Anti-TLR2 monoclonal antibody, clone UM32

Toll-like receptors take an essential part in innate immunity in response to invasion of the various harmful pathogens. We aimed to investigate TLR2, 7 and 8 expression in rat testis and epididymis throughout postnatal development. In the prepubertal period, TLR2 and 7 were variably localized to peritubular myoid cells, interstitial cells, blood vessels, epithelial cells, ductal smooth muscle cells in testis and epididymis. In the pubertal period, immunostaining of TLR2 and 7 started to be seen in primary spermatocytes, as well as other cells, in the testis. Narrow cells showed strong intracytoplasmic staining in the epididymis. In the postpubertal period, moderate to strong immunostaining of TLR2 and TLR7 was seen in spermatids at different developmental steps but weak immunoreaction in pachytene spermatocytes. Other cells in testis and epididymis showed variable immunostaining of TLR2 and 7. However, weak to moderate immunoreaction to TLR8 was detected in only interstitial cells in testis. In the mature period, immunostaining of TLR2, 7 and 8 tended to increase in different types of cells in testis and epididymis. Our findings suggest that expression of TLR2, 7 and 8 changed dynamically during postnatal development and increased towards mature period. We consider that TLR2, 7 and 8 might be associated with the regulation of spermatogenesis and the maintenance of innate immunity of testis and epididymis during postnatal development.

Background Disease progression in the absence of therapy varies significantly in mono-HIV and HCV infected individuals. Virus-specific CD8(+) T cells play an important role in restricting lentiviral replication and determining the rate of disease progression during HIV and HCV mono- and co-infection. Thus, understanding the similarities in the characteristics of CD8(+) T cells in mono-HIV and HCV infection at the transcriptomic level contributes to the development of antiviral therapy. In this study, a meta-analysis of CD8(+) T cell gene expression profiles derived from mono-HIV and HCV infected individuals at different stages of disease progression, was conducted to understand the common changes experienced by CD8(+) T cells. Methods Five microarray datasets, reporting CD8(+) T cell mRNA expression of the mono-HIV and HCV infected patients, were retrieved from Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were identified via integrative meta-analysis of expression data (INMEX) program. Network analysis methods were used to assess protein-protein interaction (PPI) networks, Gene Ontology (GO) terms and pathway enrichment for DEGs. MirDIP and miRDB online prediction tools were used to predict potential microRNAs (miRNAs) targeting hub genes. Results First, we identified 625 and 154 DEGs in the CD8(+) T cells originating from mono-HIV and HCV chronic progressor patients, respectively, compared to healthy individuals. Among them, interferon-stimulated genes (ISGs) including ISG15, IFIT3, ILI44L, CXCL8, FPR1 and TLR2, were upregulated after mono-HIV and HCV infection. Pathway enrichment analysis of DEGs showed that the "cytokine-cytokine receptor interaction" and "NF-kappa B" signaling pathways were upregulated after mono-HIV and HCV infection. In addition, we identified 92 and 50 DEGs in the CD8(+) T cells of HIV non-progressor and HCV resolver patients, respectively, compared with corresponding chronic progressors. We observed attenuated mitosis and reduced ISG expression in HIV non-progressors and HCV resolvers compared with the corresponding chronic progressors. Finally, we identified miRNA-143-3p, predicted to target both IFIT3 in HIV and STAT5A in HCV infection. Conclusions We identified DEGs and transcriptional patterns in mono-HIV and HCV infected individuals at different stages of disease progression and identified miRNA-143-3p with potential to intervene disease progression, which provides a new strategy for developing targeted therapies.