Results 191 to 200 of about 13,578 (213)

Alarmins in autoimmune diseases

Autoimmunity Reviews, 2022
Alarmins are endogenous, constitutively expressed, chemotacting and immune activating proteins or peptides released because of non-programmed cell death (i.e. infections, trauma, etc). They are considered endogenous damage-associated molecular patterns (DAMPs), able to induce a sterile inflammation.
Danieli, Maria Giovanna, Antonelli, Eleonora, Piga, Mario Andrea, Claudi, Ilaria, Palmeri, Davide, Tonacci, Alessandro, Allegra, Alessandro, Gangemi, Sebastiano   +7 more
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[Alarmins and anti-alarmin biologics in asthma].

Tuberkuloz ve toraks, 2018
Alarmins are endogenous, constitutively expressed, chemotactic, and immune activating proteins/peptides that are released as a result of degranulation, cell injury or death, or in response to immune induction. Alarmins are involved in a variety of processes including antimicrobial gene expression regulation, cellular homeostasis, wound healing ...
Begüm, Görgülü, Sevim, Bavbek
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Alarmins Initiate Host Defense

2007
In response to infection and/or tissue injury, cells of the host innate immune system rapidly produce a variety of structurally distinct mediators (we elect to call alarmins) that not only function as potent effectors of innate defense but also act to alarm the immune system by promoting the recruitment and activation of host leukocytes through ...
Joost J, Oppenheim, Poonam, Tewary, Gonzalo, de la Rosa, De, Yang   +3 more
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Anti-alarmin approaches entering clinical trials

Current Opinion in Pulmonary Medicine, 2020
Purpose of review The alarmins, thymic stromal lymphopoietin (TSLP), interleukin (IL)-25 and IL-33, are upstream regulators of T2 (type 2) inflammation and found to be expressed at high levels in airway epithelium of patients with T2 asthma. This review will summarize how alarmins regulate the inflamed asthmatic airways through
Gail M, Gauvreau, Lucie, White, Beth E, Davis   +2 more
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Alarmins of the extracellular space

Seminars in Immunology, 2018
The ability of the immune system to discriminate between healthy-self, abnormal-self, and non-self has been attributed mainly to alarmins signaling as "danger signals". It is now evident, however, that alarmins are much more complex and can perform specialized functions that can regulate a wide spectrum of processes ranging from propagation of disease ...
Jenna L, Dziki, George, Hussey, Stephen F, Badylak   +2 more
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Alarmin Detection in Senescent Cells

2018
Senescent cells secrete diverse array of proteins. One group of proteins, damage-associated molecular pattern (DAMP) proteins exhibit relocalization from inside to outside the cell. High Mobility Group Box 1 protein (HMGB1) is the founding DAMP member. HMGB1 relocalization from the nucleus provides a molecular signature during senescence.
Dong Eun, Kim, Albert R, Davalos
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Alarmins: chemotactic activators of immune responses

Current Opinion in Immunology, 2005
The recruitment and activation of antigen-presenting cells are critical early steps in mounting an immune response. Many microbial components and endogenous mediators participate in this process. Recent studies have identified a group of structurally diverse multifunctional host proteins that are rapidly released following pathogen challenge and/or ...
Joost J, Oppenheim, De, Yang
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ApoC3: an ‘alarmin’ triggering sterile inflammation

Nature Immunology, 2019
NLRP3-driven sterile inflammation facilitates the pathogenesis of various human inflammatory diseases. New work identifies apolipoprotein C3 as an endogenous NLRP3 agonist that promotes sterile inflammation and organ damage.
Tao Gong, Rongbin Zhou
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Alarmin’ lymphoid developments

Science Signaling
The alarmin cytokine IL-33 stimulates the formation of immune hubs within otherwise “cold” tumors.
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Endothelial Injury, Alarmins, and Allog raft Rejection

Critical Reviews™ in Immunology, 2008
Allograft blood vessels are important targets of clinical allograft rejection. Perioperative allograft injury to graft vasculature, especially the endothelial cell (EC) lining, increases the risk of subsequent acute and chronic vascular rejection. We hypothesize that allograft EC injured by ischemia-reperfusion (I/R) during transplantation releases ...
Deepak A, Rao, Jordan S, Pober
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