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1. Full Text Signalling pathways and molecular interactions of NOD1 and NOD2
by Watanabe, Tomohiro and Kitani, Atsushi and Murray, Peter J and Strober, Warren
Nature Reviews Immunology, ISSN 1474-1733, 01/2006, Volume 6, Issue 1, pp. 9 - 20
The NOD (nucleotide-binding oligomerization domain) proteins NOD1 and NOD2 have important roles in innate immunity as sensors of microbial components derived... 
HUMAN MONOCYTIC CELLS | INFLAMMATORY-BOWEL-DISEASE | CROHNS-DISEASE | INNATE IMMUNE-RESPONSES | TOLL-LIKE RECEPTORS | MURAMYL DIPEPTIDE RECOGNITION | LEUCINE-RICH REPEAT | HOST-MICROBIAL INTERACTIONS | IMMUNOLOGY | NF-KAPPA-B | INTESTINAL EPITHELIAL-CELLS | Adaptor Proteins, Signal Transducing - chemistry | Humans | Crohn Disease - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Nod2 Signaling Adaptor Protein | Signal Transduction - genetics | Crohn Disease - immunology | Signal Transduction - immunology | Adaptor Proteins, Signal Transducing - physiology | Animals | Crohn Disease - pathology | Intracellular Signaling Peptides and Proteins - chemistry | Adaptor Proteins, Signal Transducing - genetics | Nod1 Signaling Adaptor Protein | Adaptor Proteins, Signal Transducing - metabolism | Intracellular Signaling Peptides and Proteins - physiology | Immunity, Mucosal - genetics | Intracellular Signaling Peptides and Proteins - genetics
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2. Full Text NOD2 is a negative regulator of Toll-like receptor 2-mediated T helper type 1 responses
by Watanabe, Tomohiro and Kitani, Atsushi and Murray, Peter J and Strober, Warren
Nature Immunology, ISSN 1529-2908, 08/2004, Volume 5, Issue 8, pp. 800 - 808
The mechanism by which mutations in CARD15, which encodes nucleotide-binding oligomerization domain 2 (NOD2), cause Crohn disease is poorly understood. Because... 
ACTIVATION | INFLAMMATORY-BOWEL-DISEASE | CROHNS-DISEASE | GENE | MURAMYL DIPEPTIDE | HOST RECOGNITION | C-REL | IMMUNOLOGY | BACTERIAL PEPTIDOGLYCAN | NF-KAPPA-B | INTESTINAL EPITHELIAL-CELLS | T-Lymphocyte Subsets - immunology | Crohn Disease - genetics | Toll-Like Receptor 2 | Membrane Glycoproteins - metabolism | Crohn Disease - metabolism | Intracellular Signaling Peptides and Proteins | Receptors, Cell Surface - metabolism | Immunoblotting | NF-kappa B - metabolism | Nod2 Signaling Adaptor Protein | Reverse Transcriptase Polymerase Chain Reaction | Th1 Cells - immunology | Carrier Proteins - genetics | Signal Transduction - immunology | Toll-Like Receptors | Animals | Flow Cytometry | Mice | Mutation
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3. Full Text A Mutation in the Nlrp3 Gene Causing Inflammasome Hyperactivation Potentiates Th17 Cell-Dominant Immune Responses
by Meng, Guangxun and Zhang, Fuping and Fuss, Ivan and Kitani, Atsushi and Strober, Warren
Immunity, ISSN 1074-7613, 06/2009, Volume 30, Issue 6, pp. 860 - 874
Missense mutations of the gene encoding NLRP3 are associated with autoinflammatory disorders characterized with excessive production of interleukin-1β (IL-1β).... 
