Killer immunoglobulin-like receptor and human leukocyte antigen-C genotypes in rheumatoid arthritis primary responders and non-responders to anti-TNF-α therapy

[1]  R. Roesler,et al.  Study of killer immunoglobulin-like receptor genes and human leukocyte antigens class I ligands in a Caucasian Brazilian population with Crohn's disease and ulcerative colitis. , 2010, Human immunology.

[2]  Y. Jiao,et al.  Disparate distribution of activating and inhibitory killer cell immunoglobulin-like receptor genes in patients with systemic lupus erythematosus , 2010, Lupus.

[3]  Pilar Barrera,et al.  Tumour necrosis factor α −308G→A polymorphism is not associated with response to TNFα blockers in Caucasian patients with rheumatoid arthritis: systematic review and meta-analysis , 2009, Annals of the rheumatic diseases.

[4]  K. Taylor,et al.  Susceptibility to Crohn’s disease is mediated by KIR2DL2/KIR2DL3 heterozygosity and the HLA-C ligand , 2009, Immunogenetics.

[5]  R. Tibshirani,et al.  Blood autoantibody and cytokine profiles predict response to anti-tumor necrosis factor therapy in rheumatoid arthritis , 2009, Arthritis research & therapy.

[6]  F. Houssiau,et al.  Gene expression profiling in the synovium identifies a predictive signature of absence of response to adalimumab therapy in rheumatoid arthritis , 2009, Arthritis research & therapy.

[7]  K. Eguchi,et al.  A significantly impaired natural killer cell activity due to a low activity on a per-cell basis in rheumatoid arthritis , 2009, Modern rheumatology.

[8]  Zhangsuo Liu,et al.  [Relationship between expression of inhibitory killer cell immunoglobulin-like receptor HLA-Cw ligand and susceptibility to inflammatory bowel disease]. , 2008, Zhonghua yi xue za zhi.

[9]  C. Wijbrandts,et al.  Responsiveness to anti-tumour necrosis factor α therapy is related to pre-treatment tissue inflammation levels in rheumatoid arthritis patients , 2007, Annals of the rheumatic diseases.

[10]  A. Pawlik,et al.  Associations of killer cell immunoglobulin-like receptor genes with complications of rheumatoid arthritis , 2007, Genes and Immunity.

[11]  D. Gladman,et al.  KIRs and autoimmune disease: studies in systemic lupus erythematosus and scleroderma. , 2007, Tissue Antigens.

[12]  B. Vuylsteke,et al.  Cutting Edge: Resistance to HIV-1 Infection among African Female Sex Workers Is Associated with Inhibitory KIR in the Absence of Their HLA Ligands1 , 2006, The Journal of Immunology.

[13]  T. Ahmad,et al.  Killer Ig-like receptor (KIR) genotype and HLA ligand combinations in ulcerative colitis susceptibility , 2006, Genes and Immunity.

[14]  J. Trowsdale,et al.  HLA-C and killer cell immunoglobulin-like receptor genes in idiopathic bronchiectasis. , 2006, American journal of respiratory and critical care medicine.

[15]  M. Carrington,et al.  The impact of variation at the KIR gene cluster on human disease. , 2006, Current topics in microbiology and immunology.

[16]  G. Panayi,et al.  Natural killer cell activity in inflammatory joint disease , 1983, Clinical Rheumatology.

[17]  Derek Middleton,et al.  KIR genes. , 2005, Transplant immunology.

[18]  M. Carrington,et al.  Cutting Edge: Heterozygote Advantage in Autoimmune Disease: Hierarchy of Protection/Susceptibility Conferred by HLA and Killer Ig-Like Receptor Combinations in Psoriatic Arthritis1 , 2004, The Journal of Immunology.

[19]  F. Nagy,et al.  Investigation of the Prognostic Value of TNF-α Gene Polymorphism among Patients Treated with Infliximab, and the Effects of Infliximab Therapy on TNF-α Production and Apoptosis , 2004, Pathobiology.

[20]  H. Tiwari,et al.  The influence of genetic variation in the HLA-DRB1 and LTA-TNF regions on the response to treatment of early rheumatoid arthritis with methotrexate or etanercept. , 2004, Arthritis and rheumatism.

[21]  Salim I. Khakoo,et al.  HLA and NK Cell Inhibitory Receptor Genes in Resolving Hepatitis C Virus Infection , 2004, Science.

