Homing chemokines in rheumatoid arthritis

[1]  Darrell R. Abernethy,et al.  International Union of Pharmacology: Approaches to the Nomenclature of Voltage-Gated Ion Channels , 2003, Pharmacological Reviews.

[2]  P. Loetscher,et al.  Cutting Edge: Induction of Follicular Homing Precedes Effector Th Cell Development1 , 2001, The Journal of Immunology.

[3]  S. Kunkel,et al.  Chemokines in autoimmune disease. , 2001, Current opinion in immunology.

[4]  M. Salmon,et al.  Ectopic expression of the B cell-attracting chemokine BCA-1 (CXCL13) on endothelial cells and within lymphoid follicles contributes to the establishment of germinal center-like structures in Sjögren's syndrome. , 2001, Arthritis and rheumatism.

[5]  P. Hjelmström Lymphoid neogenesis: de novo formation of lymphoid tissue in chronic inflammation through expression of homing chemokines , 2001, Journal of leukocyte biology.

[6]  E. Kunkel,et al.  Bonzo/CXCR6 expression defines type 1-polarized T-cell subsets with extralymphoid tissue homing potential. , 2001, The Journal of clinical investigation.

[7]  Bernhard Moser,et al.  Lymphocyte traffic control by chemokines , 2001, Nature Immunology.

[8]  A. Koch,et al.  Update on synovitis , 2001, Current rheumatology reports.

[9]  A. Tzioufas,et al.  "Lymphoid" chemokine messenger RNA expression by epithelial cells in the chronic inflammatory lesion of the salivary glands of Sjögren's syndrome patients: possible participation in lymphoid structure formation. , 2001, Arthritis and rheumatism.

[10]  M. Thelen,et al.  Dancing to the tune of chemokines , 2001, Nature Immunology.

[11]  C. Mackay,et al.  Chemokines: immunology's high impact factors , 2001, Nature Immunology.

[12]  P. Lipsky,et al.  Lymphoid Chemokine B Cell-Attracting Chemokine-1 (CXCL13) Is Expressed in Germinal Center of Ectopic Lymphoid Follicles Within the Synovium of Chronic Arthritis Patients1 , 2001, The Journal of Immunology.

[13]  P. Loetscher,et al.  Cxc Chemokine Receptor 5 Expression Defines Follicular Homing T Cells with B Cell Helper Function , 2000, The Journal of experimental medicine.

[14]  E. Kremmer,et al.  Follicular B Helper T Cells Express Cxc Chemokine Receptor 5, Localize to B Cell Follicles, and Support Immunoglobulin Production , 2000, The Journal of experimental medicine.

[15]  J. Lord,et al.  Persistent Induction of the Chemokine Receptor CXCR4 by TGF-β1 on Synovial T Cells Contributes to Their Accumulation Within the Rheumatoid Synovium1 , 2000, The Journal of Immunology.

[16]  C. Weyand,et al.  Cell-cell interactions in synovitis: Interactions between T cells and B cells in rheumatoid arthritis , 2000, Arthritis Research & Therapy.

[17]  Jason G. Cyster,et al.  A chemokine-driven positive feedback loop organizes lymphoid follicles , 2000, Nature.

[18]  D. Hanahan,et al.  BLC expression in pancreatic islets causes B cell recruitment and lymphotoxin-dependent lymphoid neogenesis. , 2000, Immunity.

[19]  M. Dorf,et al.  Cutting Edge: Ectopic Expression of the Chemokine TCA4/SLC Is Sufficient to Trigger Lymphoid Neogenesis1 , 2000, The Journal of Immunology.

[20]  K. Matsushima,et al.  International union of pharmacology. XXII. Nomenclature for chemokine receptors. , 2000, Pharmacological reviews.

[21]  A. Zlotnik,et al.  Chemokines: a new classification system and their role in immunity. , 2000, Immunity.

[22]  J. Cyster,et al.  Chemokines and cell migration in secondary lymphoid organs. , 1999, Science.

[23]  L. Mazzucchelli,et al.  BCA-1 is highly expressed in Helicobacter pylori-induced mucosa-associated lymphoid tissue and gastric lymphoma. , 1999, The Journal of clinical investigation.

[24]  K. Uhlig,et al.  Predominance of mononuclear cells expressing the chemokine receptor CCR5 in synovial effusions of patients with different forms of arthritis. , 1999, Arthritis and rheumatism.

[25]  K. Okumura,et al.  Selective accumulation of CCR5+ T lymphocytes into inflamed joints of rheumatoid arthritis. , 1999, International immunology.

[26]  U. Wagner,et al.  The role of CD8+ CD40L+ T cells in the formation of germinal centers in rheumatoid synovitis. , 1998, Journal of immunology.

[27]  Jason G. Cyster,et al.  A B-cell-homing chemokine made in lymphoid follicles activates Burkitt's lymphoma receptor-1 , 1998, Nature.

[28]  M. Baggiolini,et al.  B Cell–attracting Chemokine 1, a Human CXC Chemokine Expressed in Lymphoid Tissues, Selectively Attracts B Lymphocytes via BLR1/CXCR5 , 1998, The Journal of experimental medicine.

[29]  C. Mackay,et al.  The chemokine receptors CXCR3 and CCR5 mark subsets of T cells associated with certain inflammatory reactions. , 1998, The Journal of clinical investigation.

[30]  M. Baggiolini,et al.  CCR5 is characteristic of Th1 lymphocytes , 1998, Nature.

[31]  E. Wolf,et al.  A Putative Chemokine Receptor, BLR1, Directs B Cell Migration to Defined Lymphoid Organs and Specific Anatomic Compartments of the Spleen , 1996, Cell.

[32]  R. Strieter,et al.  The role of chemokines in inflammatory joint disease , 1996, Journal of leukocyte biology.

[33]  E. Kremmer,et al.  Expression of the G-protein--coupled receptor BLR1 defines mature, recirculating B cells and a subset of T-helper memory cells. , 1994, Blood.

[34]  T. Dobner,et al.  Differentiation‐specific expression of a novel G protein‐coupled receptor from Burkitt's lymphoma , 1992, European journal of immunology.

[35]  F. Epstein,et al.  Rheumatoid arthritis. Pathophysiology and implications for therapy. , 1990, The New England journal of medicine.

[36]  S. Takemura Lymphoid neogenesis in rheumatoid synovitis , 2003 .

[37]  D. Patel,et al.  CXCR3 and CCR5 ligands in rheumatoid arthritis synovium. , 2001, Clinical immunology.

[38]  M. Baggiolini,et al.  Chemokines and their receptors in lymphocyte traffic and HIV infection. , 2000, Advances in immunology.

[39]  J. Cyster,et al.  Chemokines and B-cell homing to follicles. , 1999, Current topics in microbiology and immunology.

[40]  T. C. Adamson,et al.  Immunohistologic characterization of synovial membrane lymphocytes in rheumatoid arthritis. , 1984, Arthritis and rheumatism.