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Article ; Online: Targeted Treatment of Diseases of Immune Dysregulation.

Mohan, Smriti

Rheumatic diseases clinics of North America

2023 Volume 49, Issue 4, Page(s) 913–929

Abstract: Increasing molecular knowledge of autoinflammatory and autoimmune disorders has enabled more targeted treatment of these conditions. Treatment of inflammasomopathies is often aimed at interleukin-1 (IL-1) blockade, with potential use of other inhibitors ... ...

Abstract	Increasing molecular knowledge of autoinflammatory and autoimmune disorders has enabled more targeted treatment of these conditions. Treatment of inflammasomopathies is often aimed at interleukin-1 (IL-1) blockade, with potential use of other inhibitors targeting cytokines such as IL-18 and IL-6. Interferonopathies and some disorders with overlap features of autoimmunity and autoinflammation may improve with Janus kinase inhibition. Autoimmune conditions may also respond to inhibition of different cytokines, as well as to inhibition of T and B lymphocytes. Effective treatment is increasingly possible through targeted/precision medicine approaches.
MeSH term(s)	Humans ; Autoimmune Diseases/drug therapy ; Autoimmunity ; Cytokines ; Inflammation ; Hereditary Autoinflammatory Diseases
Chemical Substances	Cytokines
Language	English
Publishing date	2023-08-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	92118-x
ISSN	1558-3163 ; 0889-857X
ISSN (online)	1558-3163
ISSN	0889-857X
DOI	10.1016/j.rdc.2023.07.002
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Article ; Online: Electroconvulsive Therapy Is an Effective Treatment Modality in Children With Lupus Cerebritis With Persistent Catatonia.

Ince, H Yavuz / Ryan, Kaitlyn / Malas, Nasuh / Mohan, Smriti / Pierce, Jessica M

The primary care companion for CNS disorders

2022 Volume 24, Issue 6

MeSH term(s)	Child ; Humans ; Catatonia/complications ; Catatonia/therapy ; Electroconvulsive Therapy ; Treatment Outcome
Language	English
Publishing date	2022-12-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2675414-9
ISSN	2155-7780 ; 2155-7780
ISSN (online)	2155-7780
ISSN	2155-7780
DOI	10.4088/PCC.22cr03250
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Article ; Online: Orbital biopsy findings consistent with granulomatosis polyangiitis in a 14-year-old boy with Crohn's disease.

Haliyur, Rachana / Kim, Jane S / Mohan, Smriti / Iskowitz, Seth / Bommakanti, Nikhil / Bapuraj, Jayapalli Rajiv / Adler, Jeremy / Elner, Victor M / Demirci, Hakan

Orbit (Amsterdam, Netherlands)

2023 , Page(s) 1–4

Abstract: Both granulomatous polyangiitis (GPA) and Crohn's disease (CD) can cause orbital inflammation though rarely coincide and can often be differentiated by presenting features and histological findings. Here, we report the clinical and therapeutic course of ... ...

Abstract	Both granulomatous polyangiitis (GPA) and Crohn's disease (CD) can cause orbital inflammation though rarely coincide and can often be differentiated by presenting features and histological findings. Here, we report the clinical and therapeutic course of a 14-year-old White male with binocular diplopia caused by orbital myositis. Imaging and biopsy obtained at presentation revealed necrosis and necrotizing granulomatous vasculitis suspicious for GPA. He subsequently developed gastrointestinal symptoms and terminal ileitis consistent with CD. Orbital symptoms responded well to high-dose steroids and remained quiet on methotrexate maintenance therapy. While clinical history, thorough physical exam, and complete laboratory work-up are essential in the management of pediatric orbital myositis, orbital biopsy can prove critical for diagnosis and suitable treatment strategy.
Language	English
Publishing date	2023-12-13
Publishing country	England
Document type	Journal Article
ZDB-ID	603157-2
ISSN	1744-5108 ; 0167-6830
ISSN (online)	1744-5108
ISSN	0167-6830
DOI	10.1080/01676830.2023.2287625
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Article ; Online: Randomized Control Trial for Reduction of Body Weight, Body Fat Patterning, and Cardiometabolic Risk Factors in Overweight Worksite Employees in Delhi, India.

Shrivastava, Usha / Fatma, Mahrukh / Mohan, Smriti / Singh, Padam / Misra, Anoop

Journal of diabetes research

2017 Volume 2017, Page(s) 7254174

Abstract: Background: We studied the impact of the multicomponent interventions on body weight and cardiometabolic risk factors in overweight individuals working in corporate worksites.: Methods: Overweight (BMI ≥ 23 kg/m: Results: High prevalence (%) of ... ...

