Article information
Rheumatoid arthritis (RA) is a chronic, disabling disease that affects individuals during the productive years of their lives. Modern treatment for RA includes the so-called “biologic” therapy, which is based on recombinant proteins that modify the biologic processes. These agents have potent therapeutic effects and different mechanisms of action. Nevertheless, therapeutic failure still prevails. Treatment that prevents disability in RA must be started in an early manner, before the development of complications and, ideally, with a minimum possibility of therapeutic failure. As yet, there are no clinical or laboratory criteria to identify those patients with a higher probability of responding to particular types of therapy, delaying control of RA ad affecting the prevention of incapacity.
Research into gene diversity through single-nucleotide polymorphisms (SNPs) by means of microarray systems, allows the detailed analysis of gene factors associated to a given disease. SNPs have been recently applied to the study of RA, where the major polymorphisms associated to RA occur primarily in genes that code for proteins related to the initiation of an immune response and/or the control of cellular activity in the immune system, in addition to genes related to tissue repair.
The specific meaning of these findings is in its initial stages of research. On the other hand, proteomics relate to the analysis of protein expression profiles at multiple levels. Both types of studies will contribute to the knowledge of patterns of gene expression in RA compared to the general population, and will allow an understanding of the pathogenesis of RA. Moreover, proteomic and genomic profiles can be employed to designs probes that identify individuals with the risk of developing RA, individually predict the response to different therapeutic modalities (pharmacogenomics) and for the follow-up of the biologic response to therapy.
Key words:
Rheumatoid arthritis
Pathogenesis
Genomics
Proteomics
Treatment
La artritis reumatoide (AR) es una enfermedad crónica e incapacitante que afecta a individuos en etapas productivas de la vida. El tratamiento moderno de la AR incluye la denominada terapia “biológica” basada en proteínas recombinantes, modificadoras de procesos biológicos, con efectos terapéuticos potentes y diferentes mecanismos de acción, pese a lo cual persisten fracasos terapéuticos.
Un tratamiento que prevenga la discapacidad en AR debe instituirse en forma temprana, antes del desarrollo de secuelas, e idealmente con mínima posibilidad de fracaso terapéutico. No existen criterios clínicos o de laboratorio que identifiquen a pacientes con mayor probabilidad de respuesta a distintas formas de terapia, lo que retarda el control de la AR y afecta a la prevención de discapacidad.
El estudio de la diversidad genética, por medio de polimorfismos de una sola base (SNP) con sistemas de microarreglos (MA), permite el análisis detallado de los factores genéticos asociados a una enfermedad, lo cual empieza a utilizarse en AR. Los polimorfismos con mayor asociación con AR ocurren primordialmente en genes que codifican proteínas relacionadas con el inicio de la respuesta inmunitaria y/o con el control de la actividad celular, además de genes relacionados con la reparación tisular. El significado específico de esto apenas empieza a estudiarse. Por otro lado, la proteómica estudia los perfiles de expresión proteínica en cualquier individuo a múltiples niveles.
Ambos tipos de estudios ayudarían a conocer los patrones de expresión génica en AR comparados con la población general. Además de ayudar a conocer la patogenia de la AR, los perfiles proteómicos y genómicos pueden utilizarse para diseñar sondas que identifiquen a individuos con riesgo de desarrollar AR, predigan en forma individualizada la respuesta a distintos esquemas terapéuticos y que permitan seguir la respuesta biológica a la terapia.
Palabras clave:
Artritis reumatoide
Patogenia
Genómica
Proteómica
Tratamiento
Full text is only aviable in PDF
References
[1.]
M.H. Cardiel, J. Rojas-Serrano.
Community based study to estimate prevalence, burden of illness and help seeking behavior in rheumatic diseases in Mexico City. A COPCORD study.
Clin Exp Rheumatol, 20 (2002), pp. 617-624
[2.]
L. Carmona, V. Villaverde, C. Hernandez-Garcia, J. Ballina, R. Gabriel, A. Laffon.
The prevalence of rheumatoid arthritis in the general population of Spain.
