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1. Full Text POPsicle for Fever! Cooling Down the Inflammasome
by Shimada, Kenichi and Crother, Timothy R and Arditi, Moshe
Immunity, ISSN 1074-7613, 08/2015, Volume 43, Issue 2, pp. 213 - 215
Inhibition of the inflammasome might be beneficial for numerous inflammatory pathologies. In this issue of  , report that the PYRIN domain-only protein (POP1)... 
INTERLEUKIN-1 | DOMAIN | KAPPA-B | IMMUNOLOGY | Cryopyrin-Associated Periodic Syndromes - immunology | Animals | Inflammasomes - metabolism | Dendritic Cells - immunology | Humans | Macrophages, Peritoneal - immunology | Female | Monocytes - immunology | Ribonucleoproteins - metabolism | Peritonitis - immunology | Proteins | Mutation | Feedback | Rodents | Inflammatory diseases | Apoptosis
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2. Full Text Intestinal Permeability and IgA Provoke Immune Vasculitis Linked to Cardiovascular Inflammation
by Noval Rivas, Magali and Wakita, Daiko and Franklin, Michael K and Carvalho, Thacyana T and Abolhesn, Amanda and Gomez, Angela C and Fishbein, Michael C and Chen, Shuang and Lehman, Thomas J and Sato, Kazuki and Shibuya, Akira and Fasano, Alessio and Kiyono, Hiroshi and Abe, Masanori and Tatsumoto, Narihito and Yamashita, Michifumi and Crother, Timothy R and Shimada, Kenichi and Arditi, Moshe
Immunity, ISSN 1074-7613, 09/2019, Volume 51, Issue 3, pp. 508 - 521.e6
Recent experimental data and clinical, genetic, and transcriptome evidence from patients converge to suggest a key role of interleukin-1β (IL-1β) in the... 
IgA | intestinal permeability | Kawasaki disease | vasculitis | complement | coronary arteritis | interleukin-1β | CORONARY ARTERITIS | KAWASAKI-DISEASE | MANNOSE-BINDING LECTIN | INTERLEUKIN-1 RECEPTOR ANTAGONIST | MOUSE MODEL | BARRIER | SECRETORY IGA | GENOME-WIDE | IMMUNOLOGY | KIDNEY AXIS | CELIAC-DISEASE | Medical research | Medical colleges | Vasculitis | Interleukins | Analysis | Medicine, Experimental | Permeability | Immunoglobulin A | Diseases | Immunoglobulins | Disease | Pathogenesis | Mucosa | Interleukin | Inflammation | Cardiovascular pathology | IL-1β | Gene expression | Small intestine | Abdomen | Proteins | Molecular modelling | IgA nephropathy | Intestine | Coronary vessels | Vascular tissue | Bacteria | Mucocutaneous lymph node syndrome | Deposition
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3. Full Text T-Cell-Intrinsic Receptor Interacting Protein 2 Regulates Pathogenic T Helper 17 Cell Differentiation
by Shimada, Kenichi and Porritt, Rebecca A and Markman, Janet L and O’Rourke, Jacqueline Gire and Wakita, Daiko and Noval Rivas, Magali and Ogawa, Chihiro and Kozhaya, Lina and Martins, Gislâine A and Unutmaz, Derya and Baloh, Robert H and Crother, Timothy R and Chen, Shuang and Arditi, Moshe
Immunity, ISSN 1074-7613, 11/2018, Volume 49, Issue 5, pp. 873 - 885.e7
Receptor interacting protein 2 (RIP2) plays a role in sensing intracellular pathogens, but its function in T cells is unclear. We show that RIP2 deficiency in... 
