Cellular stress response and innate immune signaling: integrating pathways in host defense and inflammation
Department of Medicine, Division of Gastroenterology
Animals; *DNA Damage; Endoplasmic Reticulum Stress; Heat-Shock Response; Humans; *Immunity, Innate; Inflammation; Signal Transduction
Cellular and Molecular Physiology | Immunity
Extensive research in the past decade has identified innate immune recognition receptors and intracellular signaling pathways that culminate in inflammatory responses. Besides its role in cytoprotection, the importance of cell stress in inflammation and host defense against pathogens is emerging. Recent studies have shown that proteins in cellular stress responses, including the heat shock response, ER stress response, and DNA damage response, interact with and regulate signaling intermediates involved in the activation of innate and adaptive immune responses. The effect of such regulation by cell stress proteins may dictate the inflammatory profile of the immune response during infection and disease. In this review, we describe the regulation of innate immune cell activation by cell stress pathways, present detailed descriptions of the types of stress response proteins and their crosstalk with immune signaling intermediates that are essential in host defense, and illustrate the relevance of these interactions in diseases characteristic of aberrant immune responses, such as chronic inflammatory diseases, autoimmune disorders, and cancer. Understanding the crosstalk between cellular stress proteins and immune signaling may have translational implications for designing more effective regimens to treat immune disorders.
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Citation: J Leukoc Biol. 2013 Dec;94(6):1167-84. doi: 10.1189/jlb.0313153. Epub 2013 Aug 29. Link to article on publisher's site
Journal of leukocyte biology
Muralidharan, Sujatha and Mandrekar, Pranoti, "Cellular stress response and innate immune signaling: integrating pathways in host defense and inflammation" (2013). University of Massachusetts Medical School Faculty Publications. 506.