Rheumatology (Oxford), 41 (2002), pp. 88-95
[3.]
F. Guillemin, A. Saraux, P. Guggenbuhl, C.H. Roux, P. Fardellone, B.E. Le, et al.
Prevalence of rheumatoid arthritis in France: 2001.
Ann Rheum Dis, 64 (2005), pp. 1427-1430
[4.]
A. Linos, J.W. Worthington, W.M. O’Fallon, L.T. Kurland.
The epidemiology of rheumatoid arthritis in Rochester Minnesota: a study of incidence, prevalence, and mortality.
Am J Epidemiol, 111 (1980), pp. 87-98
[5.]
J.B. O'Sullivan, E.S. Cathcart.
The prevalence of rheumatoid arthritis. Followup evaluation of the effect of criteria on rates in Sudbury, Massachusetts.
Ann Intern Med, 76 (1972), pp. 573-577
[6.]
D. Zauli, S. Zucchini, E. Manfredini, A. Grassi, G. Ballardini, M. Fusconi, et al.
Prevalence of rheumatoid arthritis.
Rheumatology (Oxford), 42 (2003), pp. 696-697
[7.]
L. Carmona, J. Ballina, R. Gabriel, A. Laffon.
The burden of musculoskeletal diseases in the general population of Spain: results from a national survey.
Ann Rheum Dis, 60 (2001), pp. 1040-1045
[8.]
P. Emery, C. Gabay, M. Kraan, J. Gomez-Reino.
Evidence-based review of biologic markers as indicators of disease progression and remission in rheumatoid arthritis.
Rheumatol Int, 27 (2007), pp. 793-806
[9.]
L.W. Moreland.
Disease modifiers: making the right therapeutic choices for our patients.
J Rheumatol Suppl, 79 (2007), pp. 21-26
[10.]
V.S. de, L. Quartuccio.
Treatment of rheumatoid arthritis with rituximab: an update and possible indications.
Autoimmun Rev, 5 (2006), pp. 443-448
[11.]
R.M. Fleischmann, R.L. Stern, I. Iqbal.
Treatment of early rheumatoid arthritis.
Mod Rheumatol, 15 (2005), pp. 153-162
[12.]
S.M. Naguwa.
Tumor necrosis factor inhibitor therapy for rheumatoid arthritis.
Ann N Y Acad Sci, 1051 (2005), pp. 709-715
[13.]
P.E. Lipsky.
Integrating biologic therapy into the comprehensive care of patients with rheumatoid arthritis.
J Rheumatol Suppl, 72 (2005), pp. 54-57
[14.]
B. Bresnihan.
Anakinra as a new therapeutic option in rheumatoid arthritis: clinical results and perspectives.
Clin Exp Rheumatol, 20 (2002), pp. S32-S34
[15.]
J.H. Klippel.
Biologic therapy for rheumatoid arthritis.
N Engl J Med, 343 (2000), pp. 1640-1641
[16.]
R.N. Maini, P.C. Taylor, J. Szechinski, K. Pavelka, J. Broll, G. Balint, et al.
Double-blind randomized controlled clinical trial of the interleukin-6 receptor antagonist, tocilizumab, in European patients with rheumatoid arthritis who had an incomplete response to methotrexate.
Arthritis Rheum, 54 (2006), pp. 2817-2829
[17.]
M. Miyazaki, Y. Fujikawa, C. Takita, H. Tsumura.
Tacrolimus and cyclosporine A inhibit human osteoclast formation via targeting the calcineurindependent NFAT pathway and an activation pathway for c-Jun or MITF in rheumatoid arthritis.
Clin Rheumatol, 26 (2007), pp. 231-239
[18.]
T. Saxne, F.A. Wollheim.
Cyclosporin A in rheumatoid arthritis.
Ann Rheum Dis, 62 (2003), pp. 1121-1122
[19.]
