Mice – characterize the mechanism by which PLZF raises an antiviral state, IFN production and Flavopiridol 131740-09-5 ISG expression in the wild-type and PLZF were analyzed /. Remarkably, the serum levels of IFN are clearly inadequate in infected PLZF-/ – mice M. This indicates that virus-reqs Observed susceptibility was independently Ngig of the IFN production. The expression profile of a series of PLZF-dependent Ngigen ISGs, characterized in experiments on the table was evaluated ex vivo and in vivo. Significantly, the induction of IFN antiviral gene OAS1 was in primary PLZF-Ren / ver changed – Bone marrow macrophages. OAS1 is established as an effector of the antiviral effect of IFN, especially against SFV, ma S we expressed in various organs after IFN-treatment and SFV infection.
Mice – The induction of OAS1 was ma major Flavopiridol CDK inhibitor role in splenocytes from the PLZF / isolated adversely chtigt. Similarly, the antiviral ISGs and rsad2 IFIT2 in PLZF / obsolete – splenocytes or BMMS and SFV-infected organs PLZF-/ – mice M. accordance with the specificity t of the reaction PLZF, the expression of PLZF independently- ngig, but IFN-regulated transcription CCL5 was not adversely chtigt. These data suggest that the hyper sensibility of PLZF-/ – Mice due to a specific defect in the induction of antiviral genes. Xu et al. Immunity page 3. Author manuscript, increases available in PMC 19th June 2010. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript A direct comparison of the genes PLZF-independent Ngigen-dependent and was ngigen Made by comparing ifit1 IFIT2 and closely related genes.
Induced both by IFN and IFIT1 IFIT2 and the virus, and mice adversely Chtigt STAT1-deficient M. These two genes are gegens USEFUL pattern of expression in various tissues. Both genes contain ISRE binding sites in their promoter, but there is no reason PLZF binding IFIT1 in the promoter. Therefore, the induction in the absence of PLZF IFIT2 was lost, w ifit1 while still in PLZF of IFN-/ induced – mice M. Further analysis showed that the expression of PLZF in various tissues, a strong correlation between PLZF and IFIT2 induction in response to IFN. Therefore, the different expression profiles of these two related ISGs h Probably depends on their own regulation by PLZF. Although the term is largely independent IFIT1 Ngig of PLZF, PLZF degree of dependence Dependence is in the lungs of M Mice suggests found that PLZF k nnte But in an indirect way to meet the specific requirements ISG inducer.
Interestingly, the Ausma of CXCL10 expression in organs after treatment with IFN alone or IFN treatment and SFV infection, that the induction of CXCL10 by IFN in primary PLZF / adversely was chtigt – BMMS. Mice – CXCL10 was also significant in splenocytes, liver and lung of SFV-infected PLZF / isolated adversely chtigt. CXCL10 has with NK Zellaktivit t and brought protection by viral infection. Therefore, another means by which the sensitivity of PLZF nnte adapt the virus k Nnte, additionally Tzlich to the direct induction of antiviral effectors, k To IFN-mediated activation of NK cells by ISG as CXCL10. These M Possibility was investigated.
NK cell activation in PLZF / igt erm – Mice Two recent reports have shown that the effects of PLZF NK T-cell activity of t, t, the specificity of this effect due to the low expression of NK cells in Bekr EMPLOYMENT PLZF T. However yielded PLZF analysis of the expression in immune cells with human and mouse microarray database that PLZF also expressed in human NK cells. In addition, we showed that mouse NK cells in PLZF was expressed followed by sorting the different populations of spleen cells by FACS analysis of gene expression. This analysis shows the expression of relatively few CD3 + T cells and NK1.1 no detectable transcription in B cells Therefore, we studied the effect of the loss of PLZF on the function of NK cells. FACS analysis of spleen cells showed there was corresponding number of NK cells from wild type and PLZF-/ – mice M