2018
WASP-mediated regulation of anti-inflammatory macrophages is IL-10 dependent and is critical for intestinal homeostasis
Biswas A, Shouval DS, Griffith A, Goettel JA, Field M, Kang YH, Konnikova L, Janssen E, Redhu NS, Thrasher AJ, Chatila T, Kuchroo VK, Geha RS, Notarangelo LD, Pai SY, Horwitz BH, Snapper SB. WASP-mediated regulation of anti-inflammatory macrophages is IL-10 dependent and is critical for intestinal homeostasis. Nature Communications 2018, 9: 1779. PMID: 29725003, PMCID: PMC5934380, DOI: 10.1038/s41467-018-03670-6.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCell DifferentiationColitisGene DeletionGuanine Nucleotide Exchange FactorsHomeostasisHumansImmunity, MucosalInflammationInterleukin-10Interleukin-1betaInterleukin-23Intestinal MucosaMacrophagesMice, Inbred C57BLMice, TransgenicSignal TransductionWiskott-Aldrich SyndromeWiskott-Aldrich Syndrome ProteinConceptsAnti-inflammatory macrophagesMucosal homeostasisMacrophage functionDevelopment of colitisAbsence of WASpColitis developmentAutoimmune sequelaeDendritic cellsIL-10Immune toleranceIntestinal homeostasisWiskott-Aldrich syndrome proteinMacrophagesMacrophage propertiesSTAT3 phosphorylationColitisExpression of WASPWASP deficiencyHomeostasisDOCK8SequelaeMice
2013
Intestine-Specific Mttp Deletion Increases the Severity of Experimental Colitis and Leads to Greater Tumor Burden in a Model of Colitis Associated Cancer
Xie Y, Matsumoto H, Nalbantoglu I, Kerr TA, Luo J, Rubin DC, Kennedy S, Davidson NO. Intestine-Specific Mttp Deletion Increases the Severity of Experimental Colitis and Leads to Greater Tumor Burden in a Model of Colitis Associated Cancer. PLOS ONE 2013, 8: e67819. PMID: 23805328, PMCID: PMC3689718, DOI: 10.1371/journal.pone.0067819.Peer-Reviewed Original ResearchConceptsMttp-IKO miceDextran sodium sulfateDSS treatmentExperimental colitisTumor burdenColitis-associated cancerDevelopment of colitisIndependent risk factorDietary fat intakeColonic mRNA expressionLevels of TNFαColonic tumor burdenIntestine-specific deletionMicrosomal triglyceride transfer proteinDSS administrationColonic inflammationColonic injuryIL-17AInflammasome expressionSystemic injuryFat intakeFat malabsorptionColorectal cancerCytokine expressionIL-1β
2012
MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice
Hoshi N, Schenten D, Nish SA, Walther Z, Gagliani N, Flavell RA, Reizis B, Shen Z, Fox JG, Iwasaki A, Medzhitov R. MyD88 signalling in colonic mononuclear phagocytes drives colitis in IL-10-deficient mice. Nature Communications 2012, 3: 1120. PMID: 23047678, PMCID: PMC3521499, DOI: 10.1038/ncomms2113.Peer-Reviewed Original ResearchConceptsToll-like receptorsInterleukin-10Mononuclear phagocytesIL-10-deficient miceT helper 17 responsesColonic mononuclear phagocytesDevelopment of colitisInflammatory bowel diseaseColitis developmentBowel diseaseInterleukin-23MyD88 expressionInterleukin-1βInterleukin-6Intestinal homeostasisEpithelial expressionMyD88Multiple cell typesMiceCell typesReceptorsPhagocytesBacterial sensingDistinct populationsHigh levelsCytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges
Carvalho F, Nalbantoglu I, Aitken J, Uchiyama R, Su Y, Doho G, Vijay-Kumar M, Gewirtz A. Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges. Mucosal Immunology 2012, 5: 288-298. PMID: 22318495, PMCID: PMC3328601, DOI: 10.1038/mi.2012.8.Peer-Reviewed Original ResearchConceptsInflammasome activation resultsDevelopment of colitisDextran sulfate sodiumInnate immune activatorsDetection of flagellinIntestinal gene expressionPredispose miceSulfate sodiumEpithelial injuryIL-18IL-1βImmune activatorsIntestinal homeostasisSevere diseaseFlagellin administrationSalmonella infectionMonoclonal antibodiesSystemic challengesMiceNLRC4Transcription-independent pathwayIntestinal genesAdministrationActivation resultsBacterial flagellin
2010
Potentiation of Th17 cytokines in aging process contributes to the development of colitis
Ouyang X, Yang Z, Zhang R, Arnaboldi P, Lu G, Li Q, Wang W, Zhang B, Cui M, Zhang H, Liang-Chen J, Qin L, Zheng F, Huang B, Xiong H. Potentiation of Th17 cytokines in aging process contributes to the development of colitis. Cellular Immunology 2010, 266: 208-217. PMID: 21074754, PMCID: PMC3006034, DOI: 10.1016/j.cellimm.2010.10.007.Peer-Reviewed Original ResearchConceptsT cellsIL-17IL-22Aged miceTh17 cytokinesDendritic cellsYoung miceImmune responseAutoimmune/inflammatory diseasesDevelopment of colitisIL-17 productionMemory T cellsNaïve T cellsSevere colitisIL-17FInflammatory disordersInflammatory diseasesAged individualsMRNA expressionMiceColitisAged peopleSignificant differencesCytokinesHealthy onesCell-permeable Foxp3 protein alleviates autoimmune disease associated with inflammatory bowel disease and allergic airway inflammation
Choi JM, Shin JH, Sohn MH, Harding MJ, Park JH, Tobiasova Z, Kim DY, Maher SE, Chae WJ, Park SH, Lee CG, Lee SK, Bothwell AL. Cell-permeable Foxp3 protein alleviates autoimmune disease associated with inflammatory bowel disease and allergic airway inflammation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 18575-18580. PMID: 20937878, PMCID: PMC2972952, DOI: 10.1073/pnas.1000400107.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAsthmaAutoimmune DiseasesCell Membrane PermeabilityDisease Models, AnimalFemaleForkhead Transcription FactorsHumansInflammatory Bowel DiseasesLymphocyte ActivationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsRecombinant Fusion ProteinsT-Lymphocytes, RegulatoryConceptsAllergic airway inflammationT cellsAirway inflammationAllergic diseasesFOXP3 proteinOvalbumin-induced allergic airway inflammationWild-type CD4 T cellsAllergic disease modelsDevelopment of colitisInflammatory bowel diseaseRegulatory T cellsCD4 T cellsInflammatory immune responseT cell activationFoxP3 transductionBowel diseaseScurfy miceTreg functionAutoimmune diseasesAutoimmune symptomsIntranasal deliveryTherapeutic effectImmune responseSystemic deliveryClinical potential
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