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Lung Neoplasms --- Toll-Like Receptors --- immunotherapy

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The innate immune system has evolved means to recognize and react suitably to foreign entities such as infectious agents. In many cases infectious microorganisms threaten the integrity and function of the target organs or tissues; therefore, consequent to their recognition the immune system becomes activated to ensure their elimination. Toll-like receptors (TLR) constitute a family of receptors specialized in the recognition of molecular patterns typically associated with infectious agents. Different TLRs exist, each selective for molecular entities and motifs belonging to a specific pathogen group. Consequently, it is thought that the molecular nature of invading microorganisms activates specific TLRs to drive adequate anti-infectious immunity. For instance, nucleic acid-specific, intracellular receptors (TLR3/7/8/9) are used to sense viruses and drive antiviral immunity, while other receptors (such as TLR2 and TLR4) recognize and promote immunity against bacteria, yeast, and fungi. Yet, it is becoming evident that activation of TLR pathways trigger mechanisms that not only stimulate but also regulate the immune system. For instance, TLR stimulation by viruses will drive antiviral interferon but also immunoregulatory cytokine production and regulatory T cell activation. Stimulation of TLRs by bacteria or using molecular agonists can also trigger both immune stimulatory and regulatory responses. TLR stimulation by infectious agents likely serves to activate but also control anti-infectious immunity, for instance prevent potential immunopathological tissue damage which can be caused by acute immune defense mechanisms. Previous work by us and others has shown that the immunoregulatory arm of TLR stimulation can additionally help control autoreactive processes in autoimmune disease. Hence, it is becoming established that gut commensals, which also play a crucial part in the control of autoimmune disease, establish immune regulatory mechanisms through activation of particular TLRs. In sum, it appears that TLRs are key immune players that not only stimulate but also regulate immune processes in health and disease. In this Research Topic, we wish to review the dual role of TLRs as activators and regulators of immune responses. We aim to motivate data-driven opinions as to the importance of context of TLR agonism for determining immune activation vs. regulation. The presentation of ongoing original works, as well as data and opinions around other innate immune receptors pertaining to this topic, are also encouraged.

Infection --- Toll-Like Receptors --- Probiotics --- Immune stimulation --- Immunoregulation --- Autoimmune Diseases --- cancer immunotherapy --- Inflammation --- microbiome --- tolerance

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The innate immune system has evolved means to recognize and react suitably to foreign entities such as infectious agents. In many cases infectious microorganisms threaten the integrity and function of the target organs or tissues; therefore, consequent to their recognition the immune system becomes activated to ensure their elimination. Toll-like receptors (TLR) constitute a family of receptors specialized in the recognition of molecular patterns typically associated with infectious agents. Different TLRs exist, each selective for molecular entities and motifs belonging to a specific pathogen group. Consequently, it is thought that the molecular nature of invading microorganisms activates specific TLRs to drive adequate anti-infectious immunity. For instance, nucleic acid-specific, intracellular receptors (TLR3/7/8/9) are used to sense viruses and drive antiviral immunity, while other receptors (such as TLR2 and TLR4) recognize and promote immunity against bacteria, yeast, and fungi. Yet, it is becoming evident that activation of TLR pathways trigger mechanisms that not only stimulate but also regulate the immune system. For instance, TLR stimulation by viruses will drive antiviral interferon but also immunoregulatory cytokine production and regulatory T cell activation. Stimulation of TLRs by bacteria or using molecular agonists can also trigger both immune stimulatory and regulatory responses. TLR stimulation by infectious agents likely serves to activate but also control anti-infectious immunity, for instance prevent potential immunopathological tissue damage which can be caused by acute immune defense mechanisms. Previous work by us and others has shown that the immunoregulatory arm of TLR stimulation can additionally help control autoreactive processes in autoimmune disease. Hence, it is becoming established that gut commensals, which also play a crucial part in the control of autoimmune disease, establish immune regulatory mechanisms through activation of particular TLRs. In sum, it appears that TLRs are key immune players that not only stimulate but also regulate immune processes in health and disease. In this Research Topic, we wish to review the dual role of TLRs as activators and regulators of immune responses. We aim to motivate data-driven opinions as to the importance of context of TLR agonism for determining immune activation vs. regulation. The presentation of ongoing original works, as well as data and opinions around other innate immune receptors pertaining to this topic, are also encouraged.

