Haowei Wang
Neuroinflammation Senior TechnicianCards
About
Research
Publications
2021
The Type II Anti‐CD20 Antibody Obinutuzumab (GA101) Is More Effective Than Rituximab at Depleting B Cells and Treating Disease in a Murine Lupus Model
Marinov A, Wang H, Bastacky S, van Puijenbroek E, Schindler T, Speziale D, Perro M, Klein C, Nickerson K, Shlomchik M. The Type II Anti‐CD20 Antibody Obinutuzumab (GA101) Is More Effective Than Rituximab at Depleting B Cells and Treating Disease in a Murine Lupus Model. Arthritis & Rheumatology 2021, 73: 826-836. PMID: 33277983, PMCID: PMC8084886, DOI: 10.1002/art.41608.Peer-Reviewed Original ResearchConceptsMRL/lpr miceB-cell depletionSystemic lupus erythematosusDiseased MRL/lpr miceLpr miceB cellsCell depletionEarly diseaseLupus-prone MRL/lpr micePathogenic B cellsAnti-CD20 antibodyClinical end pointsCD20 monoclonal antibodyMurine lupus modelsMultiple clinical end pointsAmelioration of diseaseAdvanced disease modelsAdvanced diseaseAutoantibody titersLupus nephritisLupus modelsLupus erythematosusInflammatory settingsSingle doseCD20 mAbs
2016
PTPN22 inhibition resets defective human central B cell tolerance
Schickel JN, Kuhny M, Baldo A, Bannock JM, Massad C, Wang H, Katz N, Oe T, Menard L, Soulas-Sprauel P, Strowig T, Flavell R, Meffre E. PTPN22 inhibition resets defective human central B cell tolerance. Science Immunology 2016, 1 PMID: 27917411, PMCID: PMC5127630, DOI: 10.1126/sciimmunol.aaf7153.Peer-Reviewed Original Research
2014
Activation of Rheumatoid Factor–Specific B Cells Is Antigen Dependent and Occurs Preferentially Outside of Germinal Centers in the Lupus-Prone NZM2410 Mouse Model
Sang A, Niu H, Cullen J, Choi SC, Zheng YY, Wang H, Shlomchik MJ, Morel L. Activation of Rheumatoid Factor–Specific B Cells Is Antigen Dependent and Occurs Preferentially Outside of Germinal Centers in the Lupus-Prone NZM2410 Mouse Model. The Journal Of Immunology 2014, 193: 1609-1621. PMID: 25015835, PMCID: PMC4119566, DOI: 10.4049/jimmunol.1303000.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoantibodiesAutoantigensB-LymphocytesCell DifferentiationCells, CulturedChromatinDisease Models, AnimalFemaleGerminal CenterImmune ToleranceImmunoglobulin GLupus Erythematosus, SystemicLymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutReceptors, Antigen, B-CellRheumatoid FactorToll-Like Receptor 7Toll-Like Receptor 9ConceptsRF B cellsAb-forming cellsB cellsImmune complexesGerminal centersMouse modelMRL/lpr strainMRL/lpr miceLupus-prone mouse modelsH chain transgenic miceRheumatoid factor B cellsTLR9-dependent mannerH chain transgeneIC immunizationC57BL/6 controlsLpr miceLupus-proneTLR9 pathwayLPR strainAntigen DependentTransgenic miceGenetic background
2013
The role of B cells in neuropsychiatric disease in murine systemic lupus erythematosis (P4000)
Wen J, Stock A, Gulinello M, Putterman C, Wang H, Shlomchik M. The role of B cells in neuropsychiatric disease in murine systemic lupus erythematosis (P4000). The Journal Of Immunology 2013, 190: 42.1-42.1. DOI: 10.4049/jimmunol.190.supp.42.1.Peer-Reviewed Original ResearchB-cell depletionB cellsMRL/lpr miceNeuropsychiatric manifestationsComplete B-cell depletionAbsence of B cellsNeuropsychiatric diseasesMurine lupus modelsB cell knockoutDepression-like behaviorSystemic lupus erythematosisSystemic lupus erythematosusMRL-lpr/lpr strainBlood-brain barrierLupus modelForced swimmingLupus erythematosusNPSLELupus erythematosisOptimal treatmentMRL-lpr/lprTherapeutic depletionNeuropsychiatric abnormalitiesLupus autoantibodiesDisease manifestations
1999
Regulation of autoreactive anti-IgG (Rheumatoid Factor) B cells in normal and autoimmune mice
Wang H, Shlomchik M. Regulation of autoreactive anti-IgG (Rheumatoid Factor) B cells in normal and autoimmune mice. Immunologic Research 1999, 19: 259-270. PMID: 10493179, DOI: 10.1007/bf02786493.Peer-Reviewed Original ResearchConceptsB cellsNormal miceAutoimmune miceAutoimmune diseasesMRL/lpr/lpr miceLpr/lpr miceAutoimmune prone animalsRF B cellsChronic autoimmune diseaseSystemic autoimmune diseaseAntigen-specific mannerAutoreactive B cellsParticular underlying diseaseAutoimmune animalsRF autoantibodiesUnderlying diseaseMaternal IgGLpr miceYoung miceTransgenic miceMiceDiseaseAutoantigensRF clonesCells
1998
Maternal Ig mediates neonatal tolerance in rheumatoid factor transgenic mice but tolerance breaks down in adult mice.
Wang H, Shlomchik M. Maternal Ig mediates neonatal tolerance in rheumatoid factor transgenic mice but tolerance breaks down in adult mice. The Journal Of Immunology 1998, 160: 2263-71. PMID: 9498766, DOI: 10.4049/jimmunol.160.5.2263.Peer-Reviewed Original ResearchConceptsTransgenic miceDegree of autoreactivityRF B cellsChronic autoimmune diseaseT cell toleranceB cell deletionSelf-reactive cellsAutoimmune animalsNeonatal toleranceMaternal IgGMaternal IgTolerance breakAutoimmune diseasesB lineage cellsYoung miceNormal miceAdult miceB cellsBone marrowCell toleranceMiceLineage cellsCell deletionWk postweaningSustained expression
1997
High affinity rheumatoid factor transgenic B cells are eliminated in normal mice.
Wang H, Shlomchik M. High affinity rheumatoid factor transgenic B cells are eliminated in normal mice. The Journal Of Immunology 1997, 159: 1125-34. PMID: 9233605, DOI: 10.4049/jimmunol.159.3.1125.Peer-Reviewed Original ResearchConceptsRF B cellsRheumatoid factorB cell toleranceB cellsNormal miceCell toleranceTransgenic modelMRL/lpr miceAutoimmune MRL/lpr miceDisease-related specificitySystemic autoimmune diseaseTransgenic B cellsAutoimmune animalsAutoimmune inductionAutoimmune syndromeMultiple autoantibodiesRheumatoid arthritisLpr miceSerum IgGTolerance inductionAutoimmune diseasesCentral toleranceCognate AgNegative miceNormal animals
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