MOLIMMUNO | CELLIMMUNO | RHEUMATOID-ARTHRITIS | T(H)17 CELLS | TGF-BETA | IL-17-PRODUCING T-CELLS | INTERLEUKIN-1-BETA SECRETION | CASPASE-1 INFLAMMASOME | CYTOKINE MILIEU | IMMUNOLOGY | CIAS1 MUTATIONS | NEUTROPHIL RECRUITMENT | NALP3 INFLAMMASOME | Interleukin-18 - immunology | NLR Family, Pyrin Domain-Containing 3 Protein | Skin - metabolism | Mutation - immunology | CD4-Positive T-Lymphocytes - immunology | T-Lymphocytes, Helper-Inducer - immunology | Adenosine Triphosphate - metabolism | Receptors, Antigen, T-Cell - immunology | Interleukin-1beta - biosynthesis | Carrier Proteins - immunology | Macrophages - immunology | Skin - pathology | Cytokines - immunology | Skin - immunology | Antigen-Presenting Cells - metabolism | T-Lymphocytes, Helper-Inducer - metabolism | Cytokines - metabolism | Receptors, Antigen, T-Cell - metabolism | Mice, Inbred C57BL | CD4-Positive T-Lymphocytes - metabolism | Interleukin-1beta - immunology | Adenosine Triphosphate - immunology | Inflammation - immunology | Mutation - genetics | Antigen-Presenting Cells - immunology | Carrier Proteins - genetics | Cell Differentiation - immunology | Interleukin-18 - biosynthesis | Macrophages - metabolism | Animals | Carrier Proteins - metabolism | Inflammation - genetics | Mice | Analysis | Genetic aspects | Immune response | Studies | Bone marrow | Mutation | Gene expression | Immune system
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4. Full Text Muramyl dipeptide activation of nucleotide-binding oligomerization domain 2 protects mice from experimental colitis
by Watanabe, Tomohiro and Asano, Naoki and Murray, Peter J and Ozato, Keiko and Tailor, Prafullakumar and Fuss, Ivan J and Kitani, Atsushi and Strober, Warren
Journal of Clinical Investigation, ISSN 0021-9738, 02/2008, Volume 118, Issue 2, pp. 545 - 559
The mechanisms underlying the susceptibility of individuals with caspase recruitment domain 15 (CARD15) mutations and corresponding abnormalities of... 
Acetylmuramyl-Alanyl-Isoglutamine - administration & dosage | Adjuvants, Immunologic - administration & dosage | Dendritic Cells - immunology | Interferon Regulatory Factors - antagonists & inhibitors | Interferon Regulatory Factors - metabolism | Nod2 Signaling Adaptor Protein - genetics | Mice, Mutant Strains | Colitis - chemically induced | Toll-Like Receptors - antagonists & inhibitors | Dendritic Cells - drug effects | Colitis - immunology | Disease Models, Animal | Disease Susceptibility | Cytokines - metabolism | Immunity, Innate - drug effects | Down-Regulation | RNA, Small Interfering - pharmacology | Interferon Regulatory Factors - genetics | Crohn Disease - immunology | Animals | Nod2 Signaling Adaptor Protein - metabolism | Crohn Disease - drug therapy | Ligands | Mice | Trinitrobenzenesulfonic Acid - toxicity | Colitis - prevention & control | Cellular proteins | Usage | Genetic aspects | Colitis | Research | Health aspects | Risk factors | Enzyme-linked immunosorbent assay | Methods | Index Medicus | Abridged Index Medicus
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5. Full Text Positive and Negative Transcriptional Regulation of the Foxp3 Gene is Mediated by Access and Binding of the Smad3 Protein to Enhancer I
by Xu, Lili and Kitani, Atsushi and Stuelten, Christina and McGrady, George and Fuss, Ivan and Strober, Warren
Immunity, ISSN 1074-7613, 2010, Volume 33, Issue 3, pp. 313 - 325
The molecular mechanisms underlying retinoic acid (RA) augmentation of T cell receptor (TCR) and transforming growth factor-β (TGF-β)-induced transcription and... 
