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Apoptosis. --- Cell death --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Cell Death --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide

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Cell death. --- Cellules --- Mort. --- Cell degeneration --- Cells --- Death (Biology) --- Cell Death. --- Apoptosis. --- Therapeutics. --- Therapy --- Treatment --- Therapeutic --- Therapies --- Treatments --- Disease --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Cell Death --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide --- Death, Cell --- Cellular Senescence --- therapy

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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

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Brucellosis, caused by the facultative intracellular bacteria Brucella species, is one the most prevalent zoonosis worldwide. • The articles described in this book report several aspects of host-Brucella interactions. • The findings described here will help to advance in the comprehension of bacterial pathogenesis and contribute to the future development of drugs or vaccines to control brucellosis.

Recombinant vaccine --- divalent vaccine --- brucellosis --- Omp25 --- L7/L12 --- Brucella abortus 544 --- ST2 receptor --- Brucella abortus --- oral infection --- human endometrial cells --- internalization --- intracellular replication --- decidualization --- chemokines --- macrophages --- Brucella --- HSC --- MHC --- IL-10 --- cell cycle --- (p)ppGpp --- rsh --- neurobrucellosis --- platelets --- brain microvascular endothelial cells --- endothelial cells --- adhesins --- Ig-like domain --- monomeric autotransporters --- trimeric autotransporters --- extracellular matrix --- polar localization --- virulence factors --- vaccine candidates --- fibronectin --- canonical inflammasome --- non-canonical inflammasome --- NLR --- pyroptosis --- ASC --- caspase-11 --- caspase-1 --- IL-1β --- gDNA --- replication niche --- reservoir --- persistence --- survival --- chronic infection --- n/a

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Biologie cellulaire --- Biologie clinique --- Cancer --- Celbiologie --- Kanker --- Klinische biologie --- Neoplasms --- Cell Cycle. --- Cell Differentiation. --- Apoptosis. --- Proto-Oncogenes --- Carcinogenesis --- Tumors --- Academic collection --- Tumours --- Pathology --- Cysts (Pathology) --- Oncology --- Oncogenesis --- Pathogenesis of cancer --- Tumorigenesis --- Genetic toxicology --- Apoptosis, Extrinsic Pathway --- Apoptosis, Intrinsic Pathway --- Programmed Cell Death, Type I --- Apoptoses, Extrinsic Pathway --- Apoptoses, Intrinsic Pathway --- Extrinsic Pathway Apoptoses --- Extrinsic Pathway Apoptosis --- Intrinsic Pathway Apoptoses --- Intrinsic Pathway Apoptosis --- Necrosis --- Cell Death --- Clonal Deletion --- Superantigens --- Caspases --- Caspase 1 --- In Situ Nick-End Labeling --- Cellular Apoptosis Susceptibility Protein --- Genes, Transgenic, Suicide --- Differentiation, Cell --- Cell Differentiations --- Differentiations, Cell --- Embryo, Mammalian --- Gene Expression Regulation --- Cell Lineage --- Cell Division Cycle --- Cell Cycles --- Cell Division Cycles --- Cycle, Cell --- Cycle, Cell Division --- Cycles, Cell --- Cycles, Cell Division --- Division Cycle, Cell --- Division Cycles, Cell --- Cell Cycle Proteins --- Genes, cdc --- genetics. --- Pathogenesis --- Apoptosis --- Cell Cycle --- Cell Differentiation --- genetics --- Caspase-Dependent Apoptosis --- Classic Apoptosis --- Classical Apoptosis --- Programmed Cell Death --- Apoptosis, Caspase-Dependent --- Apoptosis, Classic --- Apoptosis, Classical --- Caspase Dependent Apoptosis --- Cell Death, Programmed --- Classic Apoptoses