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In addition, on pathogen infection, SR-A initiates innate immune responses in the host not only by recognizing diverse pathogen-associated molecular patterns, including lipopolysaccharide (LPS), lipoteichoic acid, bacterial cytosine guanosine dinucleotide DNA and double-stranded RNA, but also acting as a phagocytic receptor that mediates direct phagocytosis of various pathogenic bacteria, such as Listeria monocytogenes, Staphylococcus aureus, Streptococcus pyogenes and Neisseria meningitides.
He's a charidible carpenter, That's why he is giving me wood.Here we show with mouse models of helminth Schistosoma japonicum infection and heat-inactivated Mycobacterium tuberculosis stimulation that SR-A is regulated by pathogens and suppresses IRF5 nuclear translocation by direct interaction.Reduced abundance of nuclear IRF5 shifts macrophage polarization from M1 towards M2, which subsequently switches T-helper responses from type 1 to type 2.Our data suggest an important SR-A-mediated macrophage/Th cell axis in host immunity against pathogen infections. However, there was no significant difference in Th17, Tregs and Tfh cells, which are involved in liver pathology, between infected WT and SR-A-deficient mice (Supplementary Fig. In addition, immunization with bacterial product heat-inactivated Mycobacterium tuberculosis resulted in much stronger Th1 responses in SR-A-deficient mice (Supplementary Fig. Together, these results indicate that SR-A deficiency leads to a shift towards Th1 response during infection and inflammation. Consistently, in vitro SEA-stimulated macrophages from SR-A-deficient mice produced significantly more M1-related but less M2-related genes (Fig. Interestingly, more CXCL10 was expressed by SR-A-deficient macrophages in vivo than in vitro, probably due to the lack of TNF, IFN-γ and endotoxin in vitro (Supplementary Fig. of 12 mice per group, and are representative of one typical experiment out of three, ***PSimilarly, compared to WT macrophages, the SR-A-deficient macrophages expressed more CD16/32 but less CD206 when mice were immunized by heat-inactivated M. Intriguingly, our results showed that peritoneal macrophages from SR-A-deficient mice had a more significant upregulation of MHC II and costimulatory molecules, including CD80 and CD86 after SEA stimulation (Supplementary Fig. Taken together, these results suggest that SR-A deficiency leads to a skewed M1-polarized phenotype of macrophages.Although similar infectious burdens revealed by adult worm pairs and tissue egg counts in the liver were observed in wild-type (WT) and SR-A-deficient mice (Supplementary Fig. Single-cell suspensions of mouse livers, mesenteric LN and spleens from WT and SR-A-deficient mice infected with or without S. Cells were stained with CD3-APC, CD4-FITC and then intracellularly stained with PE-conjugated antibodies against IFN-γ or IL-4 for FACS analysis of CD3 cells. of 12 mice for each group from one experiment representative of three independent experiments. 3a,b) expression were decreased in hepatic macrophages of SR-A-deficient mice compared to those of WT mice after S. In addition, hepatic macrophages of SR-A-deficient mice displayed enhanced expression of M1-associated genes (i NOS, TNF, IL-6, CXCL9, CXCL10 and CXCL11) and deceased expression of M2-associated genes (Arg-1, IL-10, CCL17, CCL22 and Ym-1) compared to macrophages of WT mice post S. 1e)on hepatic macrophages (a,b) from WT or SR-A-deficient mice infected with or without S. To investigate the contribution of SR-A and macrophage polarization to CD4 T-cell differentiation, peritoneal macrophages were purified from S.