Physician
Pathology
Dr. Gordon C. Sharp, MD
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Gordon Sharp is an expert in the field of Pathology. He graduated from Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is one of the top medical schools in the US. Johns Hopkins University School of Medicine is ranked 3/29 in Research/PrimaryCare. He over the years received 1 awards: "Elected Member". Gordon C. Sharp has written publications. He has 87 publications published with PubMed. The lastest paper is: 'B7.2 has opposing roles during the activation versus effector stages of experimental autoimmune thyroiditis.'
Publications
- Randomized prospective study of a work place ergonomic intervention for individuals with rheumatoid arthritis and osteoarthritis.
- Antibodies to nuclear antigens in patients undergoing long-term hemodialysis.
- Human autoantibody secreted by immortalized lymphocyte cell line against the 68K polypeptide of the U1 small nuclear ribonucleoprotein.
- Analysis of anti-U1 RNA antibodies in patients with connective tissue disease. Association with HLA and clinical manifestations of disease.
- Immunogenetic studies of juvenile dermatomyositis. III. Study of antibody to organ-specific and nuclear antigens.
- Molecular genetic analysis of HLA-DR and HLA-DQ genes among anti-U1-70-kd autoantibody positive connective tissue disease patients.
- U1-70-kd autoantibody-positive mixed connective tissue disease in children. A longitudinal clinical and serologic analysis.
- Value and limitations of calcium channel blockade in the treatment of pulmonary hypertension associated with CREST--case reports.
- Increased frequency of mutations in the hprt gene of T cells isolated from patients with anti-U1-70kD-autoantibody-positive connective tissue disease.
- Autoantibodies: friend or foe?
- Enzyme-linked immunosorbent assay using isolated (U) small nuclear ribonucleoprotein polypeptides as antigens to investigate the clinical significance of autoantibodie...
- Multiple antigen recognition by individual human monoclonal antibodies of rheumatic disease patient origin.
- Is anti-U1-RNP autoantibody positive connective tissue disease genetically distinct?
- Clinical relevance of PM-1 antibody and physiochemical characterization of PM-1 antigen.
- MCTD: a concept which stood the test of time.
- Human autoantibodies against the 70-kd polypeptide of U1 small nuclear RNP are associated with HLA-DR4 among connective tissue disease patients.
- Solid-phase direct DNA sequencing of allele-specific polymerase chain reaction-amplified HLA-DR genes.
- Effects of prolactin in stimulating disease activity in systemic lupus erythematosus.
- Association of immunoglobulin Km and Gm allotypes with specific antinuclear antibodies and disease susceptibility among connective tissue disease patients.
- Effectiveness of an inpatient-based rheumatology elective.
- Genetic control of the immune response of mice to type III pneumococcal polysaccharide.
- Association of systemic lupus erythematosus and gluten enteropathy.
- Long-term anti-CD4 treatment of MRL/lpr mice ameliorates immunopathology and lymphoproliferation but fails to suppress rheumatoid factor production.
- Human RNA helicase A is a lupus autoantigen that is cleaved during apoptosis.
- Prolactin levels and antinuclear antibody profiles in women tested for connective tissue disease.
- Diverse antibody recognition patterns of the multiple Sm-D antigen polypeptides.
- Production of augmented experimental autoimmune thyroiditis lesions by combined transfer of antiserum and lymph node cells.
- Analysis of autoantibodies against RNA polymerases using immunoaffinity-purifed RNA polymerase I, II, and III antigen in an enzyme-linked immunosorbent assay.
- Antigenic domains on the U1 small nuclear ribonucleoprotein-associated 70K polypeptide: a comparison of regions selectively recognized by human and mouse autoantibodie...
- Human T cell clones reactive against U-small nuclear ribonucleoprotein autoantigens from connective tissue disease patients and healthy individuals.
- Conversion of type III pneumococcal polysaccharide low responders to high responders by immunization with a thymus-dependent form of antigen.
- Effect in neonatal thymectomy on experimental autoimmune thyroiditis in guinea pigs.
- Antiphospholipid antibodies among anti-U1-70 kDa autoantibody positive patients with mixed connective tissue disease.
- Protection against autoimmune thyroiditis in guinea pigs by thyroglobulin antiserum.
- The biological effects of anti-thyroid antibodies. Thyroid eosinophilia following passive transfer of anti-thyroglobulin antibody.
- Suppression of experimental autoimmune thyroiditis in guinea pigs by pretreatment with thyroglobulin-coupled spleen cells.
- Suppression of experimental autoimmune thyroiditis in the guinea pig by pretreatment with thyroglobulin in incomplete Freund''s adjuvant.
- Effect of guinea pig thyroglobulin in incomplete Freund's adjuvant on experimental autoimmune thyroiditis induced by in vitro-activated lymph node cells.
- Adoptive transfer of experimental autoimmune thyroiditis (EAT) in guinea pigs: requirement for Ia-positive antigen-presenting cells for in vitro activation of effector...
- Induction of experimental autoimmune thyroiditis in mice with in vitro activated splenic T cells.
- Effects of the adjuvants SGP and Quil A on the induction of experimental autoimmune thyroiditis in mice.
- The role of cellular proliferation in the induction of experimental autoimmune thyroiditis (EAT) in mice.
- Differential susceptibility of strain 2 and strain 13 guinea pigs to induction of experimental autoimmune thyroiditis.
- Adoptive transfer of experimental autoimmune thyroiditis (EAT) with in vitro activated lymph node cells from thyroglobulin-sensitized guinea pigs: characterization of ...