Abstract	Background: We studied the impact of the multicomponent interventions on body weight and cardiometabolic risk factors in overweight individuals working in corporate worksites. Methods: Overweight (BMI ≥ 23 kg/m Results: High prevalence (%) of obesity (90.9, 80.2), abdominal obesity (93.5, 84.3), excess skinfold thickness (70.3, 75.9), and low high-density lipoprotein cholesterol (HDL-c) levels (56.8, 63.7) were seen in the intervention and the control group, respectively. At the end of intervention, the following significant changes were observed in the intervention group: decrease in weight, BMI, waist circumference, serum triglycerides, and increase in HDL-c. Weight loss of more than 5% was seen in 12% and 4% individuals in the intervention and control groups, respectively. Most importantly, the sum of all the skinfold measurements (mm) in the intervention group decreased significantly more than the control group (12.51 ± 10.38 versus 3.50 ± 8.18, resp.). Conclusion: This multicomponent worksite trial showed a reduction in weight, excess subcutaneous fat, and cardiometabolic risk factors after 6 months of active intervention in overweight Asian Indians. Trial registration: This trial is registered with NCT03249610.
MeSH term(s)	Adult ; Body Fat Distribution ; Body Weight ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/prevention & control ; Diet, Reducing ; Employment ; Female ; Humans ; India/epidemiology ; Male ; Metabolic Syndrome/etiology ; Metabolic Syndrome/prevention & control ; Middle Aged ; Obesity/complications ; Obesity/epidemiology ; Obesity/metabolism ; Obesity/therapy ; Overweight/complications ; Overweight/epidemiology ; Overweight/metabolism ; Overweight/therapy ; Risk Factors ; Risk Reduction Behavior ; Weight Loss/physiology ; Weight Reduction Programs/methods ; Workplace/statistics & numerical data
Language	English
Publishing date	2017-11-29
Publishing country	England
Document type	Journal Article ; Multicenter Study ; Randomized Controlled Trial
ZDB-ID	2711897-6
ISSN	2314-6753 ; 2314-6753
ISSN (online)	2314-6753
ISSN	2314-6753
DOI	10.1155/2017/7254174
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Article ; Online: SOCS1 Haploinsufficiency Presenting as Severe Enthesitis, Bone Marrow Hypocellularity, and Refractory Thrombocytopenia in a Pediatric Patient with Subsequent Response to JAK Inhibition.

Michniacki, Thomas F / Walkovich, Kelly / DeMeyer, Lauren / Saad, Nadine / Hannibal, Mark / Basiaga, Matthew L / Horst, Kelly K / Mohan, Smriti / Chen, Liang / Brodeur, Kailey / Du, Yan / Frame, David / Ngo, Sandra / Simoneau, Jillian / Brown, Noah / Lee, Pui Y

Journal of clinical immunology

2022 Volume 42, Issue 8, Page(s) 1766–1777

Abstract: Haploinsufficiency of suppressor of cytokine signaling 1 (SOCS1) is a recently discovered autoinflammatory disorder with significant rheumatologic, immunologic, and hematologic manifestations. Here we report a case of SOCS1 haploinsufficiency in a 5-year- ...

Abstract	Haploinsufficiency of suppressor of cytokine signaling 1 (SOCS1) is a recently discovered autoinflammatory disorder with significant rheumatologic, immunologic, and hematologic manifestations. Here we report a case of SOCS1 haploinsufficiency in a 5-year-old child with profound arthralgias and immune-mediated thrombocytopenia unmasked by SARS-CoV-2 infection. Her clinical manifestations were accompanied by excessive B cell activity, eosinophilia, and elevated IgE levels. Uniquely, this is the first report of SOCS1 haploinsufficiency in the setting of a chromosomal deletion resulting in complete loss of a single SOCS1 gene with additional clinical findings of bone marrow hypocellularity and radiologic evidence of severe enthesitis. Immunologic profiling showed a prominent interferon signature in the patient's peripheral blood mononuclear cells, which were also hypersensitive to stimulation by type I and type II interferons. The patient showed excellent clinical and functional laboratory response to tofacitinib, a Janus kinase inhibitor that disrupts interferon signaling. Our case highlights the need to utilize a multidisciplinary diagnostic approach and consider a comprehensive genetic evaluation for inborn errors of immunity in patients with an atypical immune-mediated thrombocytopenia phenotype.
MeSH term(s)	Female ; Humans ; Suppressor of Cytokine Signaling 1 Protein/genetics ; Suppressor of Cytokine Signaling 1 Protein/metabolism ; Haploinsufficiency ; Leukocytes, Mononuclear/metabolism ; Bone Marrow ; COVID-19 ; SARS-CoV-2 ; Suppressor of Cytokine Signaling Proteins/genetics ; Suppressor of Cytokine Signaling Proteins/metabolism ; Interferons/metabolism ; Thrombocytopenia ; Myelodysplastic Syndromes
Chemical Substances	Suppressor of Cytokine Signaling 1 Protein ; Suppressor of Cytokine Signaling Proteins ; Interferons (9008-11-1) ; SOCS1 protein, human
Language	English
Publishing date	2022-08-17
Publishing country	Netherlands
Document type	Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-022-01346-x
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Article: Increase in pediatric recurrent fever evaluations during the first year of the COVID-19 pandemic in North America.

