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1,016 results on '"Stone, John H"'

2. Sex as a predictor of clinical phenotype and determinant of immune response in IgG4-related disease: a retrospective study of patients fulfilling the American College of Rheumatology–European League Against Rheumatism classification criteria

Author

Jha, Isha, McMahon, Grace A, Perugino, Cory A, Katz, Guy, Wallace, Zachary S, Fernandes, Ana, Jiang, Bohang, Zhang, Yuqing, McMahon, Aubree E, Guy, Thomas V, Liu, Hang, Hernandez-Barco, Yasmin G, Pillai, Shiv, and Stone, John H

Published
2024
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5. Granzyme K– and amphiregulin-expressing cytotoxic T cells and activated extrafollicular B cells are potential drivers of IgG4-related disease

Author

Koga, Risako, Maehara, Takashi, Aoyagi, Ryuichi, Munemura, Ryusuke, Murakami, Yuka, Doi, Atsushi, Kono, Michihito, Yamamoto, Hidetaka, Niiro, Hiroaki, Kiyoshima, Tamotsu, Tanabe, Mika, Nakano, Toshiaki, Matsukuma, Yuta, Kawano, Mitsuhiro, Stone, John H., Pillai, Shiv, Nakamura, Seiji, and Kawano, Shintaro

Published
2024
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6. A phase 3 randomized, double-blind, placebo-controlled study to evaluate the efficacy and safety of sarilumab in patients with giant cell arteritis

Author

Schmidt, Wolfgang A., Dasgupta, Bhaskar, Sloane, Jennifer, Giannelou, Angeliki, Xu, Yuqing, Unizony, Sebastian H., Mackie, Sarah L., Gonzalez-Gay, Miguel A., Spiera, Robert, Warrington, Kenneth J., Villiger, Peter M., Nivens, Michael C., Akinlade, Bolanle, Lin, Yong, Buttgereit, Frank, and Stone, John H.

Published
2023
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12. Evaluation of the safety, efficacy, and mechanism of action of obexelimab for the treatment of patients with IgG4-related disease: an open-label, single-arm, single centre, phase 2 pilot trial

Author

Perugino, Cory A, Wallace, Zachary S, Zack, Debra J, Quinn, Shauna M, Poma, Allen, Fernandes, Ana D, Foster, Paul, DeMattos, Steve, Burington, Bart, Liu, Hang, Allard-Chamard, Hugues, Smith, Nathan, Kai, Xin, Xing, Kelly, Pillai, Shiv, and Stone, John H

Published
2023
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14. Extrafollicular IgD−CD27−CXCR5−CD11c− DN3 B cells infiltrate inflamed tissues in autoimmune fibrosis and in severe COVID-19

Author

Allard-Chamard, Hugues, Kaneko, Naoki, Bertocchi, Alice, Sun, Na, Boucau, Julie, Kuo, Hsiao-Hsuan, Farmer, Jocelyn R., Perugino, Cory, Mahajan, Vinay S., Murphy, Samuel J.H., Premo, Katherine, Diefenbach, Thomas, Ghebremichael, Musie, Yuen, Grace, Kotta, Alekhya, Akman, Zafer, Lichterfeld, Mathias, Walker, Bruce D., Yu, Xu G., Moriyama, Masafumi, Maehara, Takashi, Nakamura, Seiji, Stone, John H., Padera, Robert F., and Pillai, Shiv

Published
2023
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19. The pediatric glucocorticoid toxicity index

Author

Brogan, Paul, Naden, Ray, Ardoin, Stacy P., Cooper, Jennifer C., De Benedetti, Fabrizio, Dicaire, Jean-Francois, Eleftheriou, Despina, Feldman, Brian, Goldin, Jon, Karol, Seth E., Price-Kuehne, Fiona, Skuse, David, Stratakis, Constantine A., Webb, Nicholas, and Stone, John H.

