scholarly journals The Role of Peptide Signals Hidden in the Structure of Functional Proteins in Plant Immune Responses

2019 ◽  
Vol 20 (18) ◽  
pp. 4343 ◽  
Author(s):  
Irina Lyapina ◽  
Anna Filippova ◽  
Igor Fesenko
Keyword(s):  
Immune Responses ◽  
Defense Responses ◽  
Innate Immune ◽  
Functional Protein ◽  
Diverse Range ◽  
Peptide Signals ◽  
Plant Pathogen Interactions ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Plants have evolved a sophisticated innate immune system to cope with a diverse range of phytopathogens and insect herbivores. Plasma-membrane-localized pattern recognition receptors (PRRs), such as receptor-like kinases (RLK), recognize special signals, pathogen- or damage-associated molecular patterns (PAMPs or DAMPs), and trigger immune responses. A growing body of evidence shows that many peptides hidden in both plant and pathogen functional protein sequences belong to the group of such immune signals. However, the origin, evolution, and release mechanisms of peptide sequences from functional and nonfunctional protein precursors, known as cryptic peptides, are largely unknown. Various special proteases, such as metacaspase or subtilisin-like proteases, are involved in the release of such peptides upon activation during defense responses. In this review, we discuss the roles of cryptic peptide sequences hidden in the structure of functional proteins in plant defense and plant-pathogen interactions.

scholarly journals The Role of Toll-Like Receptor Signaling in the Progression of Heart Failure

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Lili Yu ◽  
Zhiwei Feng
Keyword(s):  
Heart Failure ◽  
Immune Responses ◽  
Target Therapy ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Medical Systems ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns ◽  
Tlr Signaling Pathway

Medical systems worldwide are being faced with a growing need to understand mechanisms behind the pathogenesis of heart failure (HF) that is considered as a leading cause of morbidity and mortality around the world. Elevated levels of inflammatory mediators have been identified in patients with HF, which are primarily manifestations of innate immune responses mediated by pattern recognition receptors (PRRs). Toll-like receptors (TLRs), which belong to PRRs, are subjected to the release of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) to generate innate immune responses. More and more emerging data indicate that TLR signaling pathway molecules are involved in the progression of HF. Herein, we present new data with regard to the activation of TLRs in the failing heart, focusing on TLR2, TLR3, TLR4, and TLR9, and suggest the potential use of TLRs in target therapy.

scholarly journals Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension

2014 ◽  
Vol 306 (2) ◽  
pp. H184-H196 ◽  
Author(s):  
Cameron G. McCarthy ◽  
Styliani Goulopoulou ◽  
Camilla F. Wenceslau ◽  
Kathryn Spitler ◽  
Takayuki Matsumoto ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Cell Injury ◽  
Receptor Activation ◽  
Innate Immune ◽  
Immune System Activation ◽  
System Activation ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Low-grade systemic inflammation is a common manifestation of hypertension; however, the exact mechanisms that initiate this pathophysiological response, thereby contributing to further increases in blood pressure, are not well understood. Aberrant vascular inflammation and reactivity via activation of the innate immune system may be the first step in the pathogenesis of hypertension. One of the functions of the innate immune system is to recognize and respond to danger. Danger signals can arise from not only pathogenic stimuli but also endogenous molecules released following cell injury and/or death [damage-associated molecular patterns (DAMPs)]. In the short-term, activation of the innate immune system is beneficial in the vasculature by providing cytoprotective mechanisms and facilitating tissue repair following injury or infection. However, sustained or excessive immune system activation, such as in autoimmune diseases, may be deleterious and can lead to maladaptive, irreversible changes to vascular structure and function. An initial source of DAMPs that enter the circulation to activate the innate immune system could arise from modest elevations in peripheral vascular resistance. These stimuli could subsequently lead to ischemic- or pressure-induced events aggravating further cell injury and/or death, providing more DAMPs for innate immune system activation. This review will address and critically evaluate the current literature on the role of the innate immune system in hypertension pathogenesis. The role of Toll-like receptor activation on somatic cells of the vasculature in response to the release of DAMPs and the consequences of this activation on inflammation, vasoreactivity, and vascular remodeling will be specifically discussed.

scholarly journals Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Patrícia R S Rodrigues ◽  
Aljawharah Alrubayyi ◽  
Ellie Pring ◽  
Valentina M T Bart ◽  
Ruth Jones ◽  
...  
Keyword(s):  
Immune Responses ◽  
Current Knowledge ◽  
Innate Immune ◽  
Type I ◽  
Innate Immune Responses ◽  
Innate Immunology ◽  
Viral Pathogen ◽  
Health Crisis ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Abstract The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1β-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. Therefore, treatments that target inflammation and coagulation are promising strategies for reducing mortality in COVID-19.

scholarly journals The NLRP3 Inflammasome and Its Role in the Pathogenicity of Leukemia