H. Kondo, T. Abe, H. Hashimoto, S. Uchida, S. Irimajiri, M. Hara, et al.
Efficacy and safety of tacrolimus (FK506) in treatment of rheumatoid arthritis: a randomized, double blind, placebo controlled dose-finding study.
J Rheumatol, 31 (2004), pp. 243-251
[20.]
G. Suntharalingam, M.R. Perry, S. Ward, S.J. Brett, A. Castello-Cortes, M.D. Brunner, et al.
Cytokine storm in a phase 1 trial of the anti-CD28 monoclonal antibody TGN1412.
N Engl J Med, 355 (2006), pp. 1018-1028
[21.]
L.W. Moreland.
Biologic therapies on the horizon for rheumatoid arthritis.
J Clin Rheumatol, 10 (2004), pp. S32-S39
[22.]
E.W. St Clair, C.L. Wagner, A.A. Fasanmade, B. Wang, T. Schaible, A. Kavanaugh, et al.
The relationship of serum infliximab concentrations to clinical improvement in rheumatoid arthritis: results from ATTRACT, a multicenter, randomized, double-blind, placebo-controlled trial.
Arthritis Rheum, 46 (2002), pp. 1451-1459
[23.]
T. Cobo-Ibanez, E. Martin-Mola.
Etanercept: long-term clinical experience in rheumatoid arthritis and other arthritis.
Expert Opin Pharmacother, 8 (2007), pp. 1373-1397
[24.]
H.D. van der, L. Klareskog, V. Rodriguez-Valverde, C. Codreanu, H. Bolosiu, J. Melo-Gomes, et al.
Comparison of etanercept and methotrexate, alone and combined, in the treatment of rheumatoid arthritis: two-year clinical and radiographic results from the TEMPO study, a double-blind, randomized trial.
Arthritis Rheum, 54 (2006), pp. 1063-1074
[25.]
L.W. Moreland, M.E. Weinblatt, E.C. Keystone, J.M. Kremer, R.W. Martin, M.H. Schiff, et al.
Etanercept treatment in adults with established rheumatoid arthritis: 7 years of clinical experience.
J Rheumatol, 33 (2006), pp. 854-861
[26.]
A. Schattner.
Review: etanercept (25mg subcutaneously twice weekly) reduces symptoms and disease activity in rheumatoid arthritis.
ACP J Club, 141 (2004), pp. 15
[27.]
J.M. Bathon, M.C. Genovese.
The Early Rheumatoid Arthritis (ERA) trial comparing the efficacy and safety of etanercept and methotrexate.
Clin Exp Rheumatol, 21 (2003), pp. S195-S197
[28.]
B. Blumenauer, M. Judd, A. Cranney, A. Burls, D. Coyle, M. Hochberg, et al.
Etanercept for the treatment of rheumatoid arthritis.
Cochrane Data-base Syst Rev, (2003),
[29.]
M.C. Genovese, J.M. Bathon, R.W. Martin, R.M. Fleischmann, J.R. Tesser, M.H. Schiff, et al.
Etanercept versus methotrexate in patients with early rheumatoid arthritis: two-year radiographic and clinical outcomes.
Arthritis Rheum, 46 (2002), pp. 1443-1450
[30.]
T. Pincus, C. Chung, O.G. Segurado, I. Amara, G.G. Koch.
An index of patient reported outcomes (PRO-Index) discriminates effectively between active and control treatment in 4 clinical trials of adalimumab in rheumatoid arthritis.
J Rheumatol, 33 (2006), pp. 2146-2152
[31.]
D.E. Furst, M.H. Schiff, R.M. Fleischmann, V. Strand, C.A. Birbara, D. Compagnone, et al.
Adalimumab, a fully human anti tumor necrosis factoralpha monoclonal antibody, and concomitant standard antirheumatic therapy for the treatment of rheumatoid arthritis: results of STAR (Safety Trial of Adalimumab in Rheumatoid Arthritis).