Published
2022
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20. IgG4‐related disease: Association with a rare gene variant expressed in cytotoxic T cells

Author

Newman, John H, Shaver, Aaron, Sheehan, Jonathan H, Mallal, Simon, Stone, John H, Pillai, Shiv, Bastarache, Lisa, Riebau, Derek, Allard‐Chamard, Hugues, Stone, William M, Perugino, Cory, Pilkinton, Mark, Smith, Scott A, McDonnell, Wyatt J, Capra, John A, Meiler, Jens, Cogan, Joy, Xing, Kelly, Mahajan, Vinay S, Mattoo, Hamid, Hamid, Rizwan, Phillips, John A, Adams, David R, Aday, Aaron, Alejandro, Mercedes E, Allard, Patrick, Ashley, Euan A, Azamian, Mahshid S, Bacino, Carlos A, Balasubramanyam, Ashok, Barseghyan, Hayk, Batzli, Gabriel F, Beggs, Alan H, Behnam, Babak, Bellen, Hugo J, Bernstein, Jonathan A, Bican, Anna, Bick, David P, Birch, Camille L, Bonner, Devon, Boone, Braden E, Bostwick, Bret L, Briere, Lauren C, Brown, Donna M, Brush, Matthew, Burke, Elizabeth A, Burrage, Lindsay C, Butte, Manish J, Chen, Shan, Clark, Gary D, Coakley, Terra R, Cooper, Cynthia M, Cope, Heidi, Craigen, William J, D'Souza, Precilla, Davids, Mariska, Davidson, Jean M, Dayal, Jyoti G, Dell'Angelica, Esteban C, Dhar, Shweta U, Dipple, Katrina M, Donnell‐Fink, Laurel A, Dorrani, Naghmeh, Dorset, Daniel C, Douine, Emilie D, Draper, David D, Dries, Annika M, Eckstein, David J, Emrick, Lisa T, Eng, Christine M, Enns, Gregory M, Eskin, Ascia, Esteves, Cecilia, Estwick, Tyra, Fernandez, Liliana, Ferreira, Carlos, Fisher, Paul G, Fogel, Brent L, Friedman, Noah D, Gahl, William A, Glanton, Emily, Godfrey, Rena A, Goldman, Alica M, Goldstein, David B, Gould, Sarah E, Gourdine, Jean‐Philippe F, Groden, Catherine A, Gropman, Andrea L, Haendel, Melissa, Hanchard, Neil A, Handley, Lori H, Herzog, Matthew R, High, Francis, Holm, Ingrid A, Hom, Jason, Howerton, Ellen M, Huang, Yong, Jamal, Fariha, Jiang, Yong‐hui, and Johnston, Jean M

Subjects
Biological Sciences, Genetics, Rare Diseases, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Adolescent, CD4-Positive T-Lymphocytes, Genetic Variation, Humans, Immunoglobulin G, Immunoglobulin G4-Related Disease, Male, Middle Aged, T-Lymphocytes, Cytotoxic, cytotoxic lymphocytes, heritable, IgG4-RD, Undiagnosed Disease Network, Medicinal and Biomolecular Chemistry, Clinical Sciences, Medicinal and biomolecular chemistry
Abstract

BackgroundFamily screening of a 48-year-old male with recently diagnosed IgG4-related disease (IgG4-RD) revealed unanticipated elevations in plasma IgG4 in his two healthy teenaged sons.MethodsWe performed gene sequencing, immune cell studies, HLA typing, and analyses of circulating cytotoxic CD4+ T lymphocytes and plasmablasts to seek clues to pathogenesis. DNA from a separate cohort of 99 patients with known IgG4-RD was also sequenced for the presence of genetic variants in a specific gene, FGFBP2.ResultsThe three share a previously unreported heterozygous single base deletion in fibroblast growth factor binding protein type 2 (FGFBP2), which causes a frameshift in the coding sequence. The FGFBP2 protein is secreted by cytotoxic T-lymphocytes and binds fibroblast growth factor. The variant sequence in the FGFBP2 protein is predicted to form a disordered random coil rather than a helical-turn-helix structure, unable to adopt a stable conformation. The proband and the two sons had 5-10-fold higher numbers of circulating cytotoxic CD4 + T cells and plasmablasts compared to matched controls. The three members also share a homozygous missense common variant in FGFBP2 found in heterozygous form in ~40% of the population. This common variant was found in 73% of an independent, well characterized IgG4-RD cohort, showing enrichment in idiopathic IgG4-RD.ConclusionsThe presence of a shared deleterious variant and homozygous common variant in FGFBP2 in the proband and sons strongly implicates this cytotoxic T cell product in the pathophysiology of IgG4-RD. The high prevalence of a common FGFBP2 variant in sporadic IgG4-RD supports the likelihood of participation in disease.