atherosclerosis | Chlamydia pneumoniae | IL-17 | RORα | Th17 | chronic inflammation | RIP2 | T(H)17 CELLS | TGF-BETA | INNATE IMMUNE-RESPONSES | INFLAMMATION | HOST-DEFENSE | ATHEROSCLEROSIS | INFECTION | NOD2 | IMMUNOLOGY | NF-KAPPA-B | T-Lymphocyte Subsets - immunology | Encephalomyelitis, Autoimmune, Experimental - metabolism | T-Lymphocyte Subsets - cytology | Encephalomyelitis, Autoimmune, Experimental - etiology | Receptor-Interacting Protein Serine-Threonine Kinases - chemistry | Nuclear Receptor Subfamily 1, Group F, Member 1 - metabolism | Cell Differentiation - genetics | Inflammation - metabolism | Th17 Cells - metabolism | Atherosclerosis | Th17 Cells - cytology | Gene Expression | Encephalomyelitis, Autoimmune, Experimental - mortality | Immunophenotyping | Interleukin-1beta | Interleukin-17 - biosynthesis | Mice, Knockout | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | T-Lymphocyte Subsets - metabolism | Biomarkers | Inflammation - genetics | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Caspase Activation and Recruitment Domain | Oligomers | Medical research | Pneumonia | Interleukins | Bacterial pneumonia | Communicable diseases | Medicine, Experimental | Inflammation | Research institutes | T cells | Cell differentiation | Encephalomyelitis | Disease | Interleukin | Helper cells | Differentiation (biology) | Chronic infection | Infections | Lymphocytes T | Kinases | Proteins | Sexually transmitted diseases | Lymphocytes | Interleukin 1 | Chronic illnesses | Antigens | Oligomerization | Cytokines | Mortality | Gene expression | Experimental allergic encephalomyelitis | CD4 antigen | Lungs | Arteriosclerosis
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4. Full Text Abstract 423: Role of Autophagy in Macrophages During Acute Myocardial Infraction
by Chen, Shuang and Shimada, Kenichi and Crother, Timothy R and Yamashita, Michifumi and Arditi, Moshe
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 05/2018, Volume 38, Issue Suppl_1
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5. Full Text Correction: Nicotinamide exacerbates hypoxemia in ventilator-induced lung injury independent of neutrophil infiltration
by Jones, Heather D and Yoo, Jeena and Crother, Timothy R and Kyme, Pierre and Ben-Shlomo, Anat and Khalafi, Ramtin and Tseng, Ching W and Parks, William C and Arditi, Moshe and Liu, George Y and Shimada, Kenichi
PLoS ONE, ISSN 1932-6203, 05/2015, Volume 10, Issue 5, p. e0128735
NADPH | Ventilators | Hypoxemia | Lungs | Rodents | Neutrophils | Ventilation | Nicotinamide | Infiltration
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6. Full Text Abstract 4057: Gender and the immune system in lung and liver colonization of murine melanoma in a B16 metastatic model
by Markman, Janet L and Wakita, Daiko and Crother, Timothy R and Arditi, Moshe
Cancer Research, ISSN 0008-5472, 08/2015, Volume 75, Issue 15 Supplement, pp. 4057 - 4057
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7. Full Text Oxidized Mitochondrial DNA Activates the NLRP3 Inflammasome during Apoptosis
by Shimada, Kenichi and Crother, Timothy R and Karlin, Justin and Dagvadorj, Jargalsaikhan and Chiba, Norika and Chen, Shuang and Ramanujan, V. Krishnan and Wolf, Andrea J and Vergnes, Laurent and Ojcius, David M and Rentsendorj, Altan and Vargas, Mario and Guerrero, Candace and Wang, Yinsheng and Fitzgerald, Katherine A and Underhill, David M and Town, Terrence and Arditi, Moshe
Immunity, ISSN 1074-7613, 03/2012, Volume 36, Issue 3, pp. 401 - 414
We report that in the presence of signal 1 (NF-κB), the NLRP3 inflammasome was activated by mitochondrial apoptotic signaling that licensed production of... 