J Rheumatol, 30 (2003), pp. 2563-2571
[32.]
M.E. Weinblatt, E.C. Keystone, D.E. Furst, L.W. Moreland, M.H. Weisman, C.A. Birbara, et al.
Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMADA trial.
Arthritis Rheum, 48 (2003), pp. 35-45
[33.]
J. Uchida, Y. Lee, M. Hasegawa, Y. Liang, A. Bradney, J.A. Oliver, et al.
Mouse CD20 expression and function.
Int Immunol, 16 (2004), pp. 119-129
[34.]
J.K. Riley, M.X. Sliwkowski.
CD20: a gene in search of a function.
Semin Oncol, 27 (2000), pp. 17-24
[35.]
J.C. Edwards, M.J. Leandro, G. Cambridge.
B lymphocyte depletion in rheumatoid arthritis: targeting of CD20.
Curr Dir Autoimmun, 8 (2005), pp. 175-192
[36.]
B. Borisch, I. Semac, A. Soltermann, C. Palomba, D.C. Hoessli.
Anti-CD20 treatments and the lymphocyte membrane: pathology for therapy.
Verh Dtsch Ges Pathol, 85 (2001), pp. 161-166
[37.]
P. Emery, R. Fleischmann, A. Filipowicz-Sosnowska, J. Schechtman, L. Szczepanski, A. Kavanaugh, et al.
The efficacy and safety of rituximab in patients with active rheumatoid arthritis despite methotrexate treatment: results of a phase IIB randomized, double-blind, placebo-controlled, dose-ranging trial.
Arthritis Rheum, 54 (2006), pp. 1390-1400
[38.]
F. Díaz-González, I. Ferraz-Amaro.
La célula B en la patogenia de la artritis reumatoide.
Reumatol Clin, 3 (2007), pp. 176-182
[39.]
S.P. Bruce, E.G. Boyce.
Update on abatacept: a selective costimulation modulator for rheumatoid arthritis.
Ann Pharmacother, 41 (2007), pp. 1153-1162
[40.]
D.J. Todd, K.H. Costenbader, M.E. Weinblatt.
Abatacept in the treatment of rheumatoid arthritis.
Int J Clin Pract, 61 (2007), pp. 494-500
[41.]
M.H. Weisman, P. Durez, D. Hallegua, R. Aranda, J.C. Becker, I. Nuamah, et al.
Reduction of inflammatory biomarker response by abatacept in treatment of rheumatoid arthritis.
J Rheumatol, 33 (2006), pp. 2162-2166
[42.]
M. Weinblatt, B. Combe, A. Covucci, R. Aranda, J.C. Becker, E. Keystone.
Safety of the selective costimulation modulator abatacept in rheumatoid arthritis patients receiving background biologic and nonbiologic diseasemodifying antirheumatic drugs: A one-year randomized, placebocontrolled study.
Arthritis Rheum, 54 (2006), pp. 2807-2816
[43.]
M. Boers.
Abatacept in rheumatoid arthritis: a new branch on the “biologics” tree.
Ann Intern Med, 144 (2006), pp. 933-935
[44]
Allison C. Abatacept as add-on therapy for rheumatoid arthritis. Ottawa: Canadian Coordinating Office for Health Technology Assessment (CCOHTA); 2005. p. 4.
[45.]
C.E. Rudd, H. Schneider.
Unifying concepts in CD28, ICOS and CTLA4 co-receptor signalling.
Nat Rev Immunol, 3 (2003), pp. 544-556
[46.]
P.J. Noel, L.H. Boise, C.B. Thompson.
Regulation of T cell activation by CD28 and CTLA4.
Adv Exp Med Biol, 406 (1996), pp. 209-217
[47.]
J.R. O’Dell, R. Leff, G. Paulsen, C. Haire, J. Mallek, P.J. Eckhoff, et al.
Treatment of rheumatoid arthritis with methotrexate and hydroxychloroquine, methotrexate and sulfasalazine, or a combination of the three medications: results of a two-year, randomized, double-blind, placebo-controlled trial.