[22]  T. Krieg,et al.  Association of killer cell immunoglobulin-like receptors with scleroderma. , 2004, Arthritis and rheumatism.

[23]  E. G. de la Concha,et al.  Association of the major histocompatibility complex with response to infliximab therapy in rheumatoid arthritis patients. , 2004, Arthritis and rheumatism.

[24]  N. Balandraud,et al.  Polymorphism at the position -308 of TNF-α gene influences outcome of infliximab therapy in rheumatoid arthritis , 2004, Arthritis Research & Therapy.

[25]  F. Nagy,et al.  Investigation of the prognostic value of TNF-alpha gene polymorphism among patients treated with infliximab, and the effects of infliximab therapy on TNF-alpha production and apoptosis. , 2004, Pathobiology : journal of immunopathology, molecular and cellular biology.

[26]  B. Koeleman,et al.  KIR in type 1 diabetes: disparate distribution of activating and inhibitory natural killer cell receptors in patients versus HLA-matched control subjects. , 2003, Diabetes.

[27]  Nathalie Balandraud,et al.  Polymorphism at position -308 of the tumor necrosis factor alpha gene influences outcome of infliximab therapy in rheumatoid arthritis. , 2003, Arthritis and rheumatism.

[28]  Patrik Edén,et al.  Classification of Expression Patterns Using Artificial Neural Networks , 2003 .

[29]  Keith Hoots,et al.  Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS , 2002, Nature Genetics.

[30]  D. Middleton,et al.  Molecular diversity of the HLA-C gene identified in a caucasian population. , 2002, Human immunology.

[31]  Daniel J. Schaid,et al.  Major Histocompatibility Complex Class I–Recognizing Receptors Are Disease Risk Genes in Rheumatoid Arthritis , 2001, The Journal of experimental medicine.

[32]  J. Yen,et al.  Killer Cell Activating Receptors Function as Costimulatory Molecules on CD4+CD28null T Cells Clonally Expanded in Rheumatoid Arthritis1 , 2000, The Journal of Immunology.

[33]  J. Strominger,et al.  Differential binding to HLA-C of p50-activating and p58-inhibitory natural killer cell receptors. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[34]  Eric O Long,et al.  Direct binding and functional transfer of NK cell inhibitory receptors reveal novel patterns of HLA-C allotype recognition. , 1998, Journal of immunology.

[35]  D. Schaid,et al.  Expansion of unusual CD4+ T cells in severe rheumatoid arthritis. , 1997, Arthritis and rheumatism.

[36]  K. Tokunaga,et al.  Chromosomal localization of the human natural killer cell class I receptor family genes to 19q13.4 by fluorescence in situ hybridization. , 1996, Genomics.

[37]  S. Y. Yang,et al.  Locus-specific amplification of HLA class I genes from genomic DNA: locus-specific sequences in the first and third introns of HLA-A, -B, and -C alleles. , 1995, Tissue antigens.

[38]  M. Prevoo,et al.  Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. , 1995, Arthritis and rheumatism.

[39]  K. Takeda,et al.  The development of autoimmunity in C57BL/6 lpr mice correlates with the disappearance of natural killer type 1-positive cells: evidence for their suppressive action on bone marrow stem cell proliferation, B cell immunoglobulin secretion, and autoimmune symptoms , 1993, The Journal of experimental medicine.

[40]  F. Arnett.  Revised criteria for the classification of rheumatoid arthritis. , 1990, Orthopedic nursing.

[41]  M. Liang,et al.  The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. , 1988, Arthritis and rheumatism.

[42]  Shirley A. Miller,et al.  A simple salting out procedure for extracting DNA from human nucleated cells. , 1988, Nucleic acids research.

[43]  B. Combe,et al.  Modulation of Natural Killer Cell Activity in the Rheumatoid Joint and Peripheral Blood , 1984, Scandinavian journal of immunology.

[44]  J. Lyford.  The British Society for Rheumatology. , 1983, Annals of the rheumatic diseases.

[45]  A. Grayzel,et al.  Endogenous and interferon-augmented natural killer cell activity of human peripheral blood mononuclear cells in vitro. Studies of patients with multiple sclerosis, systemic lupus erythematosus or rheumatoid arthritis. , 1982, Clinical and experimental immunology.

[46]  J. Karsh,et al.  Natural cytotoxicity in rheumatoid arthritis and systemic lupus erythematosus. , 1981, Clinical immunology and immunopathology.