IN-VITRO | MECHANISM | CASPASE-1 | ATP BINDING | SALMONELLA | MICE | IL-1-BETA | IMMUNOLOGY | DAMAGE | NALP3 INFLAMMASOME | CELL-DEATH | Gene Expression | Inflammasomes - metabolism | Proto-Oncogene Proteins c-bcl-2 - immunology | DNA, Mitochondrial - metabolism | Oxidation-Reduction | Salmonella typhimurium - immunology | Salmonella typhimurium - pathogenicity | Signal Transduction | NLR Family, Pyrin Domain-Containing 3 Protein | Mice, Inbred C57BL | NF-kappa B - immunology | Macrophages - cytology | Mice, Knockout | DNA, Mitochondrial - immunology | Macrophages - metabolism | Animals | Apoptosis - immunology | Carrier Proteins - metabolism | Inflammasomes - immunology | Interleukin-1beta - biosynthesis | Mice | Proto-Oncogene Proteins c-bcl-2 - genetics | Carrier Proteins - immunology | Macrophages - immunology | Medical colleges | Cell death | DNA | Nucleosides | Mitochondrial DNA | Macrophages | Apoptosis | Microscopy | Colleges & universities | Software | Infections | Deoxyribonucleic acid--DNA
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8. Full Text Immunological Consequences of Intestinal Fungal Dysbiosis
by Wheeler, Matthew L and Limon, Jose J and Bar, Agnieszka S and Leal, Christian A and Gargus, Matthew and Tang, Jie and Brown, Jordan and Funari, Vincent A and Wang, Hanlin L and Crother, Timothy R and Arditi, Moshe and Underhill, David M and Iliev, Iliyan D
Cell Host & Microbe, ISSN 1931-3128, 06/2016, Volume 19, Issue 6, pp. 865 - 873
Compared to bacteria, the role of fungi within the intestinal microbiota is poorly understood. In this study we investigated whether the presence of a... 
MICROFLORA | SEVERE ASTHMA | ANTIBIOTICS | COMMENSAL FUNGI | MICROBIOLOGY | MICROBIOTA | CANDIDA-ALBICANS | THERAPY | VIROLOGY | INCREASED RISK | SENSITIZATION | MICE | PARASITOLOGY | Antifungal Agents - adverse effects | Fluconazole - pharmacology | Bacteria - drug effects | Hypersensitivity - immunology | Fluconazole - adverse effects | Drug Hypersensitivity - microbiology | Fungi - genetics | Fungi - immunology | Dysbiosis - immunology | Hypersensitivity - microbiology | Base Sequence | Colitis - immunology | Antifungal Agents - pharmacology | Dysbiosis - chemically induced | Fungi - drug effects | Mice, Inbred C57BL | Amphotericin B - pharmacology | Amphotericin B - adverse effects | Animals | Colitis - microbiology | Gastrointestinal Microbiome - drug effects | Intestines - microbiology | Drug Hypersensitivity - immunology | Mice | Gastrointestinal Microbiome - immunology | Dietary Supplements | Bacteria | Colitis | Microbiota (Symbiotic organisms) | Analysis | Antifungal agents
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9. Full Text Lipopolysaccharide Induces Alveolar Macrophage Necrosis via CD14 and the P2X7 Receptor Leading to Interleukin-1α Release
by Dagvadorj, Jargalsaikhan and Shimada, Kenichi and Chen, Shuang and Jones, Heather D and Tumurkhuu, Gantsetseg and Zhang, Wenxuan and Wawrowsky, Kolja A and Crother, Timothy R and Arditi, Moshe
Immunity, ISSN 1074-7613, 04/2015, Volume 42, Issue 4, pp. 640 - 653
Acute lung injury (ALI) remains a serious health issue with little improvement in our understanding of the pathophysiology and therapeutic approaches. We... 
