Research Topics
Genomes and Genes | GARY STEVEN FIRESTEINSummaryAffiliation: University of California Country: USA Publications
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Publications
Regulation of peripheral inflammation by the central nervous systemJean Marc Waldburger
Division of Rheumatology, Geneva University Hospital, Geneva, Switzerland
Curr Rheumatol Rep 12:370-8. 2010..Some of the neurotransmitters and neuroreceptors involved have been identified in preclinical models and represent novel targets for the treatment of rheumatic diseases...- PUMA-mediated apoptosis in fibroblast-like synoviocytes does not require p53Xin You
Division of Rheumatology, Allergy and Immunology, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, California 92093, USA
Arthritis Res Ther 8:R157. 2006..Therefore, approaches to gene therapy that involve increasing PUMA expression could be an effective inducer of synoviocyte cell death in rheumatoid arthritis regardless of the p53 status in the synovium... - Garden of therapeutic delights: new targets in rheumatic diseasesJean M Waldburger
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, Mail Code 0656, 9500 Gilman Drive, La Jolla, CA 92093, USA
Arthritis Res Ther 11:206. 2009..The abundance of potential targets suggests that new and creative ways of evaluating safety and efficacy are needed... - Regulation of the JNK pathway by TGF-beta activated kinase 1 in rheumatoid arthritis synoviocytesDeepa R Hammaker
Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, Gilman Dr, La Jolla, CA 92093, USA
Arthritis Res Ther 9:R57. 2007..In contrast to other cell lineages, MEKK1, MEKK2, and MEKK3 did not contribute to JNK phosphorylation in FLSs. The data identify TAK1 as a pivotal upstream kinase and potential therapeutic target to modulate synoviocyte activation in RA... - p53 tumor suppressor gene mutations in fibroblast-like synoviocytes from erosion synovium and non-erosion synovium in rheumatoid arthritisYuji Yamanishi
Department of Rheumatology, Hiroshima City Hospital, Hiroshima, Japan
Arthritis Res Ther 7:R12-8. 2005..The determining factor for invasiveness might be proximity to bone or cartilage rather than the presence of a p53 mutation... - Suppression of murine collagen-induced arthritis by targeted apoptosis of synovial neovasculatureD M Gerlag
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
Arthritis Res 3:357-61. 2001..Targeted apoptosis of synovial neovasculature can induce apoptosis and suppress clinical arthritis. This form of therapy has potential utility in the treatment of inflammatory arthritis... - Mitogen activated protein kinase inhibitors: where are we now and where are we going?S E Sweeney
University of California San Diego School of Medicine, Mail Code 0656, Division of Rheumatology, Allergy and Immunology, 9500 Gilman Drive, La Jolla, CA 92093 0656, USA
Ann Rheum Dis 65:iii83-8. 2006..These approaches might permit effective use of MAP kinase inhibitors for the treatment of rheumatic and immune-mediated diseases... - Biomedicine. Every joint has a silver liningGary S Firestein
Division of Rheumatology, Allergy and Immunology, University of California, San Diego, School of Medicine, 9500 Gilman Drive, MC 0656, La Jolla, CA 92093-0656, USA
Science 315:952-3. 2007 - Common mechanisms in immune-mediated inflammatory diseaseGary S Firestein
Division of Rheumatology, Allergy, and Immunology, Department of Medicine, University of California at San Diego, San Diego, California, USA
J Rheumatol Suppl 73:8-13; discussion 29-30. 2005..Understanding the autoimmune and inflammatory pathways implicated in disease has led to targeted drug development and improved clinical outcomes... - The T cell cometh: interplay between adaptive immunity and cytokine networks in rheumatoid arthritisGary S Firestein
Division of Rheumatology, Allergy, and Immunology and Clinical Investigation Institute, University of California San Diego School of Medicine, 9500 Gilman Drive, San Diego, CA 92093 0656, USA
J Clin Invest 114:471-4. 2004..Hence, effective therapeutic interventions can target either unique etiologic pathways related to adaptive immune responses or shared terminal mechanisms... - Pathogenesis of rheumatoid arthritis: how early is early?Gary S Firestein
Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, California, USA
Arthritis Res Ther 7:157-9. 2005..Evaluation of the cytokine profile at the earliest time points after onset of symptoms could identify novel targets that prevent progression to chronic arthritis... - Immunologic mechanisms in the pathogenesis of rheumatoid arthritisGary S Firestein
Department of Medicine, Division of Rheumatology, Allergy, and Immunology, University of California San Diego School of Medicine, 9500 Gilman Drive BSB, Rm 5098, La Jolla, CA 92093, USA
J Clin Rheumatol 11:S39-44. 2005..Although currently approved BRMs still have limitations, choosing an appropriate target, possibly early rather than late in the immune response, might result in new and improved therapies for RA... - How important are T cells in chronic rheumatoid synovitis?: II. T cell-independent mechanisms from beginning to endGary S Firestein
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0656, USA
Arthritis Rheum 46:298-308. 2002 - Evolving concepts of rheumatoid arthritisGary S Firestein
Division of Rheumatology, Allergy and Immunology, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093 0656, USA
Nature 423:356-61. 2003..Based on the pathogenic mechanisms, specific therapeutic interventions can be designed to suppress synovial inflammation and joint destruction in rheumatoid arthritis... - Regulation of peripheral inflammation by spinal p38 MAP kinase in ratsDavid L Boyle
Division of Rheumatology, Allergy, and Immunology, University of California San Diego School of Medicine, La Jolla, California, United States of America
PLoS Med 3:e338. 2006..Characterization of this mechanism could have clinical and basic research implications by supporting development of new treatments for arthritis and clarifying how the CNS regulates peripheral immune responses... - Regulation of JNK by MKK-7 in fibroblast-like synoviocytesTomoyuki Inoue
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0656, USA
Arthritis Rheum 54:2127-35. 2006..However, the functional hierarchy of MKK-4 and MKK-7 in FLS has not been determined. We determined the relative contributions of these MKKs by evaluating the effect of MKK-4 and MKK-7 gene knockdown in cultured FLS... - Mitogen-activated protein kinase kinase 3 is a pivotal pathway regulating p38 activation in inflammatory arthritisTomoyuki Inoue
Division of Rheumatology, Allergy, and Immunology, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0656, USA
Proc Natl Acad Sci U S A 103:5484-9. 2006..Therefore, selective MKK3 deficiency can suppress inflammatory arthritis and cytokine production while Toll-like receptor 4-mediated host defense remains intact... - Regulation of c-Jun phosphorylation by the I kappa B kinase-epsilon complex in fibroblast-like synoviocytesSusan E Sweeney
Division of Rheumatology, Allergy, and Immunology, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
J Immunol 174:6424-30. 2005..These data suggest a novel role for the IKKepsilon complex in synovial inflammation, extracellular matrix destruction, and activation of the viral program and innate immune response in RA... - Regulation of c-Jun N-terminal kinase by MEKK-2 and mitogen-activated protein kinase kinase kinases in rheumatoid arthritisDeepa R Hammaker
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
J Immunol 172:1612-8. 2004..These data indicate that MEKK2 is a potent activator of the JNK pathway in FLS and that signal complexes including MEKK2, MKK4, MKK7, and/or JNK are potential therapeutic targets in RA... - Wnt1 inducible signaling pathway protein-3 regulation and microsatellite structure in arthritisHyeonjoo Cheon
Division of Rheumatology, Allergy, and Immunology, University of California at San Diego School of Medicine, La Jolla, California 92093 0656, USA
J Rheumatol 31:2106-14. 2004..To investigate the contribution of WISP3 to synovial inflammation, we evaluated its expression and regulation in arthritis... - Acetylcholine regulation of synoviocyte cytokine expression by the alpha7 nicotinic receptorJean Marc Waldburger
University of California, San Diego, La Jolla, CA, USA
