number of reports have shown the functional interplay between MCs and T cells in allergic, infectious, and autoimmune processes, for example, MCs and T cells colocalizing in inflamed tissues, as in the lungs of patients with asthma and in animal models of allergic asthma. 10,11 It has also been reported that tumor necrosis factor ␣ (TNF-␣) released from MCs contributes substantially to T-cell recruitment to the draining lymph nodes (LNs) in an experimental infection model with Escherichia coli. 12 Furthermore, activated MCs induce the chemotaxis of CD8 ϩ T cells through the production of leukotrienes in vitro. 13 Further, the recruitment of early effector T cells into the airways in an asthma model is mediated by leukotriene B 4 (LTB 4 ) 14 released by MCs activated by IgE cross-linking. 15 However, the mechanisms and relevance of MC-T-cell interactions, as well as the signals required for MC activation and effector functions in settings of viral infections remain largely unknown.TLRs play an important role in innate immunity recognizing specific, nonself, conserved components shared by different pathogens. Different TLRs are involved in the specific recognition of various microbes. 16,17 Human and mouse MCs have been shown to be activated by bacterial peptidoglycan and lipopolysaccharide (LPS) via TLR2 and TLR4, respectively, producing a number of cytokines such as interleukin 5 (IL-5), IL-6, IL-10, IL-13, and TNF-␣. [18][19][20][21] On binding of viral dsRNA or its synthetic counterpart polyinosinic-polycytidyl...