BACTERIAL LIPOPOLYSACCHARIDE | STERILE INFLAMMATION | SIGNALING PATHWAY | P2X RECEPTORS | ALPHA PRODUCTION | ENDOTHELIAL-CELLS | MOUSE MODEL | IN-VIVO | ACUTE LUNG INJURY | IMMUNOLOGY | INFLAMMATORY RESPONSE | Interleukin-1alpha - immunology | Macrophages, Alveolar - pathology | Calcium - metabolism | Humans | Capillary Permeability - immunology | Neutrophil Infiltration | Necrosis - pathology | Receptors, Purinergic P2X7 - genetics | Necrosis - immunology | Cadherins - immunology | Adenosine Triphosphate - metabolism | HEK293 Cells | Interleukin-1alpha - genetics | Cadherins - genetics | Receptors, Purinergic P2X7 - immunology | Macrophages, Alveolar - immunology | Neutrophils - pathology | Lung - pathology | Protein Precursors - genetics | Signal Transduction | Neutrophils - drug effects | Gene Expression Regulation | Neutrophils - immunology | Lipopolysaccharide Receptors - immunology | Mice, Transgenic | Protein Precursors - immunology | Acute Lung Injury - pathology | Necrosis - chemically induced | Endothelial Cells - immunology | Animals | Acute Lung Injury - chemically induced | Macrophages, Alveolar - drug effects | Lung - drug effects | Lipopolysaccharides - pharmacology | Lipopolysaccharide Receptors - genetics | Acute Lung Injury - immunology | Mice | Endothelial Cells - pathology | Intubation, Intratracheal | Lung - immunology | Endothelial Cells - drug effects | endothelial cells | alveolar macrophage | Ca2+ influx | MyD88 | IL-1α | neutrophil | P2X7R | lung injury | necrosis | ARDS | ALI | sepsis | lung inflammation
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10. Full Text Caspase-1 dependent IL-1β secretion is critical for host defense in a mouse model of chlamydia pneumoniae lung infection
by Shimada, Kenichi and Crother, Timothy R and Karlin, Justin and Chen, Shuang and Chiba, Norika and Ramanujan, V. Krishnan and Vergnes, Laurent and Ojcius, David M and Arditi, Moshe
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 6, p. e21477
Chlamydia pneumoniae (CP) is an important human pathogen that causes atypical pneumonia and is associated with various chronic inflammatory disorders.... 
APOPTOSIS | INTERLEUKIN-1 | ACTIVATION | MICE DEFICIENT | IFN-GAMMA | IMMUNE-RESPONSES | MULTIDISCIPLINARY SCIENCES | INNATE | INDUCTION | BLOOD MONONUCLEAR-CELLS | NALP3 INFLAMMASOME | Lung - microbiology | Protein Biosynthesis | Chlamydia Infections - enzymology | Inflammasomes - metabolism | Reactive Oxygen Species - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Caspase 1 - metabolism | Chlamydia Infections - immunology | Disease Models, Animal | Interleukin-1beta - secretion | Lung - pathology | Macrophages, Alveolar - microbiology | Pneumonia, Bacterial - complications | Pneumonia, Bacterial - enzymology | Chlamydia Infections - complications | Mitochondria - metabolism | Toll-Like Receptor 2 - metabolism | Immunity, Innate | Macrophages, Alveolar - enzymology | Animals | Carrier Proteins - metabolism | Caspase 1 - deficiency | Survival Analysis | Pneumonia, Bacterial - immunology | Mice | Myeloid Differentiation Factor 88 - metabolism | Lung - immunology | Phagocytosis | Chlamydophila pneumoniae - immunology | Nitric Oxide Synthase Type II - metabolism | Pediatrics | Oxidative stress | Reactive oxygen species | Pneumonia | Immune clearance | Infections | Activation | Interleukin 1 receptors | Macrophages | Experiments | Caspase-1 | Sexually transmitted diseases | Mitochondria | Immunology | Chlamydia | Rodents | Interleukin 1 | Toll-like receptors | Bacteria | Alveoli | Immune system | Recombinant | Enzymes | Cytokines | Secretion | Mortality | Caspase | Protein biosynthesis | Pharmacology | Nitric-oxide synthase | Medicine | Signaling | Infectious diseases | Lungs | Protein synthesis | TLR2 protein | MyD88 protein | Potassium | Apoptosis
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11. Full Text Innate immune responses to Chlamydia pneumoniae infection: role of TLRs, NLRs, and the inflammasome
by Shimada, Kenichi and Crother, Timothy R and Arditi, Moshe
Microbes and Infection, ISSN 1286-4579, 11/2012, Volume 14, Issue 14, pp. 1301 - 1307
Chlamydiae are important human pathogens that are responsible for a wide rage of diseases with a significant impact on public health. In this review article we... 