Mansfield, Leanne M / Lapidus, Sivia K / Romero, Samira Nazzar / Moorthy, Lakshmi N / Adler-Shohet, Felice C / Hollander, Matthew / Cherian, Julie / Twilt, Marinka / Lionetti, Geraldina / Mohan, Smriti / DeLaMora, Patricia A / Durrant, Karen L / Muskardin, Theresa Wampler / Correia Marques, Mariana / Onel, Karen B / Dedeoglu, Fatma / Gutierrez, Maria J / Schulert, Grant

Frontiers in pediatrics

2023 Volume 11, Page(s) 1240242

Abstract: The impact of the COVID-19 pandemic on new diagnoses of recurrent fevers and autoinflammatory diseases is largely unknown. The Childhood Arthritis and Rheumatology Research Alliance (CARRA) PFAPA/AID Working Group aimed to investigate the impact of the ... ...

Abstract	The impact of the COVID-19 pandemic on new diagnoses of recurrent fevers and autoinflammatory diseases is largely unknown. The Childhood Arthritis and Rheumatology Research Alliance (CARRA) PFAPA/AID Working Group aimed to investigate the impact of the COVID-19 pandemic on the number of pediatric patients evaluated for recurrent fevers and autoinflammatory diseases in North America. The absolute number of new outpatient visits and the proportion of these visits attributed to recurrent fever diagnoses during the pre-pandemic period (1 March 2019-29 February 2020) and the first year of the COVID-19 pandemic (1 March 2020-28 February 2021) were examined. Data were collected from 27 sites in the United States and Canada. Our results showed an increase in the absolute number of new visits for recurrent fever evaluations in 21 of 27 sites during the COVID-19 pandemic compared to the pre-pandemic period. The increase was observed across different geographic regions in North America. Additionally, the proportion of new visits to these centers for recurrent fever in relation to all new patient evaluations was significantly higher during the first year of the pandemic, increasing from 7.8% before the pandemic to 10.9% during the pandemic year (
Language	English
Publishing date	2023-08-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2023.1240242
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Article: Corrigendum: Increase in pediatric recurrent fever evaluations during the first year of the COVID-19 pandemic in North America.

Frontiers in pediatrics

2023 Volume 11, Page(s) 1323946

Abstract: This corrects the article DOI: 10.3389/fped.2023.1240242.]. ...

Abstract	[This corrects the article DOI: 10.3389/fped.2023.1240242.].
Language	English
Publishing date	2023-11-06
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2023.1323946
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Article ; Online: Endothelial progenitor cell phenotype and function are impaired in childhood-onset systemic lupus erythematosus.

Mohan, Smriti / Barsalou, Julie / Bradley, Timothy J / Slorach, Cameron / Reynolds, John A / Hasni, Sarfaraz / Thompson, Becky / Ng, Lawrence / Levy, Deborah / Silverman, Earl / Kaplan, Mariana J

Arthritis & rheumatology (Hoboken, N.J.)

2015 Volume 67, Issue 8, Page(s) 2257–2262

Abstract: Objective: Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular risk in adult-onset and childhood-onset SLE. Type I interferons (IFNs) appear to play a prominent role in premature vascular damage in adult-onset SLE, at least ... ...