Published
2019

26. The clinical outcomes and healthcare resource utilization in IgG4-related disease: a claims-based analysis of commercially insured adults in the United States.

Author

Wallace, Zachary S, Miles, Gandarvaka, Smolkina, Ekaterina, Petruski-Ivleva, Natalia, Madziva, Duane, Guzzo, Krishan, Cook, Claire, Fu, Xiaoqing, Zhang, Yuqing, Stone, John H, and Choi, Hyon K

Subjects
MEDICAL care use, DRUG toxicity, RESEARCH funding, IMMUNOGLOBULIN G, HEALTH insurance, SEX distribution, HOSPITAL care, TREATMENT effectiveness, AGE distribution, DESCRIPTIVE statistics, RETROSPECTIVE studies, LONGITUDINAL method, CHRONIC diseases, AUTOIMMUNE diseases, MEDICAL appointments, CONFIDENCE intervals, INSURANCE companies, COMORBIDITY, MEDICAL care costs, GLUCOCORTICOIDS, ALGORITHMS, ECONOMIC aspects of diseases
Abstract

Objectives IgG4-related disease (IgG4-RD) can affect nearly any organ and is often treated with glucocorticoids, which contribute to organ damage and toxicity. Comorbidities and healthcare utilization in IgG4-RD are poorly understood. Methods We conducted a cohort study using claims data from a US managed care organization. Incident IgG4-RD cases were identified using a validated algorithm; general population comparators were matched by age, sex, race/ethnicity and index date. The frequency of 21 expert-defined clinical outcomes associated with IgG4-RD or its treatment and healthcare-associated visits and costs were assessed 12 months before and 36 months after the index date (date of earliest IgG4-RD-related claim). Results There were 524 cases and 5240 comparators. Most cases received glucocorticoids prior to (64.0%) and after (85.1%) the index date. Nearly all outcomes, many being common glucocorticoid toxicities, occurred more frequently in cases vs comparators. During follow-up, the largest differences between cases and comparators were seen for gastroesophageal reflux disease (prevalence difference: +31.2%, P  < 0.001), infections (+17.3%, P  < 0.001), hypertension (+15.5%, P  < 0.01) and diabetes mellitus (+15.0%, P  < 0.001). The difference in malignancy increased during follow-up from +8.8% to +12.5% (P  < 0.001). Some 17.4% of cases used pancreatic enzyme replacement therapy during follow-up. Over follow-up, cases were more often hospitalized (57.3% vs 17.2%, P  < 0.01) and/or had an emergency room visit (72.0% vs 36.7%, P  < 0.01); all costs were greater in cases than comparators. Conclusions Patients with IgG4-RD are disproportionately affected by adverse outcomes, some of which may be preventable or modifiable with vigilant clinician monitoring. Glucocorticoid-sparing treatments may improve these outcomes. [ABSTRACT FROM AUTHOR]

Published
2024
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37. Cytotoxic [CD4.sup.+] T lymphocytes may induce endothelial cell apoptosis in systemic sclerosis

Author

Maehara, Takashi, Kaneko, Naoki, Perugino, Cory A., Mattoo, Hamid, Kers, Jesper, Allard-Chamard, Hugues, Mahajan, Vinay S., Liu, Hang, Murphy, Samuel J.H., Ghebremichael, Musie, Fox, David, Payne, Aimee S., Lafyatis, Robert, Stone, John H., Khanna, Dinesh, and Pillai, Shiv

Subjects
Apoptosis -- Analysis, B cells -- Analysis, Scleroderma (Disease) -- Development and progression, Endothelium -- Analysis, Skin -- Analysis, T cells -- Analysis, Biochemistry, Cell death, Lymphocytes, Fibrosis, Diseases, Health care industry
Abstract