Arthritis Rheum 58:3439-49. 2008..To test this possibility, we evaluated the expression of alpha7R and its potential role as a target in rheumatoid arthritis (RA)... - Measurement of inflammatory biomarkers in synovial tissue extracts by enzyme-linked immunosorbent assaySanna Rosengren
Center for Innovative Therapy, Division of Rheumatology, Allergy, and Immunology, University of California--San Diego School of Medicine, La Jolla, California, USA
Clin Diagn Lab Immunol 10:1002-10. 2003..These methods allow monitoring of biomarker protein levels in synovial tissue and could potentially be applied to early-phase clinical trials to provide a preliminary estimate of drug efficacy... - Expression and activation of mitogen-activated protein kinase kinases-3 and -6 in rheumatoid arthritisMartine Chabaud-Riou
Division of Rheumatology, Allergy, and Immunology, University of California at San Diego School of Medicine, La Jolla, California 92093, USA
Am J Pathol 164:177-84. 2004..By forming a complex with p38 in synovial tissue and FLS, these kinases can potentially be targeted to regulate the production of proinflammatory cytokine production in inflamed synovium... - Gadd45beta deficiency in rheumatoid arthritis: enhanced synovitis through JNK signalingCamilla I Svensson
University of California San Diego School of Medicine, La Jolla, CA 92093, USA
Arthritis Rheum 60:3229-40. 2009..This study was carried out to evaluate whether low Gadd45beta expression in RA enhances JNK activation and overproduction of MMPs in RA, and whether Gadd45beta deficiency increases arthritis severity in passive K/BxN murine arthritis... - IL-6 and matrix metalloproteinase-1 are regulated by the cyclin-dependent kinase inhibitor p21 in synovial fibroblastsHarris Perlman
Division of Rheumatology, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA
J Immunol 170:838-45. 2003..These data suggest that alterations in p21 expression may activate AP-1 leading to enhanced proinflammatory cytokine and MMP production and development of autoimmune disease... - Regulation of p38 MAPK by MAPK kinases 3 and 6 in fibroblast-like synoviocytesTomoyuki Inoue
Division of Rheumatology, Allergy, and Immunology, University of California, San Diego, School of Medicine, La Jolla, CA 92093 0656, USA
J Immunol 174:4301-6. 2005..These data demonstrate that MKK3 and MKK6 make individual contributions to p38 activation in FLS after cytokine stimulation, but that both must be blocked for maximum inhibition... - Expression of the MAPK kinases MKK-4 and MKK-7 in rheumatoid arthritis and their role as key regulators of JNKMonisha Sundarrajan
University of California, San Diego, School of Medicine, La Jolla, 92093, USA
Arthritis Rheum 48:2450-60. 2003..We therefore evaluated the interactions between the various MAP kinase components and determined their subcellular localization... - Expression and regulation of aggrecanase in arthritis: the role of TGF-betaYuji Yamanishi
Division of Rheumatology, Allergy, and Immunology, University of California at San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093, USA
J Immunol 168:1405-12. 2002..In contrast, aggrecanase-2 protein may be regulated by a post-translational mechanism in OA and RA ST. Synovial and FLS production of aggrecanase can contribute to cartilage degradation in RA and OA... - Retinoblastoma suppression of matrix metalloproteinase 1, but not interleukin-6, through a p38-dependent pathway in rheumatoid arthritis synovial fibroblastsKathleen Bradley
Saint Louis University, School of Medicine, St Louis, Missouri 63104, USA
Arthritis Rheum 50:78-87. 2004..Therefore, we sought to determine if the tumor suppressor gene product retinoblastoma (Rb), a negative regulator of cell cycle activity, inhibits IL-6, MMP-1, and p38 in RA synovial fibroblasts... - Kinetic analysis of synovial signalling and gene expression in animal models of arthritisAkihisa Fukushima
Division of Rheumatology, Allergy and Immunology, University of California, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0656, USA
Ann Rheum Dis 69:918-23. 2010..Animal models of arthritis are frequently used to evaluate novel therapeutic agents. However, their ability to predict responses in humans is variable... - A novel spleen tyrosine kinase inhibitor blocks c-Jun N-terminal kinase-mediated gene expression in synoviocytesHoon-Suk Cha
