Showing papers by "Himanshu Kumar published in 2013"

Recognition of bacterial infection by innate immune sensors

Abstract: Microbial challenges to the host initiate an array of defense processes through the activation of innate and adaptive immunity. Innate immunity consists of sensors or pattern-recognition receptors (PRRs) that are expressed on immune and non-immune cells and sense conserved pathogen-derived molecules or pathogen-associated molecular patterns (PAMPs) in various compartments of the host cells. Recognition of the PAMPs by PRRs triggers antimicrobial effector responses via the induction of proinflammatory cytokines and type I IFNs. Several families of PRRs, such as Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and DNA sensors and their respective PAMPs have been well studied in innate immunity and host defense. Here, we review the recent findings on bacterial recognition by TLRs and NLRs and the signaling pathways activated by these sensors.

Sweeten PAMPs: Role of Sugar Complexed PAMPs in Innate Immunity and Vaccine Biology

Abstract: Innate sensors play a critical role in the early innate immune responses to invading pathogens through sensing of diverse biochemical signatures also known as pathogen associated molecular patterns (PAMPs). These biochemical signatures primarily consist of a major family of biomolecules such as proteins, lipids, nitrogen bases, and sugar and its complexes, which are distinct from host molecules and exclusively expressed in pathogens and essential to their survival. The family of sensors known as pattern recognition receptors (PRRs) are germ-line encoded, evolutionarily conserved molecules, and consist of Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), NOD-like receptors (NLRs), C-type lectin-like receptors (CLRs), and DNA sensors. Sensing of PAMP by PRR initiates the cascade of signaling leading to the activation of transcription factors, such as NF-κB and interferon regulatory factors (IRFs), resulting in a variety of cellular responses, including the production of interferons (IFNs) and pro-inflammatory cytokines. In this review, we discuss sensing of different types of glycosylated PAMPs such as β-glucan (a polymeric sugar) or lipopolysaccharides, nucleic acid, and so on (sugar complex PAMPs) by different families of sensors, its role in pathogenesis, and its application in development of potential vaccine and vaccine adjuvants.

Innate Immune Recognition Mechanisms and Translational Opportunities

Abstract: Innate immune sensors are a family of receptors which play a pivotal role in immune surveillance in various cellular compartments, recognizing numerous motifs derived from pathogens or associated with altered self molecules. Sensing of pathogenic components of self or nonself origin leads to a variety of integrated responses such as induction of proinflammatory and antiviral cytokines and lipid mediators, as well as upregulation of costimulatory molecules on a variety of cells. Furthermore, these sensors play a crucial role in cell survival, autophagy and pluripotency, and therefore, they are essential for the maintenance of cellular metabolic homeostasis. Finally, these sensors also play a substantial role in elicitation of specific immune responses, deploying and regulating the development of appropriate adaptive immunity against pathogens. This issue focuses on the biology of innate immune sensors, particularly Toll-like receptors and C-type lectin receptors, mutations in such sensors and/or their signaling components associated with disorders and the role of innate immune sensors in the mechanism of response to particulate vaccine adjuvants.

This information is current as Plasmacytoid Dendritic Cells Production in α of Viral Replication for IFN- Feedback Signaling Masks the Requirement Recognition Along with Type I IFN Positive Cutting Edge: TLR-Dependent Viral

Abstract: Kawai, Osamu Takeuchi and Shizuo AkiraYutaro Kumagai, Himanshu Kumar, Shohei Koyama, Tarohttp://www.jimmunol.org/content/182/7/3960doi: 10.4049/jimmunol.0804315J Immunol€2009; 182:3960-3964; ;Referenceshttp://www.jimmunol.org/content/182/7/3960.full#ref-list-1This article cites 22 articles, 12 of which you can access for free at: Subscriptionshttp://jimmunol.org/subscriptionsInformation about subscribing to The Journal of Immunology is online at: Permissionshttp://www.aai.org/ji/copyright.htmlSubmit copyright permission requests at: Email Alertshttp://jimmunol.org/cgi/alerts/etocReceive free email-alerts when new articles cite this article. Sign up at: