Professor, Medicine, UCSF School of Medicine
Rheumatology
Dr. William E. Seaman, MD
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William E. Seaman works in the field of Rheumatology. He researched medicine at Harvard Medical School. Harvard Medical School is a one of the best medicals schools. Harvard Medical School is ranked 1/12 in Research/PrimaryCare. He received 1 awards: "Elected Member". William Seaman is also a published MD. He has 92 paper published. The most recent paper is: Mouse Ly-49D recognizes H-2Dd and activates natural killer cell cytotoxicity.
Publications
- Traumatic brain injury induces macrophage subsets in the brain.
- Synergistic Ca2+ responses by G{alpha}i- and G{alpha}q-coupled G-protein-coupled receptors require a single PLC{beta} isoform that is sensitive to both G{beta}{gamma} ...
- Iron Uptake Mediated by Binding of H-Ferritin to the TIM-2 Receptor in Mouse Cells.
- Clostridium difficile toxin B differentially affects GPCR-stimulated Ca2+ responses in macrophages: independent roles for Rho and PLA2.
- Binding and uptake of H-ferritin are mediated by human transferrin receptor-1.
- TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria.
- Signaling and cross-talk by C5a and UDP in macrophages selectively use PLCbeta3 to regulate intracellular free calcium.
- The innate immune response to Salmonella enterica serovar Typhimurium by macrophages is dependent on TREM2-DAP12.
- Cutting edge: inhibition of TLR and FcR responses in macrophages by triggering receptor expressed on myeloid cells (TREM)-2 and DAP12.
- TREM2, a DAP12-associated receptor, regulates osteoclast differentiation and function.
- Clinical academic rheumatology: comment on the article by Wickersham et al.
- TIM-2 is expressed on B cells and in liver and kidney and is a receptor for H-ferritin endocytosis.
- Expression and activation of signal regulatory protein alpha on astrocytomas.
- CMRF-35-like molecule-1, a novel mouse myeloid receptor, can inhibit osteoclast formation.
- Pattern recognition by TREM-2: binding of anionic ligands.
- Letter: Effect of salicylates on creatinine clearance.
- A single lentiviral vector platform for microRNA-based conditional RNA interference and coordinated transgene expression.
- Cocaine increases natural killer cell activity.
- Natural killing activity in Sjögren's syndrome. An analysis of defective mechanisms.
- Analysis of the major patterns of B cell gene expression changes in response to short-term stimulation with 33 single ligands.
- Ligand interactions by activating and inhibitory Ly-49 receptors.
- Cloning and characterization of a novel mouse myeloid DAP12-associated receptor family.
- Activating Ly-49D and inhibitory Ly-49A natural killer cell receptors demonstrate distinct requirements for interaction with H2-D(d).
- Natural killer cells and natural killer T cells.
- Natural killing of xenogeneic cells mediated by the mouse Ly-49D receptor.
- Mouse Ly-49D recognizes H-2Dd and activates natural killer cell cytotoxicity.
- DAP12-mediated signal transduction in natural killer cells. A dominant role for the Syk protein-tyrosine kinase.
- The alpha2 domain of H-2Dd restricts the allelic specificity of the murine NK cell inhibitory receptor Ly-49A.
- Natural killer cells and recognition of MHC class I molecules: new perspectives and challenges in immunology.
- Divergent functions of lectin-like receptors on NK cells.
- Mouse Ly-49A interrupts early signaling events in natural killer cell cytotoxicity and functionally associates with the SHP-1 tyrosine phosphatase.
- Recognition and signaling by mouse Ly-49 receptors.
- An autosomal dominant locus, Nka, mapping to the Ly-49 region of a rat natural killer (NK) gene complex, controls NK cell lysis of allogeneic lymphocytes.
- The Ly-49 and NKR-P1 gene families encoding lectin-like receptors on natural killer cells: the NK gene complex.
- A natural killer cell receptor specific for a major histocompatibility complex class I molecule.
- Ly-49A, a receptor for H-2Dd, has a functional carbohydrate recognition domain.
- NKR-P1A is a target-specific receptor that activates natural killer cell cytotoxicity.
- A family of murine NK cell receptors specific for target cell MHC class I molecules.
- Natural killing by spleen cells from W/Wv and Sl/Sld anemic mice.
- Suppression of natural killing in vitro by monocytes and polymorphonuclear leukocytes: requirement for reactive metabolites of oxygen.
- Effect of 89Sr on immunity and autoimmunity in NZB/NZW F1 mice.
- Thymic influences on autoimmunity in MRL-lpr mice.
- Natural killing of tumor cells by human peripheral blood cells. Suppression of killing in vitro by tumor-promoting phorbol diesters.
- Surface antigens on mouse natural killer cells: use of monoclonal antibodies to inhibit or to enrich cytotoxic activity.
- The Lyt-2, Lyt-3 macromolecules: structural and functional studies.
- Human and murine natural killer cell activity may require lipoxygenation of arachidonic acid.
- Human natural killer cell activity is reversibly inhibited by antagonists of lipoxygenation.
- Monocytosis in the BXSB model for Systemic lupus erythematosus.
- Treatment of autoimmune MRL/Ipr mice with monoclonal antibody to Thy-1.2: a single injection has sustained effects on lymphoproliferation and renal Disease.
- Suppression or enhancement of natural killing does not alter tolerance to bovine gamma globulin.
- Lyt-2 and lyt-3 antigens are on two different polypeptide subunits linked by disulfide bonds. Relationship of subunits to T cell cytolytic activity.
- The proliferating cells in autoimmune MRL/lpr mice lack L3T4, an antigen on "helper" T cells that is involved in the response to class II major histocompatibility anti...
- Avascular necrosis of the talus, scaphoid, and metatarsal head in Systemic lupus erythematosus.
- Proceedings: Aspirin-induced hepatotoxicity in patients with RA or Systemic lupus erythematosus (SLE).
- Letter: Aspirin and hepatotoxicity: addendum.
- Aspirin-induced hepatotoxicity in patients with Systemic lupus erythematosus.
- Successful treatment of autoimmunity in NZB/NZW F1 mice with monoclonal antibody to L3T4.
- Harvesting of leukocytes from intestinal lumen in murine giardiasis and preliminary characterization of these cells.
- Treatment of murine lupus with monoclonal anti-T cell antibody.
- Human synovial dendritic cells. Direct observation of transition to fibroblasts.
- Depletion of natural killer cells in mice by monoclonal antibody to NK-1.1. Reduction in host defense against malignancy without loss of cellular or humoral immunity.
- Inositol trisphosphate is generated by a rat natural killer cell tumor in response to target cells or to crosslinked monoclonal antibody OX-34: possible signaling role...
- Randomized, double-blind, placebo-controlled study of the treatment of the painful shoulder.
- Selective manipulation of the immune response in vivo by monoclonal antibodies.
- Inhibition of humoral immunity in vivo by monoclonal antibody to L3T4: studies with soluble antigens in intact mice.
- Reversal of advanced murine lupus in NZB/NZW F1 mice by treatment with monoclonal antibody to L3T4.
- Analysis of the function of L3T4+ T cells by in vivo treatment with monoclonal antibody to L3T4.
- Induction of immune tolerance by administration of monoclonal antibody to L3T4.
- Regulation of autoimmunity and donor cell engraftment by recipient Lyt-2+ cells during the graft-versus-host reaction.
- Rejection of skin grafts and generation of cytotoxic T cells by mice depleted of L3T4+ cells.
- Receptor-specific mechanisms for the responses of human leukocytes to leukotrienes.
- Identification and characterization of a cell-surface molecule that is selectively induced on rat lymphokine-activated killer cells.
- Induction of immune tolerance during administration of monoclonal antibody to L3T4 does not depend on depletion of L3T4+ cells.
- Divergent regulation of phospholipase C-alpha and phospholipase C-gamma transcripts during activation of a human T cell line.
- NKR-P1, an activating molecule on rat natural killer cells, stimulates phosphoinositide turnover and a rise in intracellular calcium.
- Molecular cloning of gp42, a cell-surface molecule that is selectively induced on rat natural killer cells by interleukin 2: glycolipid membrane anchoring and capacity...
- cDNA cloning of mouse NKR-P1 and genetic linkage with LY-49. Identification of a natural killer cell gene complex on mouse chromosome 6.
- Characterization of signal-transducing molecules on natural killer cells.
- Molecular cloning of the NK1.1 antigen, a member of the NKR-P1 family of natural killer cell activation molecules.
- The OX-44 molecule couples to signaling pathways and is associated with CD2 on rat T lymphocytes and a natural killer cell line.
- Effect of aspirin on liver tests in patients with RA or SLE and in normal volunteers.
- Systemic lupus erythematosus. Contrasts and comparisons.
- beta-Estradiol reduces natural killer cells in mice.
- Effect of estrogen on natural killer cells.
- Natural killer cells, bone, and the bone marrow: studies in estrogen-treated mice and in congenitally osteopetrotic (mi/mi) mice.
- Natural killing in estrogen-treated mice responds poorly to poly I.C despite normal stimulation of circulating interferon.
- Hepatic injury due to acetaminophen or salicylates.
- Overview of the Alliance for Cellular Signaling.
- Characterization of TREM-3, an activating receptor on mouse macrophages: definition of a family of single Ig domain receptors on mouse chromosome 17.
- Tim-2 is the receptor for H-ferritin on oligodendrocytes.
- A role for TREM2 ligands in the phagocytosis of apoptotic neuronal cells by microglia.
Schools
Harvard Medical School
Massachusetts General Hospital
National Institute Arth Nih
Conditions Treated
- Arthritis
- Bursitis
- Enthesopathy of Hip (incl. Trochanteric Bursitis)
- Fibromyalgia
- View All
Doctors Specialties
- Rheumatology
Accepted Insurances
- CHAMPVA
- Medicare MCR
- United Healthcare
Awards
- Elected Member
Education
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Massachusetts General Hospital -
Harvard Medical School
Hospital
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San Francisco General Hospital and Trauma Center -
San Francisco VA Medical Center -
UCSF Medical Center
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