Abstract	Objective: Systemic lupus erythematosus (SLE) is characterized by increased cardiovascular risk in adult-onset and childhood-onset SLE. Type I interferons (IFNs) appear to play a prominent role in premature vascular damage in adult-onset SLE, at least in part, by inducing impairments in the phenotype and function of endothelial progenitor cells (EPCs), thereby hampering vascular repair. It is not clear whether EPC dysfunction is present in childhood-onset SLE in association with a type I IFN signature. Methods: The phenotype and numbers of EPCs were quantified in patients with childhood-onset SLE, patients with juvenile idiopathic arthritis (JIA), and matched healthy control subjects. In a separate cohort of patients with childhood-onset SLE, markers of subclinical atherosclerosis and endothelial dysfunction were quantified using standardized protocols and analyzed for associations with serum type I IFN activity. Results: EPC numbers and function were significantly decreased in patients with childhood-onset SLE compared with patients with JIA and healthy control subjects. Serum from patients with childhood-onset SLE impaired differentiation of EPCs into mature endothelial cells in healthy controls, and this effect was blocked by inhibition of the type I IFN pathway. Type I IFN activity in serum was not significantly associated with subclinical atherosclerosis and endothelial function in patients with childhood-onset SLE. Conclusion: As in adult-onset SLE, childhood-onset SLE is characterized by phenotypic and functional EPC abnormalities, which are likely triggered by type I IFNs. Although cross-sectional analysis revealed no global association between type I IFN signatures and vascular measures of subclinical atherosclerosis, longitudinal assessments are needed to evaluate whether progression of vascular damage in patients with childhood-onset SLE is associated with type I IFNs, as observed in patients with adult-onset SLE.
MeSH term(s)	Adolescent ; Arthritis, Juvenile/epidemiology ; Arthritis, Juvenile/immunology ; Arthritis, Juvenile/physiopathology ; Asymptomatic Diseases ; Atherosclerosis/epidemiology ; Atherosclerosis/physiopathology ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/physiopathology ; Carotid Intima-Media Thickness ; Case-Control Studies ; Cell Differentiation/physiology ; Child ; Cross-Sectional Studies ; Endothelial Progenitor Cells/cytology ; Female ; Humans ; Interferon Type I/antagonists & inhibitors ; Interferon Type I/immunology ; Lupus Erythematosus, Systemic/epidemiology ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/physiopathology ; Male ; Phenotype ; Pulse Wave Analysis ; Risk Factors ; Vasodilation/physiology
Chemical Substances	Interferon Type I
Language	English
Publishing date	2015-04-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.39149
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Article ; Online: DEK-targeting DNA aptamers as therapeutics for inflammatory arthritis.

Nature communications

2017 Volume 8, Page(s) 14252

Abstract: Novel therapeutics are required for improving the management of chronic inflammatory diseases. Aptamers are single-stranded RNA or DNA molecules that have recently shown utility in a clinical setting, as they can specifically neutralize biomedically ... ...

Abstract	Novel therapeutics are required for improving the management of chronic inflammatory diseases. Aptamers are single-stranded RNA or DNA molecules that have recently shown utility in a clinical setting, as they can specifically neutralize biomedically relevant proteins, particularly cell surface and extracellular proteins. The nuclear chromatin protein DEK is a secreted chemoattractant that is abundant in the synovia of patients with juvenile idiopathic arthritis (JIA). Here, we show that DEK is crucial to the development of arthritis in mouse models, thus making it an appropriate target for aptamer-based therapy. Genetic depletion of DEK or treatment with DEK-targeted aptamers significantly reduces joint inflammation in vivo and greatly impairs the ability of neutrophils to form neutrophil extracellular traps (NETs). DEK is detected in spontaneously forming NETs from JIA patient synovial neutrophils, and DEK-targeted aptamers reduce NET formation. DEK is thus key to joint inflammation, and anti-DEK aptamers hold promise for the treatment of JIA and other types of arthritis.
MeSH term(s)	Adult ; Animals ; Aptamers, Nucleotide/therapeutic use ; Arthritis, Juvenile/immunology ; Arthritis, Juvenile/therapy ; Chemotactic Factors/antagonists & inhibitors ; Chemotactic Factors/genetics ; Chemotactic Factors/immunology ; Chemotactic Factors/metabolism ; Chromosomal Proteins, Non-Histone/antagonists & inhibitors ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/immunology ; Chromosomal Proteins, Non-Histone/metabolism ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Disease Models, Animal ; Extracellular Traps/immunology ; Extracellular Traps/metabolism ; Female ; Healthy Volunteers ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils/immunology ; Oncogene Proteins/antagonists & inhibitors ; Oncogene Proteins/genetics ; Oncogene Proteins/immunology ; Oncogene Proteins/metabolism ; Poly-ADP-Ribose Binding Proteins/antagonists & inhibitors ; Poly-ADP-Ribose Binding Proteins/genetics ; Poly-ADP-Ribose Binding Proteins/immunology ; Poly-ADP-Ribose Binding Proteins/metabolism ; Primary Cell Culture ; Synovial Fluid/chemistry ; Synovial Fluid/cytology ; Synovial Fluid/immunology ; Zymosan/immunology
Chemical Substances	Aptamers, Nucleotide ; Chemotactic Factors ; Chromosomal Proteins, Non-Histone ; DEK protein, mouse ; DNA-Binding Proteins ; DEK protein, human ; Oncogene Proteins ; Poly-ADP-Ribose Binding Proteins ; Zymosan (9010-72-4)
Language	English
Publishing date	2017-02-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/ncomms14252
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Article ; Online: High Levels of DEK Autoantibodies in Sera of Patients With Polyarticular Juvenile Idiopathic Arthritis and With Early Disease Flares Following Cessation of Anti-Tumor Necrosis Factor Therapy.