Division of Rheumatology, Allergy and Immunology, University of California, San Diego, School of Medicine, La Jolla, CA 92093, USA
J Pharmacol Exp Ther 317:571-8. 2006..These data demonstrate that Syk activation plays an essential role in TNFalpha-induced cytokine and matrix metalloproteinase production in RA FLS, especially by suppressing activation of the JNK pathway... - PUMA regulation and proapoptotic effects in fibroblast-like synoviocytesHoon-Suk Cha
University of California-San Diego, La Jolla, California, USA
Arthritis Rheum 54:587-92. 2006..However, HA-PUMA transfection into FLS resulted in rapid apoptosis with the activation of caspase 3. CONCLUSION: PUMA can induce apoptosis by FLS and represents a potential target in RA... - Inhibiting inflammation in rheumatoid arthritisGary S Firestein
Division of Rheumatology, Allergy, and Immunology and the University of California at San Diego Clinical Investigation Institute, University of California at San Diego School of Medicine, La Jolla, USA
N Engl J Med 354:80-2. 2006 - Antiviral gene expression in rheumatoid arthritis: role of IKKepsilon and interferon regulatory factor 3Susan E Sweeney
University of California San Diego, School of Medicine, La Jolla, CA 92093, USA
Arthritis Rheum 56:743-52. 2007..This study was designed to investigate the role of the IKK-related kinase IKKepsilon and IFN regulatory factor 3 (IRF-3) in the activation of antiviral genes in rheumatoid arthritis (RA)... - Innate immunity as a hired gun: but is it rheumatoid arthritis?Maripat Corr
Division of Rheumatology, Allergy, and Immunology, University of California, San Diego, La Jolla, CA 92093, USA
J Exp Med 195:F33-5. 2002 - Joint damage and inflammation in c-Jun N-terminal kinase 2 knockout mice with passive murine collagen-induced arthritisZuoning Han
University of California San Diego School of Medicine, La Jolla 92093, USA
Arthritis Rheum 46:818-23. 2002..The present study was undertaken to investigate whether selective loss of JNK-2 function decreases joint destruction in JNK-2 knockout mice, in order to determine the role of this isoform in inflammatory arthritis... - The genetics of the target tissue in rheumatoid arthritisMaripat Corr
Division of Rheumatology, Allergy, and Immunology, University of California, San Diego, School of Medicine, La Jolla, California, USA
Rheum Dis Clin North Am 28:79-94. 2002..Further studies of large populations are likely to segregate out factors affecting specific ethnic, clinical, and genetic subgroups... - Synoviocyte innate immune responses: II. Pivotal role of IFN regulatory factor 3Susan E Sweeney
Division of Rheumatology, Allergy, and Immunology, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
J Immunol 184:7162-8. 2010..Targeting synoviocyte IRF3 represents a potential approach to suppress diverse mediators while limiting suppression of IRF7-mediated immune responses... - Vanadate, an inhibitor of stromelysin and collagenase expression, suppresses collagen induced arthritisStephen J Oliver
Division of Rheumatology, UCLA School of Medicine, Los Angeles, California, USA
J Rheumatol 34:1802-9. 2007..We evaluated whether a vanadium AP-1 inhibitor could reduce MMP expression and subsequent joint damage in CIA... - Primer: signal transduction in rheumatic disease--a clinician's guideSusan E Sweeney
Division of Rheumatology, Allergy and Immunology, University of California San Diego, Department of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0656, USA
Nat Clin Pract Rheumatol 3:651-60. 2007..Understanding these intracellular pathways might lead to new approaches to the treatment of inflammatory disease, including the use of orally bioavailable small molecules that regulate cytokine function and production... - Synoviocyte innate immune responses: I. Differential regulation of interferon responses and the JNK pathway by MAPK kinasesToshio Yoshizawa
Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA
J Immunol 181:3252-8. 2008..MKK7 is the primary activator of JNK in TNF, LPS, and PGN responses. However, TLR3 requires both MKK4 and MKK7, with the former activating c-Jun and the latter activating both c-Jun and IRF3 through JNK-dependent mechanisms... - Spinal adenosine receptor activation inhibits inflammation and joint destruction in rat adjuvant-induced arthritisDavid L Boyle
