Immunology, Antigen, Autoantibody, Antibody and Autoimmunity are his primary areas of study. His biological study spans a wide range of topics, including Systemic lupus erythematosus, Graft-versus-host disease and Cell biology. His Antigen research also works with subjects such as
His study in Autoantibody is interdisciplinary in nature, drawing from both Lupus nephritis, Autoimmune disease, Toll-like receptor and CD20. His studies in Antibody integrate themes in fields like Inflammation, Molecular biology, Spleen and B-1 cell. His Autoimmunity study combines topics from a wide range of disciplines, such as Mutation, Germline mutation, Immunoglobulin G, Lupus erythematosus and Proinflammatory cytokine.
Mark J. Shlomchik mostly deals with Immunology, B cell, Antigen, Cell biology and Antibody. He regularly ties together related areas like Systemic lupus erythematosus in his Immunology studies. His B cell research includes themes of Molecular biology and CD40, B-1 cell.
In his research on the topic of Antigen, Chromatin is strongly related with B-cell receptor. His research integrates issues of Cell, Receptor, breakpoint cluster region, Cellular differentiation and Naive B cell in his study of Cell biology. His Autoantibody research is multidisciplinary, incorporating perspectives in Transgene, Rheumatoid factor, Inflammation, Proinflammatory cytokine and Autoimmune disease.
Mark J. Shlomchik mainly investigates Immunology, B cell, Germinal center, Antigen and Cell biology. His work in Immunology is not limited to one particular discipline; it also encompasses Systemic lupus erythematosus. His B cell study incorporates themes from Molecular biology and Bone marrow.
He interconnects Humoral immunity, Phosphorylation, Affinity maturation and Somatic cell in the investigation of issues within Germinal center. His Antigen research incorporates elements of Immune system and Immunological memory. His Cell biology study combines topics in areas such as Receptor, breakpoint cluster region and Naive B cell.
His primary areas of investigation include Germinal center, Cell biology, Phosphorylation, Antigen and breakpoint cluster region. His Germinal center study is related to the wider topic of B cell. His B cell research is multidisciplinary, relying on both mTORC1, Cell signaling and Somatic cell.
The concepts of his Cell biology study are interwoven with issues in Receptor, Major histocompatibility complex and Memory B cell. His Antigen research includes elements of Myeloid, Immunity, Immunological memory and Heart transplantation. His research in breakpoint cluster region intersects with topics in Protein kinase B, PTEN, Germline mutation and Protein kinase A.
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Chromatin–IgG complexes activate B cells by dual engagement of IgM and Toll-like receptors
Elizabeth A. Leadbetter;Ian R. Rifkin;Andreas M. Hohlbaum;Britte C. Beaudette.
Prevention of graft versus host disease by inactivation of host antigen-presenting cells.
Warren D. Shlomchik;Matthew S. Couzens;Cheng Bi Tang;Jennifer McNiff.
Toll-like receptor 7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus.
Sean R. Christensen;Jonathan Shupe;Kevin Nickerson;Michael Kashgarian.
RNA-associated autoantigens activate B cells by combined B cell antigen receptor/Toll-like receptor 7 engagement
Christina M. Lau;Courtney Broughton;Abigail S. Tabor;Shizuo Akira.
Journal of Experimental Medicine (2005)
A Novel Mouse with B Cells but Lacking Serum Antibody Reveals an Antibody-independent Role for B Cells in Murine Lupus
Owen T.M. Chan;Lynn G. Hannum;Ann M. Haberman;Michael P. Madaio.
Journal of Experimental Medicine (1999)
The role of clonal selection and somatic mutation in autoimmunity.
Mark J. Shlomchik;Ann Marshak-Rothstein;Claudia B. Wolfowicz;Thomas L. Rothstein.
Anti-DNA antibodies from autoimmune mice arise by clonal expansion and somatic mutation.
M Shlomchik;M Mascelli;H Shan;M Z Radic.
Journal of Experimental Medicine (1990)
Activation of Autoreactive B Cells by CpG dsDNA
Gregory A Viglianti;Christina M Lau;Timothy M Hanley;Benjamin A Miko.
From T to B and back again: positive feedback in systemic autoimmune disease.
Mark J. Shlomchik;Joseph E. Craft;Mark J. Mamula.
Nature Reviews Immunology (2001)
Epidermal langerhans cell-deficient mice develop enhanced contact hypersensitivity.
Daniel H. Kaplan;Mathew C. Jenison;Sem Saeland;Warren D. Shlomchik.
Profile was last updated on December 6th, 2021.
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