Mor-Vaknin, Nirit / Rivas, Miguel / Legendre, Maureen / Mohan, Smriti / Yuanfan, Ye / Mau, Theresa / Johnson, Anne / Huang, Bin / Zhao, Lili / Kimura, Yukiko / Spalding, Steven J / Morris, Paula W / Gottlieb, Beth S / Onel, Karen / Olson, Judyann C / Edelheit, Barbara S / Shishov, Michael / Jung, Lawrence K / Cassidy, Elaine A /

Prahalad, Sampath / Passo, Murray H / Beukelman, Timothy / Mehta, Jay / Giannini, Edward H / Adams, Barbara S / Lovell, Daniel J / Markovitz, David M

Arthritis & rheumatology (Hoboken, N.J.)

2018 Volume 70, Issue 4, Page(s) 594–605

Abstract: Objective: The nuclear oncoprotein DEK is an autoantigen associated with juvenile idiopathic arthritis (JIA), especially the oligoarticular subtype. DEK is a secreted chemotactic factor. Abundant levels of DEK and DEK autoantibodies are found in ... ...

Abstract	Objective: The nuclear oncoprotein DEK is an autoantigen associated with juvenile idiopathic arthritis (JIA), especially the oligoarticular subtype. DEK is a secreted chemotactic factor. Abundant levels of DEK and DEK autoantibodies are found in inflamed synovium in JIA. We undertook this study to further characterize the nature of DEK autoantibodies in screening serum samples from 2 different cohorts that consisted mostly of patients with JIA. Methods: DEK autoantibody levels were analyzed in sera from 33 JIA patients, 13 patients with other inflammatory conditions, and 11 healthy controls, as well as in 89 serum samples from JIA patients receiving anti-tumor necrosis factor (anti-TNF) therapy. Recombinant His-tagged full-length DEK protein (1-375 amino acids [aa]) and the 187-375-aa and 1-350-aa His-tagged DEK fragments made in a baculovirus system were used for enzyme-linked immunosorbent assay (ELISA) and immunoblotting. The C-terminal 25-aa fragment of DEK was expressed in a glutathione S-transferase-tagged vector. ELISA results were calculated as area under the curve by the trapezoidal rule. Results: DEK autoantibody levels were significantly higher in patients with polyarticular JIA than in those with oligoarticular JIA, and were higher in patients with polyarticular JIA who had more active disease after cessation of anti-TNF therapy. Immunoblotting against the C-terminal 25-aa fragment of DEK confirmed that this section of the DEK molecule is the most immunogenic domain. Conclusion: DEK autoantibody levels are higher in patients with polyarticular JIA than in those with oligoarticular JIA, and higher in patients who have disease flares after cessation of anti-TNF therapy. The C-terminal 25-aa fragment is the most immunogenic portion of DEK. These findings are significant with respect to the nature of DEK autoantibodies, their contribution to JIA pathogenesis, and their implications for JIA management.
MeSH term(s)	Adolescent ; Antirheumatic Agents/immunology ; Arthritis, Juvenile/blood ; Arthritis, Juvenile/drug therapy ; Arthritis, Juvenile/immunology ; Autoantibodies/blood ; Autoantibodies/immunology ; Case-Control Studies ; Child ; Chromosomal Proteins, Non-Histone/immunology ; Female ; Humans ; Male ; Oncogene Proteins/immunology ; Poly-ADP-Ribose Binding Proteins/immunology ; Symptom Flare Up ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Withholding Treatment
Chemical Substances	Antirheumatic Agents ; Autoantibodies ; Chromosomal Proteins, Non-Histone ; DEK protein, human ; Oncogene Proteins ; Poly-ADP-Ribose Binding Proteins ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2018-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.40404
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