Division of Rheumatology, Allergy and Immunology, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
Arthritis Rheum 46:3076-82. 2002..To examine the effect of spinal cord adenosine (Ado) receptor stimulation on rat adjuvant-induced arthritis (AIA)... - Quantitative biomarker analysis of synovial gene expression by real-time PCRDavid L Boyle
Center for Innovative Therapy, Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, California, USA
Arthritis Res Ther 5:R352-60. 2003..The technique can potentially be used in serial biopsy studies to provide insights into mechanism of action and therapeutic effect of new anti-inflammatory agents... - Rheumatoid arthritis: regulation of synovial inflammationSusan E Sweeney
Division of Rheumatology, Allergy, and Immunology, UCSD School of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
Int J Biochem Cell Biol 36:372-8. 2004.... - Prevention of cold-associated acute inflammation in familial cold autoinflammatory syndrome by interleukin-1 receptor antagonistHal M Hoffman
Division of Rheumatology, Allergy, and Immunology, University of California at San Diego School of Medicine, La Jolla, CA 92093 0635, USA
Lancet 364:1779-85. 2004..The genetic basis of this disease has been elucidated. Cryopyrin, the protein that is altered in FCAS, is one of the adaptor proteins that activate caspase 1, resulting in release of interleukin 1... - Spinal adenosine agonist reduces c-fos and astrocyte activation in dorsal horn of rats with adjuvant-induced arthritisLinda S Sorkin
Department of Anesthesiology and Division of Rheumatology, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093 0818, USA
Neurosci Lett 340:119-22. 2003..Astrocyte activation was only partially attenuated by adenosine A1 receptor agonist treatment... - Regulation of peripheral inflammation by spinal adenosine: role of somatic afferent fibersLinda S Sorkin
Department of Anesthesiology, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093, USA
Exp Neurol 184:162-8. 2003..Information on pain and inflammation in the periphery is transmitted to the nervous system, where increased spinal adenosine levels can suppress peripheral inflammation... - Telomerase-transduced osteoarthritic fibroblast-like synoviocyte cell lineYubo Sun
Division of Rheumatology and Immunology, Department of Medicine, University of Miami School of Medicine, Miami, FL 33101, USA
Biochem Biophys Res Commun 323:1287-92. 2004.... - Fibroblast-like synoviocytes: key effector cells in rheumatoid arthritisBeatrix Bartok
Division of Rheumatology, Allergy, and Immunology, UCSD School of Medicine, La Jolla, CA 92093, USA
Immunol Rev 233:233-55. 2010..New agents that target FLS could potentially complement the current therapies without major deleterious effect on adaptive immune responses... - Immunostimulatory DNA sequences influence the course of adjuvant arthritisArash Ronaghy
Department of Medicine, Division of Rheumatology, Allergy and Immunology, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
J Immunol 168:51-6. 2002..In this model, we postulate that massive and prolonged activation of macrophages, dendritic cells, and osteoclast precursors in the bone marrow may prime the joints for the induction of inflammatory Th1 immune responses to Mtb Ags... - HIF-1alpha is essential for myeloid cell-mediated inflammationThorsten Cramer
Molecular Biology Section, Division of Biological Sciences, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA
Cell 112:645-57. 2003..This role for HIF-1alpha demonstrates its direct regulation of survival and function in the inflammatory microenvironment... - Inflammatory mediators promote production of shed LRP1/CD91, which regulates cell signaling and cytokine expression by macrophagesMatvey Gorovoy
Department of Pathology, University of California San Diego School of Medicine, La Jolla, CA 92093, USA
J Leukoc Biol 88:769-78. 2010..7 cells, including TNF-?, MCP-1/CCL2, and IL-10. These results demonstrate that sLRP1 is generated in inflammation and may regulate inflammation by its effects on macrophage physiology... - Microsatellite instability and suppressed DNA repair enzyme expression in rheumatoid arthritisSang Heon Lee