RETINOIC-ACID | INDUCTION | DRIVEN | IMMUNOLOGY | EXPRESSION | T-CELLS | TH17 CELLS | Promoter Regions, Genetic | Phosphorylation | Protein-Serine-Threonine Kinases - physiology | Mice, Inbred C57BL | NFATC Transcription Factors - metabolism | Gene Expression Regulation | Transforming Growth Factor beta - physiology | Smad3 Protein - metabolism | Receptors, Transforming Growth Factor beta - physiology | Retinoid X Receptors - physiology | Forkhead Transcription Factors - genetics | Receptors, Antigen, T-Cell - physiology | Animals | Enhancer Elements, Genetic | Transcription Factor AP-1 - physiology | Female | Transcription, Genetic | Mice | Binding Sites | Tretinoin - pharmacology | Genetic aspects | Chemical properties | T cells | Transforming growth factors | Protein binding | Proteins | Studies | Transcription factors | Cytokines | Mutagenesis | Plasmids | Sperm | Genes | Cloning | Kinases | Binding sites | Deoxyribonucleic acid--DNA
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6. Full Text The role of NLRP3 and IL-1β in the pathogenesis of inflammatory bowel disease
by Mao, Liming and Kitani, Atsushi and Strober, Warren and Fuss, Ivan J
Frontiers in Immunology, ISSN 1664-3224, 11/2018, Volume 9, p. 2566
It is logical to assume that a major pro-inflammatory mechanism, i.e., the NLRP3 inflammasome would play a prominent role in the pathogenesis of the... 
NLRP3 | Inflammasome | IL-18 | Interleukin-1β | IBD-inflammatory bowel diseases | inflammasome | interleukin-1β
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7. Full Text IL-13 signaling through the IL-13α2 receptor is involved in induction of TGF-β1 production and fibrosis
by Fichtner-Feigl, Stefan and Strober, Warren and Kawakami, Koji and Puri, Raj K and Kitani, Atsushi
Nature Medicine, ISSN 1078-8956, 01/2006, Volume 12, Issue 1, pp. 99 - 106
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8. Full Text NOD1 contributes to mouse host defense against Helicobacter pylori via induction of type I IFN and activation of the ISGF3 signaling pathway
by Watanabe, Tomohiro and Asano, Naoki and Fichtner-Feigl, Stefan and Gorelick, Peter L and Tsuji, Yoshihisa and Matsumoto, Yuko and Chiba, Tsutomu and Fuss, Ivan J and Kitani, Atsushi and Strober, Warren
Journal of Clinical Investigation, ISSN 0021-9738, 05/2010, Volume 120, Issue 5, pp. 1645 - 1662
Nucleotide-binding oligomerization domain 1 (NOD 1) is an intracellular epithelial cell protein known to play a role in host defense at mucosal surfaces. Here... 
INDEPENDENT ANTIVIRAL RESPONSE | PROTECTS MICE | MEDICINE, RESEARCH & EXPERIMENTAL | INTERFERON-ALPHA/BETA | INNATE IMMUNE RECOGNITION | EXPERIMENTAL COLITIS | INFLAMMATORY DISEASE | NF-KAPPA-B | INTESTINAL EPITHELIAL-CELLS | EFFECTOR-CELLS | T-LYMPHOCYTES | Peptides - chemistry | Signal Transduction | Humans | Mice, Inbred C57BL | Male | Interferon-Stimulated Gene Factor 3, gamma Subunit - metabolism | Nod1 Signaling Adaptor Protein - metabolism | Animals | Helicobacter pylori - metabolism | Interferon-Stimulated Gene Factor 3 - metabolism | Interferon Type I - metabolism | Protein Binding | Female | Helicobacter Infections - metabolism | Ligands | Chemokines - metabolism | Mice | Th1 Cells - cytology
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9. Full Text Cell contact-dependent immunosuppression by CD4+CD25+ regulatory T cells is mediated by cell surface-bound transforming growth factor β
by Nakamura, K and Kitani, A and Strober, W
Journal of Experimental Medicine, ISSN 0022-1007, 09/2001, Volume 194, Issue 5, pp. 629 - 644
CD4(+)CD25(+) T cells have been identified as a population of immunoregulatory T cells, which mediate suppression of CD4(+)CD25(-) T cells by cell-cell contact... 