Arthritis Rheum, 46 (2002), pp. 1164-1170
[48.]
J.R. O’Dell, C.E. Haire, N. Erikson, W. Drymalski, W. Palmer, P.J. Eckhoff, et al.
Treatment of rheumatoid arthritis with methotrexate alone, sulfasalazine and hydroxychloroquine, or a combination of all three medications.
N Engl J Med, 334 (1996), pp. 1287-1291
[49.]
T. Sokka, P. Hannonen, T. Mottonen.
Conventional disease-modifying antirheumatic drugs in early arthritis.
Rheum Dis Clin North Am, 31 (2005), pp. 729-744
[50.]
I. del Rincón, A. Escalante.
HLA-DRB1 alleles associated with susceptibility or resistance to rheumatoid arthritis, articular deformities, and disability in Mexican Americans.
Arthritis Rheum, 42 (1999), pp. 1329-1338
[51.]
P.A. Gourraud, P. Dieude, J.F. Boyer, L. Nogueira, A. Cambon-Thomsen, B. Mazieres, et al.
A new classification of HLA-DRB1 alleles differentiates predisposing and protective alleles for autoantibody production in rheumatoid arthritis.
Arthritis Res Ther, 9 (2007), pp. R27
[52.]
T.W. Huizinga, C.I. Amos, A.H. van der Helm-van Mil, W. Chen, F.A. van Gaalen, D. Jawaheer, et al.
Refining the complex rheumatoid arthritis phenotype based on specificity of the HLA-DRB1 shared epitope for antibodies to citrullinated proteins.
Arthritis Rheum, 52 (2005), pp. 3433-3438
[53.]
L. Michou, P. Croiseau, E. Petit-Teixeira, S.T. du Montcel, I. Lemaire, C. Pierlot, et al.
Validation of the reshaped shared epitope HLA-DRB1 classification in rheumatoid arthritis.
Arthritis Res Ther, 8 (2006), pp. R79
[54.]
J.R. O’Dell, B.S. Nepom, C. Haire, V.H. Gersuk, L. Gaur, G.F. Moore, et al.
HLA-DRB1 typing in rheumatoid arthritis: predicting response to specific treatments.
Ann Rheum Dis, 57 (1998), pp. 209-213
[55.]
C. Seidl, U. Koch, T. Buhleier, B. Moller, R. Wigand, E. Markert, et al.
Association of (Q)R/KRAA positive HLA-DRB1 alleles with disease progression in early active and severe rheumatoid arthritis.
J Rheumatol, 26 (1999), pp. 773-776
[56]
Madsen BE, Villesen P, Wiuf C. A periodic pattern of SNPs in the human genome. Genome Research. 2007. Available from: http://www.genome.org/cgi/doi/10.1101/gr.6223207
[57.]
N. Maniatis, A. Collins, N.E. Morton.
Effects of single SNPs, haplotypes, and whole-genome LD maps on accuracy of association mapping.
Genet Epidemiol, 31 (2007), pp. 179-188
[58.]
M.A. Eberle, M.J. Rieder, L. Kruglyak, D.A. Nickerson.
Allele frequency matching between SNPs reveals an excess of linkage disequilibrium in genic regions of the human genome.
PLoS Genet, 2 (2006), pp. e142
[59.]
J.N. Hirschhorn, C.M. Lindgren, M.J. Daly, A. Kirby, S.F. Schaffner, N.P. Burtt, et al.
Genomewide linkage analysis of stature in multiple populations reveals several regions with evidence of linkage to adult height.
Am J Hum Genet, 69 (2001), pp. 106-116
[60.]
R. Judson, B. Salisbury, J. Schneider, A. Windemuth, J.C. Stephens.
How many SNPs does a genome-wide haplotype map require?.
Pharmacogenomics, 3 (2002), pp. 379-391
[61.]
Genome-wide association study of 14 000 cases of seven common diseases and 3,000 shared controls.