Chlamydia pneumoniae | Inflammasome | TLR | NLR | INFECTIOUS DISEASES | SIGNALING PATHWAYS | ACTIVATION | IFN-GAMMA | MITOCHONDRIA | TRACHOMATIS | ATHEROSCLEROSIS | MICROBIOLOGY | IMMUNOLOGY | III SECRETION | CYTOCHROME-C | ELECTRON-MICROSCOPIC OBSERVATIONS | PEPTIDOGLYCAN SYNTHESIS | Vascular Diseases - immunology | Chlamydia Infections - immunology | Receptors, Cytoplasmic and Nuclear - immunology | Animals | Vascular Diseases - microbiology | Humans | Inflammasomes - immunology | Toll-Like Receptors - immunology | Immunity, Innate | Chlamydophila pneumoniae - immunology | Pneumonia | Immune response | Chlamydia | Bacterial pneumonia | Children | Health aspects | Public health | Diseases | Infection | Pathogens | Immunity | inflammasome
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12. Full Text Toll-Like Receptor 2 signaling protects mice from tumor development in a mouse model of Colitis-induced cancer
by Lowe, Emily L and Crother, Timothy R and Rabizadeh, Shervin and Hu, Bing and Wang, Hanlin and Chen, Shuang and Shimada, Kenichi and Wong, Michelle H and Michelsen, Kathrin S and Arditi, Moshe
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 9, p. e13027
Inflammatory bowel disease (IBD) is a disorder of chronic inflammation with increased susceptibility to colorectal cancer. The etiology of IBD is unclear but... 
INFLAMMATORY-BOWEL-DISEASE | TGF-BETA | DENDRITIC CELLS | EPITHELIAL-CELLS | NITRIC-OXIDE SYNTHASE | COLORECTAL-CANCER | IN-VIVO | BIOLOGY | REGULATORY T-CELLS | SPONTANEOUS INTESTINAL TUMORIGENESIS | CUTTING EDGE | Aberrant Crypt Foci - etiology | Toll-Like Receptor 2 - genetics | Colitis - genetics | Humans | Colitis - complications | Male | Aberrant Crypt Foci - immunology | Colorectal Neoplasms - etiology | Female | Colitis - immunology | Aberrant Crypt Foci - prevention & control | Disease Models, Animal | Signal Transduction | Mice, Inbred C57BL | Colorectal Neoplasms - prevention & control | Aberrant Crypt Foci - pathology | Immunity, Innate | Mice, Knockout | Neoplastic Processes | Animals | Colorectal Neoplasms - immunology | Interleukin-6 - immunology | Toll-Like Receptor 2 - immunology | Mice | Colorectal Neoplasms - pathology | Gastrointestinal diseases | Oncology, Experimental | Colorectal cancer | Colitis | Research | Risk factors | Cancer | Diseases | Immunohistochemistry | Haplotypes | Pediatrics | Inflammatory bowel diseases | Epithelial cells | Physicians | Colorectal carcinoma | Homeostasis | Innate immunity | Genomes | Immunity | Interleukin 6 | Proteins | Microorganisms | Histopathology | Immunology | Lymphocytes | Etiology | Intestine | Rodents | Toll-like receptors | Bacteria | Tumorigenesis | Immune system | Medical research | Immune response | Cytokines | Stat3 protein | Inflammation | Epithelium | Crohns disease | Medicine | Inflammatory bowel disease | Signaling | Infectious diseases | TLR2 protein | Regulation | Aberration | Immunofluorescence | Tumors
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13. Full Text Ogg1-Dependent DNA Repair Regulates NLRP3 Inflammasome and Prevents Atherosclerosis
by Tumurkhuu, Gantsetseg and Shimada, Kenichi and Dagvadorj, Jargalsaikhan and Crother, Timothy R and Zhang, Wenxuan and Luthringer, Daniel and Gottlieb, Roberta A and Chen, Shuang and Arditi, Moshe
Circulation Research, ISSN 0009-7330, 09/2016, Volume 119, Issue 6, pp. e76 - e90
RATIONALE:Activation of NLRP3 (nucleotide-binding domain and leucine-rich repeat pyrin domain containing 3) inflammasome-mediating interleukin (IL)-1β... 
