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- W2907521807 abstract "The mammalian immune system consists of the innate and adaptive arm/s that protect the host against pathogenic infections in a highly coordinated process involving multiple steps. Innate immune cells such as macrophages and dendritic cells (DCs) are responsible fordetermining the initiation of specific events and thus they tailor specific immune responses to eliminate the invading pathogen. Host innate immune responses are triggered by sensing of PAMPs (pathogen associated molecular patterns) or DAMPs (damage associated molecularpatterns) via pattern recognition receptors (PRRs) and these inturn facilitate adaptive immune responses. The four major families of PRRs including Toll- like receptors (TLRs), NOD-like receptors (NLRs), RIG-I like receptors (RLRs) and C-type lectin receptors (CLRs) recognizea wide range of PAMPs and DAMPs. Engagement of PRRs with these stimuli promotes the differential induction of PRRs-driven signaling cascades such as inflammation, apoptosis, and autophagy among others that result in organized actions of multiple immune cells toeradicate microbial infection. However, in spite of having such effective and efficient immune system, some of the pathogens are able to breach immune layers and establish a successful infection while escaping host key immune surveillance mechanisms. One such pathogen of rising concern, Mycobacterium tuberculosis (Mtb) causing tuberculosis (TB), has evolved with mankind and causes an alarming 1.4 million deaths annually, in accordance with recent WHO reports.Mtb is an intracellular pathogen, whose primary target cells are macrophages. These are crucial effector immune cells that provide defense against a vast array of pathogens through the presentation of abundant cell surface receptors including TLRs that sensitize the host andexecute the tailoring of immune responses during mycobacterial infection. In particular, TLR2 has been shown to elicit inflammatory responses including the increased expression of effector molecules such as tumor necrosis factor (TNF) α, interferon gamma (IFN-γ), xiinterleukins (ILs), chemokines and inflammatory cytokines in this process. Accumulating evidences indicate the role of phagosomal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)2 in producing oxidative stress in order to clear pathogen. Recent reports have suggested essential role of NOX2 in efficient killing of mycobacteria. For example, p47-phox (NOX2 subunit) null mouse showed increased susceptibility tomycobacteria infection. Interestingly, another recent study suggested the crucial role of host NAD(P)H quinone oxidoreductase 1 (NQO1) in promoting mycobacterial survival. Yet the contribution of NQO1 in regulating immune responses during pathogenic mycobacteria infection needs further investigation. Additionally, few reports indicate the role for hostderived reductases in regulating apoptosis. More importantly, several studies propose that mycobacteria can inhibit apoptosis and promote its survival. Therefore, dissecting the molecular mechanism in…" @default.
- W2907521807 created "2019-01-11" @default.
- W2907521807 creator A5013772982 @default.
- W2907521807 date "2018-10-01" @default.
- W2907521807 modified "2023-09-27" @default.
- W2907521807 title "Delineating the Roles for WNT Signaling During PRRs Driven Inflammatory Responses : Implications for Host-Pathogen Interaction" @default.
- W2907521807 hasPublicationYear "2018" @default.
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