Division of Rheumatology, Allergy, and Immunology, Division of Gastroenterology, School of Medicine, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
J Immunol 170:2214-20. 2003..We propose that oxidative stress not only creates DNA adducts that are potentially mutagenic, but also suppresses the mechanisms that limit the DNA damage... - P53 down-regulates matrix metalloproteinase-1 by targeting the communications between AP-1 and the basal transcription complexYubo Sun
Department of Medicine, University of Miami School of Medicine, Miami, Florida 33101, USA
J Cell Biochem 92:258-69. 2004..Finally, by using p53 truncated mutant constructs, we demonstrate that both the N-terminal activation domain and the C-terminal oligomerization domains of p53 were required for the down-regulation of MMP1 transcription... - Role of MAPK kinase 6 in arthritis: distinct mechanism of action in inflammation and cytokine expressionToshio Yoshizawa
Division of Rheumatology, Allergy and Immunology, University of California San Diego, School of Medicine, La Jolla, CA 92093, USA
J Immunol 183:1360-7. 2009..Although MKK3 and MKK6 activate the p38 pathway, they regulate distinct subsets of proinflammatory cytokines. MKK6 appears mainly to facilitate p38 and MK2 colocalization in the nucleus rather than to phosphorylate p38... - Proinflammatory cytokine expression in the endolymphatic sac during inner ear inflammationHitoshi Satoh
Division of Otolaryngology Head and Neck Surgery, University of California, San Diego, CA 92093, USA
J Assoc Res Otolaryngol 4:139-47. 2003.... - Interactive cytokine regulation of synoviocyte lubricant secretionMegan E Blewis
Department of Bioengineering, University of California San Diego, La Jolla, CA, USA
Tissue Eng Part A 16:1329-37. 2010.... - Regional analysis of p53 mutations in rheumatoid arthritis synoviumYuji Yamanishi
Division of Rheumatology, Allergy, and Immunology, University of California at San Diego School of Medicine, La Jolla, CA 92093, USA
Proc Natl Acad Sci U S A 99:10025-30. 2002..A relatively low percentage of cells containing p53 mutations can potentially affect neighboring cells and enhance inflammation through the elaboration of proinflammatory cytokines... - TLR2 signaling in chondrocytes drives calcium pyrophosphate dihydrate and monosodium urate crystal-induced nitric oxide generationRu Liu-Bryan
Veterans Affairs Medical Center, San Diego, CA 92161, USA
J Immunol 174:5016-23. 2005..Our results indicate the potential for innate immunity at the level of the articular chondrocyte to directly contribute to inflammatory and degenerative tissue reactions associated with both gout and pseudogout... - Tumor necrosis factor-alpha, an initiator, and etanercept, an inhibitor of cochlear inflammationHitoshi Satoh
Division of Otolaryngology--Head and Neck Surgery, University of California, San Diego, La Jolla 92093-0666, USA
Laryngoscope 112:1627-34. 2002.... - Signal transduction in rheumatoid arthritisSusan E Sweeney
Division of Rheumatology, Allergy, and Immunology, University of California-San Diego, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093, USA
Curr Opin Rheumatol 16:231-7. 2004..Many other pathways could be targeted and offer new therapeutic options for rheumatoid arthritis... - Regulation of arthritis by p53: critical role of adaptive immunityEgle Simelyte
University of California, San Diego, School of Medicine, La Jolla, CA, USA
Arthritis Rheum 52:1876-84. 2005..CONCLUSION: Adaptive immune responses, rather than antibody-mediated responses, in p53(-/-) mice account for increased disease severity in the active CIA model... - Recombinant human relaxin in the treatment of systemic sclerosis with diffuse cutaneous involvement: a randomized, double-blind, placebo-controlled trialDinesh Khanna
David Geffen School of Medicine, and School of Public Health, University of California, Los Angeles, USA
Arthritis Rheum 60:1102-11. 2009.... - Innate immunity contributes to cochlear adaptive immune responsesShigehisa Hashimoto
Division of Otolaryngology-Head and Neck Surgery, University of California, San Diego, 9500 Gilman Dr, CA 92093-0666, USA
