30 research outputs found
Expression of Scavenger receptor A on antigen presenting cells is important for CD4+ T-cells proliferation in EAE mouse model
Identification of Candidate Susceptibility and Resistance Genes of Mice Infected with Streptococcus suis Type 2
Streptococcus suis type 2 (SS2) is an important swine pathogen and zoonosis agent. A/J mice are significantly more susceptible than C57BL/6 (B6) mice to SS2 infection, but the genetic basis is largely unknown. Here, alterations in gene expression in SS2 (strain HA9801)-infected mice were identified using Illumina mouse BeadChips. Microarray analysis revealed 3,692 genes differentially expressed in peritoneal macrophages between A/J and B6 mice due to SS2 infection. Between SS2-infected A/J and control A/J mice, 2646 genes were differentially expressed (1469 upregulated; 1177 downregulated). Between SS2-infected B6 and control B6 mice, 1449 genes were differentially expressed (778 upregulated; 671 downregulated). These genes were analyzed for significant Gene Ontology (GO) categories and signaling pathways using the Kyoto Encylopedia of Genes and Genomes (KEGG) database to generate a signaling network. Upregulated genes in A/J and B6 mice were related to response to bacteria, immune response, positive regulation of B cell receptor signaling pathway, type I interferon biosynthesis, defense and inflammatory responses. Additionally, upregulated genes in SS2-infected B6 mice were involved in antigen processing and presentation of exogenous peptides, peptide antigen stabilization, lymphocyte differentiation regulation, positive regulation of monocyte differentiation, antigen receptor-mediated signaling pathway and positive regulation of phagocytosis. Downregulated genes in SS2-infected B6 mice played roles in glycolysis, carbohydrate metabolic process, amino acid metabolism, behavior and muscle regulation. Microarray results were verified by quantitative real-time PCR (qRT-PCR) of 14 representative deregulated genes. Four genes differentially expressed between SS2-infected A/J and B6 mice, toll-like receptor 2 (Tlr2), tumor necrosis factor (Tnf), matrix metalloproteinase 9 (Mmp9) and pentraxin 3 (Ptx3), were previously implicated in the response to S. suis infection. This study identified candidate genes that may influence susceptibility or resistance to SS2 infection in A/J and B6 mice, providing further validation of these models and contributing to understanding of S. suis pathogenic mechanisms
The long pentraxin 3 : a key component of innate immunity, modulates the inflammatory response to non self and self ligands
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Co-regulation of the long pentraxin PTX3 and the hyaluronic acid binding protein TSG-6 in leukocytes : potential involvement in hyaluronic acid-rich extracellular matrix assembly in inflammation
The long pentraxin PTX3 as a prototypic humoral pattern recognition receptor : interplay with cellular innate immunity
The innate immune system consists of a cellular arm and a humoral arm. Components of humoral immunity include diverse molecular families, which represent functional ancestors of antibodies. They play a key role as effectors and modulators of innate resistance in animals and humans, interacting with cellular innate immunity. The prototypic long pentraxin, pentraxin 3 (PTX3), represents a case in point of this interplay. Gene targeting of this evolutionarily conserved long pentraxin has unequivocally defined its role at the crossroads of innate immunity, inflammation, matrix deposition, and female fertility. Phagocytes represent a key source of this fluid-phase pattern recognition receptor, which, in turn, facilitates microbial recognition by phagocytes acting as an opsonin. Moreover, PTX3 has modulatory functions on innate immunity and inflammation. Here, we review the studies on PTX3 which emphasize the complexity and complementarity of the crosstalk between the cellular and humoral arms of innate immunity
Tuning of inflammatory cytokines and toll-like receptors by TIR8/SIGIRR, a member of the IL-1 receptor family with unique structur and regulation
Co-regulation in leukocytes of the long pentraxin PTX3 and TSG-6, two co-operating molecules involved in the assembly of hyaluronan-rich extracellular matrices.
Co-regulation of the long pentraxin PTX3 and the hyaluronic acid binding protein TSG-6 in leukocytes : potential involvement in hyaluronic acid-rich extracellular matrix assembly in inflammation
Complex pattern of HTLV-2 splicing and expression in PBMCs from infected patients
HTLV express multiple gene products from the same coding region by employing different strategies, including alternative splicing. Our investigations were focused on the analysis of the levels of expression of different HTLV-2 transcripts, to test their temporal expression at different stages of viral cycle and their quantitation by real time RT-PCR, in infected cell lines and in primary cultures of PBMCs from infected subjects.
An early transcription of tax/rex regulatory mRNA was observed, followed by a gradual and steady increase of gag/pol and env structural transcripts and of other accessory mRNAs. We identified a novel 3\u2019 splice acceptor site, used by both HTLV-2 A and B subtypes to generate alternative doubly spliced mRNAs within the pX region and also a novel env isoform preferentially expressed in 2B subtypes and behaving as a late gene. Among the singly spliced mRNAs coding for other accessory proteins, the p28, p22/p20-II isoform was found to be highly expressed as compared to its alternative p28, p22/p20-I form. The APH-2 transcript from the negative strand behaved as a late gene in stably infected cells, while in ex-vivo PBMCs its kinetics appeared to be variable so that a clear pattern of expression was not yet assessed.
In conclusion, the temporal transcription of different HTLV-2 transcripts follows a distinct expression pattern: tax/rex is the first mRNA to be expressed, thus indicating that it is necessary at the beginning of the infection cycle to transactivate and regulate viral and cellular transcripts, while gag/pol and env structural genes are expressed later in the viral cycle