Systemic sclerosis (SSc) is an autoimmune fibrotic disease whose pathogenesis is poorly understood and lacks effective therapies. We undertook quantitative analyses of T cell infiltrates in the skin of 35 untreated patients with early diffuse SSc and here show that [CD4.sup.+] cytotoxic T cells and [CD8.sup.+] T cells contribute prominently to these infiltrates. We also observed an accumulation of apoptotic cells in SSc tissues, suggesting that recurring cell death may contribute to tissue damage and remodeling in this fibrotic disease. HLA-DR-expressing endothelial cells were frequent targets of apoptosis in SSc, consistent with the prominent vasculopathy seen in patients with this disease. A circulating effector population of cytotoxic [CD4.sup.+] T cells, which exhibited signatures of enhanced metabolic activity, was clonally expanded in patients with systemic sclerosis. These data suggest that cytotoxic T cells may induce the apoptotic death of endothelial and other cells in systemic sclerosis. Cell loss driven by immune cells may be followed by overly exuberant tissue repair processes that lead to fibrosis and tissue dysfunction., Introduction Systemic sclerosis (SSc) is a systemic autoimmune inflammatory disorder of unknown etiology characterized by prominent fibrosis that may affect many organs including the skin, lungs, kidneys, and gastrointestinal tract [...]

Published
2020
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41. Reply

Author

Matza, Mark A., Fernandes, Ana D., Stone, John H., and Unizony, Sebastian H.

Published
2021
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46. Meta‐analysis of genetic polymorphisms in granulomatosis with polyangiitis (Wegener's) reveals shared susceptibility loci with rheumatoid arthritis

Author

Chung, Sharon A, Xie, Gang, Roshandel, Delnaz, Sherva, Richard, Edberg, Jeffrey C, Kravitz, Megan, Dellaripa, Paul F, Hoffman, Gary S, Mahr, Alfred D, Seo, Philip, Specks, Ulrich, Spiera, Robert F, St.Clair, E William, Stone, John H, Plenge, Robert M, Siminovitch, Katherine A, Merkel, Peter A, and Monach, Paul A

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Epidemiology, Health Sciences, Clinical Sciences, Arthritis, Digestive Diseases, Autoimmune Disease, Clinical Research, Prevention, Lupus, Human Genome, Rheumatoid Arthritis, Inflammatory Bowel Disease, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Adolescent, Adult, Aged, Aged, 80 and over, Arthritis, Rheumatoid, Female, Genetic Loci, Genetic Predisposition to Disease, Genotype, Granulomatosis with Polyangiitis, Humans, Male, Middle Aged, Polymorphism, Genetic, Risk Factors, Immunology, Public Health and Health Services, Arthritis & Rheumatology, Clinical sciences
Abstract

ObjectiveTo examine the association of previously identified autoimmune disease susceptibility loci with granulomatosis with polyangiitis (Wegener's) (GPA), and to determine whether the genetic susceptibility profiles of other autoimmune diseases are associated with those of GPA.MethodsGenetic data from 2 cohorts were meta-analyzed. Genotypes for 168 previously identified single-nucleotide polymorphisms (SNPs) associated with susceptibility to different autoimmune diseases were ascertained in a total of 880 patients with GPA and 1,969 control subjects of European descent. Single-marker associations were identified using additive logistic regression models. Associations of multiple SNPs with GPA were assessed using genetic risk scores based on susceptibility loci for Crohn's disease, type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis (RA), celiac disease, and ulcerative colitis. Adjustment for population substructure was performed in all analyses, using ancestry-informative markers and principal components analysis.ResultsGenetic polymorphisms in CTLA4 were significantly associated with GPA in the single-marker meta-analysis (odds ratio [OR] 0.79, 95% confidence interval [95% CI] 0.70-0.89, P = 9.8 × 10(-5) ). The genetic risk score for RA susceptibility markers was significantly associated with GPA (OR 1.05 per 1-unit increase in genetic risk score, 95% CI 1.02-1.08, P = 5.1 × 10(-5) ).ConclusionRA and GPA may arise from a similar genetic predisposition. Aside from CTLA4, other loci previously found to be associated with common autoimmune diseases were not statistically significantly associated with GPA in this study.

Published
2012

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