GIAN Course from 17th to 28th February
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Innate immunity is first line of defense system and promptly activated after microbial infection to initiate protective responses through production of inflammatory cytokines from various immune cells. Innate immune system consists of humoral components such as complements, acute phase proteins and cellular components such as Monocytes, Macrophages, Dendritic cells, Eosinophils, Basophils, Neutrophils, Mast cells and Natural-killer cells. The humoral components have a broad range of actions against microorganisms, including gram-positive and gram-negative bacteria, fungi and viruses. The cellular components either directly kill the microbial pathogens through phagocytosis or induce production of cytokines, which helps in the elimination of pathogens. The innate immune cells express various pattern recognition receptors (PRRs) which recognize signature molecules of the pathogen. These signature molecules are essential for the survival of the pathogen and known as a pathogen associated molecular pattern (PAMPs). These PRRs recognizes different PAMPs of the pathogen in various compartments of the cells and trigger induction of inflammatory cytokines for the host defense. Furthermore, the innate immune responses are also required for the development of the pathogen specific adaptive immunity through B and T lymphocytes.
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Balancing anti-viral innate immunity and immune homeostasis
Schematic representation of the regulation of the anti-viral signaling pathway, after sensing by viral products by their cognate pattern recognition receptors (PRRs).
Induction of oncogenesis by HCMV deubiqutinase
HCMV-DUB facilitates deubiquitination of TRAF6, TRAF3, IRAK1, IRF7 and STING to inhibit I-IFN synthesis, which in turn inhibits the expression of several pro-apoptotic genes and induces the expression of anti-apoptotic genes.
Bispecific targeting of the 3′UTR of RIG-I and PB1 by miR-485.
A) Model showing the targeting of RIG-I by miR-485 and the subsequent effects on antiviral responses and the replication of NDV and H5N1 when present at low viral titers. (B) Model showing the targeting of H5N1 PB1 by miR-485 and the subsequent effects on antiviral responses and H5N1 replication at high viral titers.
Regulatory role of IPS1 in cancer ablation
NDV infection and polyIC transfection induce type I IFN-dependent and -independent anticancer activity via the IPS-1, IRF3 and IRF7 axis. The mechanism of the type I IFN relies on high NDV replication, upregulation of TRAIL or downregulation of the BCL2, BIRC3 and PRKCE genes
All of us do not have equal talent, but all of us have an equal opportunity to develop our talents"
: Dr. APJ Abdul Kalam
(Former President of India)