CD4-positive T lymphocytes | Receptors, interleukin 2 | T lymphocytes, suppressor-effector | Autoimmune diseases | Transforming growth factors | autoimmune diseases | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | LYMPHOCYTE-ASSOCIATED ANTIGEN-4 | THROMBOSPONDIN-1 | RECEPTOR | INDUCTION | IMMUNOLOGY | transforming growth factors | INTESTINAL INFLAMMATION | IN-VITRO | COLITIS | IMMUNOLOGICAL SELF-TOLERANCE | AUTOIMMUNE-DISEASE | receptors, interleukin 2
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10. Full Text Cutting Edge: Regulatory T Cells Induce CD4+CD25-Foxp3- T Cells or Are Self-Induced to Become Th17 Cells in the Absence of Exogenous TGF-beta
by Xu, LiLi and Kitani, Atsushi and Fuss, Ivan and Strober, Warren
The Journal of Immunology, ISSN 0022-1767, 06/2007, Volume 178, Issue 11, pp. 6725 - 6729
Recent studies have shown that TGF-beta together with IL-6 induce the differentiation of IL-17-producing T cells (Th17) T cells. We therefore examined whether... 
EXPRESSION | GROWTH-FACTOR-BETA | IMMUNOLOGY | T-Lymphocyte Subsets - immunology | T-Lymphocytes, Regulatory - metabolism | T-Lymphocyte Subsets - cytology | Coculture Techniques | Interleukin-17 - physiology | Interleukin-2 Receptor alpha Subunit - biosynthesis | Transforming Growth Factor beta - biosynthesis | T-Lymphocytes, Regulatory - immunology | Lymphocyte Activation - immunology | Forkhead Transcription Factors - metabolism | Mice, Mutant Strains | Interleukin-6 - physiology | T-Lymphocytes, Regulatory - cytology | Female | Forkhead Transcription Factors - biosynthesis | Mice, Inbred C57BL | Cells, Cultured | Transforming Growth Factor beta - physiology | Interleukin-17 - biosynthesis | Cell Differentiation - immunology | Animals | Interleukin-2 Receptor alpha Subunit - metabolism | T-Lymphocyte Subsets - metabolism | Mice | Transforming Growth Factor beta - metabolism
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11. Full Text TGF-β1 Plays an Important Role in the Mechanism of CD4 +CD25+ Regulatory T Cell Activity in Both Humans and Mice
by Nakamura, Kazuhiko and Kitani, Atsushi and Fuss, Ivan and Pedersen, Aasta and Harada, Naohiko and Nawata, Hajime and Strober, Warren
Journal of Immunology, ISSN 0022-1767, 01/2004, Volume 172, Issue 2, pp. 834 - 842
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12. Full Text Nucleotide Binding Oligomerization Domain 2 Deficiency Leads to Dysregulated TLR2 Signaling and Induction of Antigen-Specific Colitis
by Watanabe, Tomohiro and Kitani, Atsushi and Murray, Peter J and Wakatsuki, Yoshio and Fuss, Ivan J and Strober, Warren
Immunity, ISSN 1074-7613, 2006, Volume 25, Issue 3, pp. 473 - 485
In this study, we determined conditions leading to the development of colitis in mice with nucleotide binding oligomerization domain 2 (NOD2) deficiency, a... 