atherosclerosis | macrophages | inflammasomes | DNA repair | mitochondria | SYSTEMIC-LUPUS-ERYTHEMATOSUS | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | ACTIVATED PROTEIN-KINASE | ACCELERATED ATHEROSCLEROSIS | DEFICIENT MICE | MITOCHONDRIAL-DNA | MAMMALIAN-CELLS | ENDOTHELIAL-CELLS | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | GLYCOSYLASE 1 | HEMATOLOGY | Inflammasomes - metabolism | DNA, Mitochondrial - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Atherosclerosis - genetics | Humans | DNA Glycosylases - genetics | DNA Repair - physiology | Diet, Western - adverse effects | Atherosclerosis - metabolism | Inflammasomes - genetics | Mice, Knockout | NLR Family, Pyrin Domain-Containing 3 Protein - genetics | DNA Glycosylases - deficiency | Animals | DNA, Mitochondrial - genetics | Mice | Atherosclerosis - prevention & control | DNA Glycosylases - metabolism | inflammasome | Ogg1 | Vascular Disease | Animal Models of Human Disease | macrophage | Inflammation
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14. Full Text The NOD/RIP2 pathway is essential for host defenses against chlamydophila pneumoniae lung infection
by Shimada, Kenichi and Chen, Shuang and Dempsey, Paul W and Sorrentino, Rosalinda and Alsabeh, Randa and Slepenkin, Anatoly V and Peterson, Ellena and Doherty, Terence M and David, Underhill and Crother, Timothy R and Moshe, Arditi
PLoS Pathogens, ISSN 1553-7366, 04/2009, Volume 5, Issue 4, pp. e1000379 - e1000379
Here we investigated the role of the Nod/Rip2 pathway in host responses to Chlamydophila pneumoniae-induced pneumonia in mice. Rip2(-/-) mice infected with C.... 
IFN-GAMMA | RECEPTOR-INTERACTING PROTEIN-2 | MICROBIOLOGY | INTRACELLULAR BACTERIAL-INFECTION | CHLAMYDIA-TRACHOMATIS INFECTION | VIROLOGY | FOAM CELL-FORMATION | IMMUNE-RESPONSES | IN-VIVO | TOLL-LIKE RECEPTORS | NITRIC-OXIDE | NF-KAPPA-B | PARASITOLOGY | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Nitric Oxide Synthase Type II - biosynthesis | Nod Signaling Adaptor Proteins - immunology | RNA, Messenger - analysis | Chlamydophila Infections - pathology | Pneumonia, Bacterial - metabolism | Flow Cytometry | Chlamydophila pneumoniae - metabolism | Bone Marrow Cells - immunology | Nod Signaling Adaptor Proteins - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - immunology | Pneumonia, Bacterial - pathology | Macrophages - immunology | Chemokines - immunology | Neutrophil Infiltration - immunology | Nitric Oxide - biosynthesis | Enzyme-Linked Immunosorbent Assay | Chlamydophila Infections - metabolism | Chlamydophila Infections - immunology | Immunity, Innate | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Pneumonia, Bacterial - immunology | Signal Transduction - physiology | Chemokines - metabolism | Mice | Bone Marrow Cells - metabolism | Chlamydophila pneumoniae - immunology | Chlamydia infections | Pneumonia | Immune response | Bacterial pneumonia | Physiological aspects | Causes of | Development and progression | Genetic aspects | Research | Gene expression | Cell culture | Lungs | Rodents | Bone marrow | Bacteria | Experiments | Recruitment
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