2021 ◽  
Vol 22 (3) ◽  
pp. 1271
Author(s):  
Laura Urwanisch ◽  
Michela Luciano ◽  
Jutta Horejs-Hoeck
Keyword(s):  
Nlrp3 Inflammasome ◽  
Innate Immune System ◽  
Inflammatory Cell ◽  
Current Knowledge ◽  
Innate Immune ◽  
Leukemic Cells ◽  
Different Types ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Chronic inflammation contributes to the development and progression of various tumors. Especially where the inflammation is mediated by cells of the innate immune system, the NLRP3 inflammasome plays an important role, as it senses and responds to a variety of exogenous and endogenous pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). The NLRP3 inflammasome is responsible for the maturation and secretion of the proinflammatory cytokines interleukin-1β (IL-1β) and IL-18 and for the induction of a type of inflammatory cell death known as pyroptosis. Overactivation of the NLRP3 inflammasome can be a driver of various diseases. Since leukemia is known to be an inflammation-driven cancer and IL-1β is produced in elevated levels by leukemic cells, research on NLRP3 in the context of leukemia has increased in recent years. In this review, we summarize the current knowledge on leukemia-promoting inflammation and, in particular, the role of the NLRP3 inflammasome in different types of leukemia. Furthermore, we examine a connection between NLRP3, autophagy and leukemia.

scholarly journals Role of Damage-Associated Molecular Pattern/Cell Death Pathways in Vaccine-Induced Immunity

Viruses ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 2340
Author(s):  
Sun Min Lee ◽  
Paul Kim ◽  
Jinsuh You ◽  
Eui Ho Kim
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Natural Infection ◽  
Cell Death Pathways ◽  
Molecular Pattern ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns ◽  
Induced Immunity ◽  
Pathogenic Infection

Immune responses induced by natural infection and vaccination are known to be initiated by the recognition of microbial patterns by cognate receptors, since microbes and most vaccine components contain pathogen-associated molecular patterns. Recent discoveries on the roles of damage-associated molecular patterns (DAMPs) and cell death in immunogenicity have improved our understanding of the mechanism underlying vaccine-induced immunity. DAMPs are usually immunologically inert, but can transform into alarming signals to activate the resting immune system in response to pathogenic infection, cellular stress and death, or tissue damage. The activation of DAMPs and cell death pathways can trigger local inflammation, occasionally mediating adaptive immunity, including antibody- and cell-mediated immune responses. Emerging evidence indicates that the components of vaccines and adjuvants induce immunogenicity via the stimulation of DAMP/cell death pathways. Furthermore, strategies for targeting this pathway to enhance immunogenicity are being investigated actively. In this review, we describe various DAMPs and focus on the roles of DAMP/cell death pathways in the context of vaccines for infectious diseases and cancer.

scholarly journals Parasitic Infections: A Role for C-Type Lectins Receptors

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Alicia Vázquez-Mendoza ◽  
Julio César Carrero ◽  
Miriam Rodriguez-Sosa
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Innate Immune ◽  
Parasitic Infections ◽  
Dependent Manner ◽  
Innate Immune Responses ◽  
Parasite Infections ◽  
Antigen Presenting ◽  
Molecular Patterns

Antigen-presenting cells (APCs) sense the microenvironment through several types of receptors that recognize pathogen-associated molecular patterns. In particular, C-type lectins receptors (CLRs), which are expressed by distinct subsets of dendritic cells (DCs) and macrophages (MØs), recognize and internalize specific carbohydrate antigens in a Ca2+-dependent manner. The targeting of these receptors is becoming an efficient strategy for parasite recognition. However, relatively little is known about how CLRs are involved in both pathogen recognition and the internalization of parasites. The role of CLRs in parasite infections is an area of considerable interest because this research will impact our understanding of the initiation of innate immune responses, which influences the outcome of specific immune responses. This paper attempts to summarize our understanding of the effects of parasites’ interactions with CLRs.

scholarly journals Bacterial Endophytes: The Hidden Actor in Plant Immune Responses Against Biotic Stress

2021 ◽  
Author(s):  
Nadira Oukala ◽  
Kamel Aissat ◽  
Victoria Pastor
Keyword(s):  
Immune Responses ◽  
Defense Responses ◽  
Plant Tissues ◽  
Bacterial Endophytes ◽  
Entire Plant ◽  
Bacterial Endosymbionts ◽  
Promote Plant Growth ◽  
Plant Pathogen Interactions ◽  
The Impact

Bacterial endophytes interact closely with plant tissues and constitute an essential part of the plant microbiome. These interactions can promote plant growth and elicit specific defense responses against abiotic stresses and pathogen attacks. In this paper, we review the role of endophytic bacteria in modulating defenses of the host rendering the entire plant more resistant to pathogens and pests. The endophyte-induced resistance will probably introduce a new factor when consid-ering plant-pathogen interactions. The impact of the bacterial endosymbionts on the host leading to the priming state is also discussed since it confers a specific adaptation of the plant to the biotic threat.

