Intracellular sensing of stress and danger signals initiates inflammatory innate immune responses by triggering inflammasome assembly, caspase-1 activation and pyroptotic cell death as well as the release of interleukin 1β (IL-1β), IL-18 and danger signals. NLRP3 broadly senses infectious patterns and sterile danger signals, resulting in the tightly coordinated and regulated assembly of the NLRP3 inflammasome, but the precise mechanisms are incompletely understood. Here, we identified NLRP11 as an essential component of the NLRP3 inflammasome in human macrophages. NLRP11 interacted with NLRP3 and ASC, and deletion of NLRP11 specifically prevented NLRP3 inflammasome activation by preventing inflammasome assembly, NLRP3 and ASC polymerization, caspase-1 activation, pyroptosis and cytokine release but did not affect other inflammasomes. Restored expression of NLRP11, but not NLRP11 lacking the PYRIN domain (PYD), restored inflammasome activation. NLRP11 was also necessary for inflammasome responses driven by NLRP3 mutations that cause cryopyrin-associated periodic syndrome (CAPS). Because NLRP11 is not expressed in mice, our observations emphasize the specific complexity of inflammasome regulation in humans.

The virus causing mosaic of muskmelon in the Punjab is transmitted through seed, sap and aphids but not through beetle, whitefly, fungi or contact. It systemically infected Nicotiana tabacum (var. “White Burley” and CTRI‐Special), N. glutinosa, N. rustica and Capsicum annuum besides various cucurbit hosts when inoculated mechanically. The virus gave positive reaction with the antiserum of cucumber mosaic virus and the particles are spherical in shape. The virus has been identified as a distinct strain of cucumber mosaic virus and is designated as muskmelon strain of cucumber mosaic virus (CMV‐mst.).

Growth and sporulation of C. capsici were lesser in different solid and liquid media containing of virus infected leaves than in media containing extracts of healthy leaves. Spore germination and formation of appressoria in different dilutions of the extract were poor as compared to healthy leaf extracts The antimetabolite/inhibitor in TMV infected plants is water soluble.

West Nile Virus (WNV) is the leading cause of mosquito-borne neuroinvasive disease in the United States. Upon entry into the central nervous system (CNS), WNV infects neurons, causing neuronal injury and inflammation, potentially resulting in long-term sequelae and death. Studies have shown that infiltrating virus-specific CD8+ T cells are dependent on dendritic cell-mediated reactivation in the CNS to restrict viral replication and pathogenesis within the CNS. Previous reports have shown that CD8+DEC-205+ dendritic cells (DCs) rapidly accumulate within the CNS during WNV encephalitis; however, their specific role in host defense has not been demonstrated. DEC-205, an endocytic receptor expressed by DC subsets, is responsible for cross-presentation and can promote either antigen (Ag) specific effector T cell activation or immunological T cell tolerance. Using a mouse model of WNV encephalitis, we show that DEC-205 critically regulates effector T cell responses within the CNS. DEC-205−/− mice exhibited enhanced mortality compared to wild-type (WT) controls. The enhanced susceptibility of the DEC-205−/− mice arose from an increased viral burden; however, this was associated with increased numbers of infiltrating and activated T cells and increased inflammatory myeloid cells suggesting that DEC-205 promotes protective immune responses within the CNS that limit immunopathology during a neurotropic viral infection. These data clarify the role of DEC-205+ DCs in the restriction of viral pathogenesis and implicate DEC-205+ DCs as a key regulator of protective immune responses within the CNS.

West Nile Virus (WNV) is the leading cause of mosquito-borne neuroinvasive disease in the United States. Upon entry into the central nervous system (CNS, WNV infects neurons causing neuronal injury and inflammation potentially resulting in long-term sequelae and death. In order to restrict viral replication and pathogenesis within the CNS, infiltrating virus-specific CD8+ T cells are dependent on dendritic cell (DC) mediated reactivation. While previous reports have shown that DCs rapidly accumulate within the CNS during infection, the subset necessary to induce T-cell mediated protection against WNV has not been clarified. Previously, DEC-205+ DCs were detected within the CNS during WNV infection. DEC-205, an endocytic receptor expressed on a subset of DCs, promotes cross-presentation and induction of anti-viral immunity. However, the specific role of DEC-205+ DCs in establishing immunity against WNV encephalitis is not known. We hypothesize that DEC-205+ DCs restrict WNV pathogenesis by activating anti-viral T cell immunity in the CNS. We show that DEC-205−/− mice have increased clinical disease and mortality compared to wild-type (WT) controls. The enhanced susceptibility of the DEC-205−/− mice arose from increased viral burden, however, this was associated with increased neuronal chemokine expression and numbers of infiltrating T cells and inflammatory myeloid cells. These results suggest that DEC-205+ DCs promote protective immune responses to CNS viral infection that limits immunopathology. These findings will uncover the mechanism by which DEC-205+ DCs modulate protective immune responses within the CNS in order to restrict a neurotropic viral infection.