- Induction of severe granulomatous experimental autoimmune thyroiditis in mice by effector cells activated in the presence of anti-interleukin 2 receptor antibody.
- The cellular basis for the Ia restriction in murine experimental autoimmune thyroiditis.
- Augmentation of transfer of experimental autoimmune thyroiditis (EAT) in mice by irradiation of recipients.
- A thyroxine-containing thyroglobulin peptide induces both lymphocytic and granulomatous forms of experimental autoimmune thyroiditis.
- Effects of anti-I-A and anti-I-E monoclonal antibodies on the induction and expression of experimental autoimmune thyroiditis in mice.
- Regulation of the induction and resolution of granulomatous experimental autoimmune thyroiditis in mice by CD8+ T cells.
- Intrathyroidal cell phenotype in murine lymphocytic and granulomatous experimental autoimmune thyroiditis.
- Transforming growth factor-beta has contrasting effects in the presence or absence of exogenous interleukin-12 on the in vitro activation of cells that transfer experi...
- Prevention and reversal of experimental autoimmune thyroiditis (EAT) in mice by administration of anti-L3T4 monoclonal antibody at different stages of disease developm...
- The kinetics of cytokine gene expression in the thyroids of mice developing granulomatous experimental autoimmune thyroiditis.
- A critical role for TRAIL in resolution of granulomatous experimental autoimmune thyroiditis.
- Adoptive transfer murine model of granulomatous experimental autoimmune thyroiditis.
- Apoptosis of thyrocytes and effector cells during induction and resolution of granulomatous experimental autoimmune thyroiditis.
- Spontaneous autoimmune thyroiditis in NOD.H-2h4 mice.
- Induction of granulomatous experimental autoimmune thyroiditis in mice with in vitro activated effector T cells and anti-IFN-gamma antibody.
- IFN-gamma-deficient mice develop severe granulomatous experimental autoimmune thyroiditis with eosinophil infiltration in thyroids.
- Interleukin-12 promotes activation of effector cells that induce a severe destructive granulomatous form of murine experimental autoimmune thyroiditis.
- Induction of granulomatous experimental autoimmune thyroiditis in IL-4 gene-disrupted mice.
- Differential requirement for autoantibody-producing B cells for induction of lymphocytic versus granulomatous experimental autoimmune thyroiditis.
- B7.2 has opposing roles during the activation versus effector stages of experimental autoimmune thyroiditis.
- Expression and regulation of Fas and Fas ligand on thyrocytes and infiltrating cells during induction and resolution of granulomatous experimental autoimmune thyroiditis.
- Induction of experimental autoimmune thyroiditis in IL-12-/- mice.
- Characterization of thyroid fibrosis in a murine model of granulomatous experimental autoimmune thyroiditis.
- Wegener''s granulomatosis: survey of 701 patients in North America. Changes in outcome in the 1990s.
- Effect of transgenic overexpression of FLIP on lymphocytes on development and resolution of experimental autoimmune thyroiditis.
- CD8+ T cells induce thyroid epithelial cell hyperplasia and fibrosis.
- Transgenic expression of TGF-beta on thyrocytes inhibits development of spontaneous autoimmune thyroiditis and increases regulatory T cells in thyroids of NOD.H-2h4 mice.
- Eosinophils infiltrate thyroids, but have no apparent role in induction or resolution of experimental autoimmune thyroiditis in interferon-gamma(-/-) mice.
- TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice.
- Interleukin-10 promotes resolution of granulomatous experimental autoimmune thyroiditis.
- Expression of transgenic FLIP on thyroid epithelial cells inhibits induction and promotes resolution of granulomatous experimental autoimmune thyroiditis in CBA/J mice.
- Murine FLIP transgene expressed on thyroid epithelial cells promotes resolution of granulomatous experimental autoimmune thyroiditis in DBA/1 mice.
- Decreasing TNF-alpha results in less fibrosis and earlier resolution of granulomatous experimental autoimmune thyroiditis.
- Thyrocytes responding to IFN-gamma are essential for development of lymphocytic spontaneous autoimmune thyroiditis and inhibition of thyrocyte hyperplasia.
- Thyroid epithelial cell hyperplasia in IFN-gamma deficient NOD.H-2h4 mice.
- Chemokine expression during development of fibrosis versus resolution in a murine model of granulomatous experimental autoimmune thyroiditis.
- Fas ligand is required for resolution of granulomatous experimental autoimmune thyroiditis.
- Balance of proliferation and cell death between thyrocytes and myofibroblasts regulates thyroid fibrosis in granulomatous experimental autoimmune thyroiditis (G-EAT).
- Mechanisms of spontaneous resolution versus fibrosis in granulomatous experimental autoimmune thyroiditis.
- FLIP and FasL expression by inflammatory cells vs thyrocytes can be predictive of chronic inflammation or resolution of autoimmune thyroiditis.
- Inhibition of TGFbeta1 by anti-TGFbeta1 antibody or lisinopril reduces thyroid fibrosis in granulomatous experimental autoimmune thyroiditis.
- Dual roles for IFN-gamma, but not for IL-4, in spontaneous autoimmune thyroiditis in NOD.H-2h4 mice.
Schools
Johns Hopkins University School of Medicine
Johns Hopkins Hospital
National Canc Institute
Stanford University Hospital
Stanford University School
Doctors Specialties
- Internal Medicine
- Pathology
Accepted Insurances
Awards
- Elected Member
Education
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Stanford University -
Johns Hopkins University -
Johns Hopkins University School of Medicine
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