Audiol Neurootol 10:35-43. 2005..If true in humans, this implies that priming may be an important component in the development of immune-mediated hearing loss... - Acoustic trauma augments the cochlear immune response to antigenMasumichi Miyao
Division of Otolaryngology Head and Neck Surgery, University of California, La Jolla, California 92093 0666, USA
Laryngoscope 118:1801-8. 2008..To test whether noise-exposure, which activates a cochlear immune response with cytokine expression and infiltration of circulating leukocytes could augment the response to antigen (Ag)... - Acquisition, culture, and phenotyping of synovial fibroblastsSanna Rosengren
Methods Mol Med 135:365-75. 2007..Surface markers that can be used to characterize FLS include positive staining for VCAM-1, CD44, CD55, CD90 (Thy-1), and cadherin-11, coupled with the absence of macrophage markers such as CD14 or CD68... - Amelioration of arthritis by intraarticular dominant negative Ikk beta gene therapy using adeno-associated virus type 5Sander W Tas
Division of Clinical Immunology and Rheumatology, Academic Medical Center/University of Amsterdam, 1100 DE Amsterdam, The Netherlands
Hum Gene Ther 17:821-32. 2006..This translational research represents a crucial next step toward the development of gene therapy for application in humans... - Fibroblast-like synoviocytes derived from patients with rheumatoid arthritis show the imprint of synovial tissue heterogeneity: evidence of a link between an increased myofibroblast-like phenotype and high-inflammation synovitisPia V Kasperkovitz
VU Medical Center, Amsterdam, The Netherlands
Arthritis Rheum 52:430-41. 2005.... - Real-time quantitative PCR to detect changes in synovial gene expression in rheumatoid arthritis after corticosteroid treatmentDanielle M Gerlag
Division of Clinical Immunology and Rheumatology, F4 218, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE, Amsterdam, The Netherlands
Ann Rheum Dis 66:545-7. 2007..These data suggest that Q-PCR can be used to measure synovial mRNA expression of mediators implicated in the pathogenesis of RA in small proof-of-concept trials... - Reduction of proinflammatory cytokine expression in the synovium by targeting IKKbeta in vivo in a rat modelSander W Tas
University of Amsterdam, Amsterdam, The Netherlands
Arthritis Rheum 54:3716-8. 2006 - Regulation of joint destruction and inflammation by p53 in collagen-induced arthritisYuji Yamanishi
University of California at San Diego School of Medicine, La Jolla La Jolla, California 92093, USA
Am J Pathol 160:123-30. 2002.... - Synovial tissue analysis in clinical trialsBarry Bresnihan
Department of Rheumatology, St Vincent s University Hospital, Dublin, Ireland
J Rheumatol 32:2481-4. 2005..This special interest group is working on establishing the evidence to have this endpoint meet the OMERACT filter criteria... - A biomarker by any other nameGary S Firestein
Nat Clin Pract Rheumatol 2:635. 2006 - Regulation of apoptosis in fibroblast-like synoviocytes by the hypoxia-induced Bcl-2 family member Bcl-2/adenovirus E1B 19-kd protein-interacting protein 3Wafa Kammouni
University of Manitoba, Winnipeg, Manitoba, Canada
Arthritis Rheum 56:2854-63. 2007..Since hypoxia is a regulator of apoptosis, and since RA synovium is hypoxic, we conducted this study to examine the effects of hypoxia on the Bcl-2 pathway and the role this may play in regulating apoptosis in FLS... - Transforming growth factor beta expression during an inner ear immune responseHitoshi Satoh
Division of Otolaryngology-Head and Neck Surgery, University of California San Diego, USA
Ann Otol Rhinol Laryngol 115:81-8. 2006..This finding suggests that the process of cochlear fibrosis starts early and that proper treatment could prevent cochlear fibrosis... - NF-kappaB: Holy Grail for rheumatoid arthritis?Gary S Firestein
Arthritis Rheum 50:2381-6. 2004
Research Grants
- 'c-Jun N-terminal kinase and joint destruction in RA'Gary Firestein; Fiscal Year: 2006..Finally, we will determine the role of JNK in animal models of arthritis. These data will support our hypothesis that JNK plays a pivotal role in the FLS biology and is a potential target for chondroprotective therapy. ..
