Objective:To investigate the immune defence against acute encephalitis induced by the highly neurovirulent recombinant R404BP strain of influenza A virus.Methods:A murine model system for a lethal encephalitis due to influenza has been established by stereotaxic microinjection with the recombinant R404BP strain of influenza A virus into the olfactory bulb of the senescence-accelerated mouse(SAM) strain P1 mice. The mortality of infected mice, clearance of infected neurons and induced cellular immune responses were investigated.Results:The SAM-P1 mice showed a higher rate of mortality with prolonged virus shedding. The increased susceptibility was associated with impaired activity of both NK cells and virus-specific cytotoxic T lymphocytes.Conclusion:The decreased Th1 immune responses in the senescence-accelerated mouse might be responsible for the low defence system against neurovirulent recombinant influenza A virus.

Objective:To investigate the effect of perforin-mediated cytotoxicity in primary influenza virus infection.Methods:Perforin-deficient and wild-type C57BL/6 mice were infected intranasally with influenza virus A/PR/8/34. Pulmonary viral growth was determined at various days after infection by pfu experiment. Perforin-mediated apoptotic degeneration was observed by Immunohistochemical staining. LDH-release method was used for detection of specific CTL and NK cell activity from spleen cells.Results:Mice deficient in the perforin gene showed an increased virus growth and prolonged virus shedding. The appearance of apoptotic degeneration in virally infected lung cells was delayed in perforin-deficient mice. The cytolytic activities of natural killer cells and virus-specific cytotoxic T lymphocytes were significantly lower than that of wild-type mice.Conclusion:Perforin plays a critical role in the host defense system against primary influenza virus infection.

Type 2 innate lymphoid cells ( ILC2s) are recently identified members of the innate lymphoid cell ( ILC) family. These cells are capable of producing Th2-type cytokines such as IL-5 and IL-13 in response to epithelial cell-derived cytokines IL-25 and IL-33 and play critical roles in allergic diseases such as bronchial asthma. Further investigations on ILC2s will enhance the better understanding of type 2 immune responses and may provide new strategies for the treatment of allergic asthma. In this review, we fo-cus on the origin, location and biological function of ILC2s as well as their possible roles in the pathogenesis of bronchial asthma.

ObjectiveTo investigate whether γδ T cells act as a regulatory factor during respiratory syncytial virus (RSV) infections was responsible for the subsequent changes in asthmatic-type inflammation in allergic mice.MethodsMice were sensitized and challenged with OVA,and infected intranasaly with RSV before or after OVA sensitization.Lung sections were stained with HE for determination of inflammatory reaction.Real-time RT-PCR was used to analyze the expression of cytokine mRNA of γδ T cells in the lung and spleen of tested mice.The number of γδ T cells in the spleen and lung of BALB/c mice was determined by flow cytometry.Adoptive transfer of γδ T cells was performed to identify the role of γδ T cells in allergic asthma.ResultsOVA-sensitized and challenged mice exhibited significantly peribronchial inflammation with larger number of mononuclear cells and granulocytes in the lung tissue sections.RSV infection before OVA-sensitization diminished the grade of inflammatory responses induced by OVA treatment.The expression of IFN-γ mRNA was increased siguificantly in RSV-infected,OVA-sensitized mice.In contrast,the level of IL-4 mRNA was diminished.The number of total γδ T cells as well as activated γδ T cells was decreased in the spleen and lung of OVA-sensitized mice by prior RSV infection.Adoptive transfer of γδ T cells obtained from OVA-sensitized and challenged mice induced a slight inflammation in the lung of normal mice,and enhanced inflammatory responses in RSV-infected OVA-sensitized mice.Conclusionγδ T cells may play an important role in the development of allergen-induced allergic airway inflammation.

Objective To investigate the role of CD4+T cells in airway inflammation induced by respiratory syncytial virus (RSV) infection. Methods Animal models of acute RSV infection were estab-lished. Lung tissues were stained with hematoxylin and eosin (HE) to observe histopathological changes. Total number of CD4+T cells and the number of CD4+T cells secreting Th1/Th2 cytokines (IFN-γ, IL-4, IL-5 and IL-13) in spleen were detected by flow cytometry. Adoptive transfer of CD4+T cells was performed to identify the role of CD4+T cells in RSV-induced airway inflammation. Results RSV infection increased the total number of splenic CD4+T cells,particularly Th2-type CD4+T cells. The absolute numbers of IL-4/IL-5/IL-13-secreting CD4+T cells were increased significantly after RSV infection. Furthermore, adoptive transfer of CD4+T cells into BALB/c mice not only promoted the infiltration of mononuclear cells in lung,but also enhanced the secretion of Th2 cytokines during RSV infection. Conclusion CD4+T cells are involved in RSV-induced airway inflammation through secreting Th2 cytokines.