scholarly journals TLRs as a Promise Target Along With Immune Checkpoint Against Gastric Cancer

2021 ◽  
Vol 8 ◽  
Author(s):  
Lin Cui ◽  
Xiuqing Wang ◽  
Dekai Zhang
Keyword(s):  
Gastric Cancer ◽  
Pattern Recognition ◽  
Immune Responses ◽  
Therapeutic Agents ◽  
Pattern Recognition Receptors ◽  
Innate Immune ◽  
Therapeutic Approaches ◽  
The World ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Gastric cancer (GC) is one of the most common cancers in the world, and the incidence of gastric cancer in Asia appears to increase in recent years. Although there is a lot of improvement in treatment approaches, the prognosis of GC is poor. So it is urgent to search for a novel and more effective treatment to improve the survival rate of patients. Both innate immunity and adaptive immunity are important in cancer. In the innate immune system, pattern recognition receptors (PRRs) activate immune responses by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Toll-like receptors (TLRs) are a class of pattern recognition receptors (PRRs). Many studies have reported that TLRs are involved in the occurrence, development, and treatment of GC. Therefore, TLRs are potential targets for immunotherapy to gastric cancer. However, gastric cancer is a heterogeneous disorder, and TLRs function in GC is complex. TLRs agonists can be potentially used not only as therapeutic agents to treat gastric cancer but also as adjuvants in conjunction with other immunotherapies. They might provide a promising new target for GC treatment. In the review, we sort out the mechanism of TLRs involved in tumor immunity and summarize the current progress in TLRs-based therapeutic approaches and other immunotherapies in the treatment of GC.

scholarly journals Targeting Innate Immunity to Combat Cutaneous Stress: The Vitiligo Perspective

2021 ◽  
Vol 12 ◽  
Author(s):  
Katia Boniface ◽  
Thierry Passeron ◽  
Julien Seneschal ◽  
Meri K. Tulic
Keyword(s):  
Immune Response ◽  
Current Knowledge ◽  
Therapeutic Strategies ◽  
Innate Immune ◽  
Danger Signals ◽  
Multiple Factors ◽  
Autoimmune Condition ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Multiple factors are involved in the process leading to melanocyte loss in vitiligo including environmental triggers, genetic polymorphisms, metabolic alterations, and autoimmunity. This review aims to highlight current knowledge on how danger signals released by stressed epidermal cells in a predisposed patient can trigger the innate immune system and initiate a cascade of events leading to an autoreactive immune response, ultimately contributing to melanocyte disappearance in vitiligo. We will explore the genetic data available, the specific role of damage-associated-molecular patterns, and pattern-recognition receptors, as well as the cellular players involved in the innate immune response. Finally, the relevance of therapeutic strategies targeting this pathway to improve this inflammatory and autoimmune condition is also discussed.

scholarly journals Mitochondrial antiviral signalling protein is crucial for the development of pulmonary fibrosis

2020 ◽  
pp. 2000652
Author(s):  
Sang-Hun Kim ◽  
Jung Yeon Lee ◽  
Chang Min Yoon ◽  
Hyeon Jun Shin ◽  
Sei Won Lee ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Therapeutic Strategy ◽  
Innate Immune ◽  
Therapeutic Effects ◽  
Innate Immune Responses ◽  
Approved Drugs ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Danger signals, or damage-associated molecular patterns (DAMPs), instigate mitochondrial innate immune responses wherein Mitochondrial Antiviral Signalling protein (MAVS) functions as a key platform molecule to mediate them. The role of MAVS in the pathogenesis of idiopathic pulmonary fibrosis (IPF), however, has not been identified yet. A possibility whether the MAVS signalling can be modulated by currently existing drugs has not been explored, either. Here, using an established model of pulmonary fibrosis, we demonstrate that MAVS plays as a critical mediator of multiple DAMPs signalling pathways and the consequent lung fibrosis after bleomycin-induced injury in vivo. After bleomycin injury, the expression of MAVS was mainly observed in macrophages. In addition, multimeric MAVS aggregation, a key event of MAVS signalling activation, was significantly increased and persisted in bleomycin-injured lungs. Interestingly, a proapoptotic BH3 mimetic ABT-263 attenuated the expression of MAVS and its signalling and, consequently, the development of experimental pulmonary fibrosis. In contrast, the therapeutic effects of Pirfenidone or Nintedanib, two approved drugs for IPF treatment, were not related to the modulation of MAVS or its signalling. Importantly, multimeric MAVS aggregation was significantly increased in lungs from the patients with IPF as well. In conclusion, MAVS may play an important role in the development of pulmonary fibrosis, and targeting MAVS with BH3 mimetics may provide a novel therapeutic strategy for IPF, a major unmet disorder.

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