- Regulation of p38 and inflammation by MAPK kinasesGary Firestein; Fiscal Year: 2007..These studies will provide detailed information on the mechanism of p38 activation in inflammatory arthritis and test the hypothesis that selective targeting of MKKs like MKKS will be beneficial in RA. ..
- Training grant in Rheumatic DiseasesGary Firestein; Fiscal Year: 2007..The first two hospitals have, in addition, a Clinical Research Center for hospitalization of patients participating in investigational programs. ..
- Innate immunity and the IKKi complex in Rheumatoid Arthritis (RA) synoviumGary Firestein; Fiscal Year: 2007..These experiments will provide insight into IKK-related kinases and pathogenic mechanisms that contribute to synovitis and joint destruction. ..
- Innate immunity and the IKKi complex in Rheumatoid Arthritis (RA) synoviumGary Firestein; Fiscal Year: 2009..These experiments will provide insight into IKK-related kinases and pathogenic mechanisms that contribute to synovitis and joint destruction. ..
- Regulation of p38 and inflammation by MAPK kinasesGary Firestein; Fiscal Year: 2009..These studies will provide detailed information on the mechanism of p38 activation in inflammatory arthritis and test the hypothesis that selective targeting of MKKs like MKKS will be beneficial in RA. ..
- Innate immunity and the IKKi complex in Rheumatoid Arthritis (RA) synoviumGARY STEVEN FIRESTEIN; Fiscal Year: 2010..These experiments will provide insight into IKK-related kinases and pathogenic mechanisms that contribute to synovitis and joint destruction. ..
- Regulation of p38 and inflammation by MAPK kinasesGARY STEVEN FIRESTEIN; Fiscal Year: 2010..These studies will provide detailed information on the mechanism of p38 activation in inflammatory arthritis and test the hypothesis that selective targeting of MKKs like MKKS will be beneficial in RA. ..
- c-Jun N-terminal kinase and joint destruction in RAGARY STEVEN FIRESTEIN; Fiscal Year: 2010..This project will explore how JNK in RA is regulated by upstream kinases and determine the potential for inhibiting one of these signaling molecules as a therapeutic target. ..
- SYNOVIAL DYSFUNCTION DUE TO P53 ABNORMALITIES IN RAGary Firestein; Fiscal Year: 2006..abstract_text> ..
- REGULATION OF PERIPHERAL INFLAMMATION BY THE CNSGary Firestein; Fiscal Year: 2002..These studies will provide a basis for understanding the central nervous system-immune system connection as well as explore novel therapeutic targets. ..
- SYNOVIAL DYSFUNCTION DUE TO P53 ABNORMALITIES IN RAGary Firestein; Fiscal Year: 2001..A p53-targeted therapeutic approach using a defective adenoviral vector lacking the E1B 55 kD protein will be tested in vivo and in vitro. ..
- IKKi expression and regulation in rheumatoid arthritisGary Firestein; Fiscal Year: 2005..We propose to test the hypothesis that IKKi is an important signal transduction pathway that regulates inflammation in chronic arthritis and is a novel target for development of anti-rheumatic agents. ..
- Regulation of p38 and inflammation by MAPK kinasesGARY STEVEN FIRESTEIN; Fiscal Year: 2010..These studies will provide detailed information on the mechanism of p38 activation in inflammatory arthritis and test the hypothesis that selective targeting of MKKs like MKKS will be beneficial in RA. ..