MOLIMMUNO | HUMDISEASE | SIGNALING | LEISHMANIA-MAJOR | INFLAMMATORY-BOWEL-DISEASE | MEDIATED-IMMUNITY | CROHNS-DISEASE | ESCHERICHIA-COLI | MICE | KAPPA-B | NOD2 | IMMUNOLOGY | INTESTINAL EPITHELIAL-CELLS | T-CELLS | Toll-Like Receptor 2 - genetics | Colitis - genetics | Humans | Inflammatory Bowel Diseases - immunology | Antigens, Bacterial - immunology | Male | Inflammatory Bowel Diseases - metabolism | Epitopes - immunology | Intracellular Signaling Peptides and Proteins - deficiency | Toll-Like Receptor 2 - deficiency | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - genetics | Colitis - immunology | Intracellular Signaling Peptides and Proteins - genetics | Antigen-Presenting Cells - metabolism | Cells, Cultured | Mice, Transgenic | Nod2 Signaling Adaptor Protein | Protein Structure, Tertiary - genetics | Signal Transduction - genetics | Intestinal Mucosa - microbiology | Antigen-Presenting Cells - immunology | Mice, Knockout | Animals | Toll-Like Receptor 2 - physiology | Colitis - metabolism | Mice | Intracellular Signaling Peptides and Proteins - physiology | Antigens | Medical colleges | Peptides | Albumin | Crohn's disease | Biological response modifiers | T cells | Diseases | Oligomers | Crohn's disease in children | Children | Colitis | Interferon gamma | Inflammatory bowel disease | Proteins | Studies | Statistical analysis | Lymphocytes | Rodents | Ligands | Kinases | Experiments | Crohns disease
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13. Full Text IL-13 signaling through the IL-13α 2 receptor is involved in induction of TGF-β 1 production and fibrosis
by Kawakami, Koji and Fichtner-Feigl, Stefan and Strober, Warren and Puri, Raj K and Kitani, Atsushi
Nature Medicine, ISSN 1078-8956, 01/2006, Volume 12, Issue 1, pp. 99 - 106
Interleukin (IL)-13 is a major inducer of fibrosis in many chronic infectious and autoimmune diseases. In studies of the mechanisms underlying such induction,... 
NK-T-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | ULCERATIVE-COLITIS | TISSUE FIBROSIS | INTERLEUKIN-13 | GROWTH FACTOR-BETA-1 GENE | OXAZOLONE COLITIS | CELL BIOLOGY | IN-VIVO | MICE | PULMONARY-FIBROSIS | ALPHA-2 CHAIN
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14. Full Text Cellular and molecular mechanisms underlying NOD2 risk‐associated polymorphisms in Crohn's disease
by Strober, Warren and Asano, Naoki and Fuss, Ivan and Kitani, Atsushi and Watanabe, Tomohiro
Immunological Reviews, ISSN 0105-2896, 07/2014, Volume 260, Issue 1, pp. 249 - 260
Summary The discovery that polymorphisms in the NOD2 (nucleotide‐binding oligomerization domain containing 2) gene are associated with a greatly increased risk... 
defensins | Crohn's disease | colitis | NOD2 | microbiome | IRF‐4 | Colitis | Defensins | IRF-4 | Microbiome | STIMULATION | DENDRITIC CELLS | INVASIVE ESCHERICHIA-COLI | RECEPTOR | COLONIZATION | GUT MICROBIOTA | INDUCTION | IMMUNOLOGY | COMMENSAL | ILEAL MUCOSA | PANETH CELLS | Crohn Disease - genetics | Intestinal Mucosa - metabolism | Nod2 Signaling Adaptor Protein - deficiency | Defensins - biosynthesis | Humans | Inflammatory Bowel Diseases - immunology | Crohn Disease - metabolism | Nod2 Signaling Adaptor Protein - genetics | Intestines - metabolism | Inflammatory Bowel Diseases - metabolism | Intestines - immunology | Microbiota | Intestinal Mucosa - immunology | Inflammatory Bowel Diseases - genetics | Crohn Disease - microbiology | Paneth Cells - metabolism | Genetic Predisposition to Disease | Genetic Association Studies | Immunomodulation | Intestinal Mucosa - microbiology | Immunity, Innate | Crohn Disease - immunology | Polymorphism, Genetic | Animals | Intestines - microbiology | Nod2 Signaling Adaptor Protein - metabolism | Inflammatory Bowel Diseases - microbiology | Microbiota (Symbiotic organisms) | Genetic aspects
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