Infection --- Toll-Like Receptors --- Probiotics --- Immune stimulation --- Immunoregulation --- Autoimmune Diseases --- cancer immunotherapy --- Inflammation --- microbiome --- tolerance

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The group of pattern recognition receptors (PRRs) includes families of Toll-like receptors (TLRs), NOD-like receptors (NLRs), C-type lectin receptors (CLRs), RIG-I-like receptors (RLRs), and AIM-2-like receptors (ALRs). Conceptually, receptors constituting these families are united by two general features. Firstly, they directly recognize common antigen determinants of virtually all classes of pathogens (so-called pathogen-associated molecular patterns, or simply PAMPs) and initiate immune response against them via specific intracellular signaling pathways. Secondly, they recognize endogenous ligands (since they are usually released during cell stress, they are called damage-associated molecular patterns, DAMPs), and, hence, PRR-mediated immune response can be activated without an influence of infectious agents. So, pattern recognition receptors play the key role performing the innate and adaptive immune response. In addition, many PRRs have a number of other vital functions apart from participation in immune response realization. The fundamental character and diversity of PRR functions have led to amazingly rapid research in this field. Such investigations are very promising for medicine as immune system plays a key role in vast majority if not all human diseases, and the process of discovering the new aspects of the immune system functioning is rapidly ongoing. The role of Toll-like receptors in cancer was analyzed in certain reviews but the data are still scattered. This collection of reviews systematizes the key information in the field.

Toll-Like Receptors --- C-type lectin receptors --- nod-like receptors --- DNA Repair --- Pattern Recognition Receptors --- Inflammation --- RIG-I-like receptors --- Autophagy --- Cancer --- Apoptosis

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The innate immune system is the first line of defense against bacterial and viral infections and sterile inflammation through the recognition of pathogen-associated molecular patterns (PAMPs) by pathogen recognition receptors (PRRs) resulting in the production of proinflammatory and antiviral cytokines and chemokines. Several damage-associated molecular patterns (DAMPs), which were released by passive or active mechanisms under sterile conditions, are additionally recognized by PRRs and can cause or even aggravate the inflammatory response. In this special issue many aspects of innate immunity are summarized. Mechanisms of different DAMPs to induce pro- and anti-inflammatory activities, functions of different immune cells, as well as the crosstalk between coagulation and innate immunity were described. Furthermore, aspects of autoinflammatory diseases, types of programmed cell death pathways, and insect immunity are covered. Finally, therapeutic options for the treatment of diseases related to autoimmunity or infections are suggested. Overall, this special issue presents a broad overview of activities related to sterile inflammation and defense mechanisms of innate immunity.

Medicine --- inflammation --- type I interferons --- interleukin-1β --- crosstalk --- hepatic non-parenchymal cells --- albumin --- chronic liver diseases --- bacteria --- cytomegalovirus --- endothelin receptor --- repurposing --- cell culture --- Drosophila suzukii --- hemocytes --- plasmatocytes --- extracellular traps --- HMGB1 --- RAGE --- TLR4 --- DAMP --- SIRT1 --- α7-nicotinic acetylcholine receptor --- nociceptor --- cancer --- COVID-19 --- proteostasis --- autoinflammation --- ribosomopathies --- proteinopathies --- proteasomopathies --- extracellular RNA --- cytokines --- macrophages --- endothelial cells --- toll-like receptors --- angiogenesis --- γδ T cells --- gamma delta T cells --- proliferation --- macrophage polarization --- neutrophils --- neutrophil extracellular traps --- NETs --- ischemia --- PANoptosis --- PANoptosome --- pyroptosis --- apoptosis --- necroptosis --- inflammatory cell death --- inflammasome --- innate immunity --- infection --- NLR --- caspase --- IRF1 --- ZBP1 --- RIPK1 --- RIPK3 --- MLKL --- NLRP3 --- AIM2 --- Pyrin --- caspase-1 --- ASC --- caspase-8 --- caspase-3 --- caspase-7 --- plasticity --- redundancy --- SMOC1 --- thrombin --- n/a