A5063791039- Complement system in diseases
- Multiple Sclerosis Research Studies
- Neuroinflammation and Neurodegeneration Mechanisms
- Cell Adhesion Molecules Research
- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- Cytokine Signaling Pathways and Interactions
- T-cell and B-cell Immunology
- Immunodeficiency and Autoimmune Disorders
- Reproductive System and Pregnancy
- Ion channel regulation and function
- Galectins and Cancer Biology
- Dermatological and Skeletal Disorders
- interferon and immune responses
- Glycosylation and Glycoproteins Research
- Peripheral Neuropathies and Disorders
- Parathyroid Disorders and Treatments
- MicroRNA in disease regulation
- Cell death mechanisms and regulation
- Systemic Lupus Erythematosus Research
- S100 Proteins and Annexins
- Angiogenesis and VEGF in Cancer
- Cerebrovascular and genetic disorders
- Connective Tissue Growth Factor Research
- Heterotopic Ossification and Related Conditions
National Institutes of Health
2014-2024
National Heart Lung and Blood Institute
2019-2024
National Institute of Arthritis and Musculoskeletal and Skin Diseases
2013-2021
University of Maryland, Baltimore
2007-2016
VA Maryland Health Care System
2005-2016
Neurology, Inc
2007-2009
University of Maryland, College Park
2007-2008
Johns Hopkins University
2005
Multiple Sclerosis (MS) is characterized by central nervous system perivenular and parenchymal mononuclear cell infiltrates consisting of activated T cells macrophages. We recently demonstrated that elevated expression the voltage-gated potassium channel, Kv1.3, a functional marker effector memory (T EM ) in experimental allergic encephalomyelitis myelin-specific derived from peripheral blood patients with MS. Herein, we show Kv1.3 highly expressed postmortem MS brain inflammatory...
The deficiency of adenosine deaminase 2 (DADA2) is an autosomal recessively inherited disease that has undergone extensive phenotypic expansion since being first described in patients with fevers, recurrent strokes, livedo racemosa, and polyarteritis nodosa 2014. It now recognized may develop multisystem spans multiple medical subspecialties. Here, we describe the findings from a large single center longitudinal cohort 60 patients, broad presentation, as well highlight cohort’s experience...
Background: Arterial calcification due to deficiency of CD73 (ACDC; OMIM 211800) is a rare genetic disease resulting in calcium deposits arteries and small joints causing claudication, resting pain, severe joint deformities. Currently, there are no standard treatments for ACDC. Our previous work identified etidronate as potential targeted ACDC treatment, using vitro vivo models with patient-derived cells. In this study, we test the safety effectiveness attenuating progression lower-extremity...
Potassium (K(+)) channels on immune cells have gained attention recently as promising targets of therapy for immune-mediated neurological diseases such multiple sclerosis (MS). We examined K(+) dendritic (DCs), which infiltrate the brain in MS and may impact disease course.We identified blood-derived DCs by whole-cell patch-clamp analysis, confirmed immunofluorescent staining. also stained sections from patients control subjects. To test functionality, we blocked K(v)1.3 K(v)1.5 stimulated...
Abstract Activation of the terminal complement cascade involving C5 to C9 proteins has a beneficial role for oligodendrocytes (OLG) in experimental allergic encephalomyelitis, an animal model multiple sclerosis, by protecting them from apoptotic cell death. We have previously shown that sublytic C5b-9 complexes, through posttranslational regulation Bad, inhibit mitochondrial pathway apoptosis induced serum deprivation. In present study, we examined possible involvement caspase-8 and Fas OLG...
Abstract Complement activation is involved in the initiation of Ab-mediated inflammatory demyelination experimental autoimmune encephalomyelitis (EAE). At a sublytic dose, C5b-9 membrane attack complex protects oligodendrocytes (OLG) from apoptosis. Using C5-deficient (C5-d) mice, we previously showed dual role for C5: enhancement acute EAE, and promotion remyelination during recovery. In this study, investigated C5 apoptosis myelin-induced EAE. C5-d C5-sufficient (C5-s) mice had similar...