Nature, 447 (2007), pp. 661-678
[62.]
R.M. Plenge, M. Seielstad, L. Padyukov, A.T. Lee, E.F. Remmers, B. Ding, et al.
TRAF1-C5 as a risk locus for rheumatoid arthritis – a genomewide study.
N Engl J Med, 357 (2007), pp. 1199-1209
[63.]
L. Michou, S. Lasbleiz, A.C. Rat, P. Migliorini, A. Balsa, R. Westhovens, et al.
Linkage proof for PTPN22, a rheumatoid arthritis susceptibility gene a human autoimmunity gene.
Proc Natl Acad Sci USA, 104 (2007), pp. 1649-1654
[64.]
D. Smyth, J.D. Cooper, J.E. Collins, J.M. Heward, J.A. Franklyn, J.M. Howson, et al.
Replication of an association between the lymphoid tyrosine phosphatase locus (LYP/PTPN22) with type 1 diabetes, and evidence for its role as a general autoimmunity locus.
Diabetes, 53 (2004), pp. 3020-3023
[65.]
S. Cha, C.B. Choi, T.U. Han, C.P. Kang, C. Kang, S.C. Bae.
Association of anticyclic citrullinated peptide antibody levels with PADI4 haplotypes in early rheumatoid arthritis and with shared epitope alleles in very late rheumatoid arthritis.
Arthritis Rheum, 56 (2007), pp. 1454-1463
[66.]
K. Ikari, M. Kuwahara, T. Nakamura, S. Momohara, M. Hara, H. Yamanaka, et al.
Association between PADI4 and rheumatoid arthritis: a replication study.
Arthritis Rheum, 52 (2005), pp. 3054-3057
[67.]
S. Tokuhiro, R. Yamada, X. Chang, A. Suzuki, Y. Kochi, T. Sawada, et al.
An intronic SNP in a RUNX1 binding site of SLC22A4, encoding an organic cation transporter, is associated with rheumatoid arthritis.
Nat Genet, 35 (2003), pp. 341-348
[68.]
S.Y. Hwang, J.Y. Kim, K.W. Kim, M.K. Park, Y. Moon, W.U. Kim, et al.
IL17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-kappaB– and PI3-kinase/Akt-dependent pathways.
Arthritis Res Ther, 6 (2004), pp. R120-R128
[69.]
J. Moreno, L. Adorini, G.J. Hammerling.
Co-dominant restriction by a mixed-haplotype I-A molecule (alpha k beta b) for the lysozyme peptide 5261 in H-2k x H-2b F1 mice.
J Immunol, 144 (1990), pp. 3296-3304
[70.]
K. Raza, M. Breese, P. Nightingale, K. Kumar, T. Potter, D.M. Carruthers, et al.
Predictive value of antibodies to cyclic citrullinated peptide in patients with very early inflammatory arthritis.
J Rheumatol, 32 (2005), pp. 231-238
[71.]
F.A. van Gaalen, A.J. van, T.W. Huizinga, G.M. Schreuder, F.C. Breedveld, E. Zanelli, et al.
Association between HLA class II genes and autoantibodies to cyclic citrullinated peptides (CCPs) influences the severity of rheumatoid arthritis.
Arthritis Rheum, 50 (2004), pp. 2113-2121
[72.]
A. Barton, J. Bowes, S. Eyre, K. Spreckley, A. Hinks, S. John, et al.
A functional haplotype of the PADI4 gene associated with rheumatoid arthritis in a Japanese population is not associated in a United Kingdom population.
Arthritis Rheum, 50 (2004), pp. 1117-1121
[73.]
J. Wu, A. Katrekar, L.A. Honigberg, A.M. Smith, M.T. Conn, J. Tang, et al.
Identification of substrates of human protein-tyrosine phosphatase PTPN22.
J Biol Chem, 281 (2006), pp. 11002-11010
[74.]
T. Vang, M. Congia, M.D. Macis, L. Musumeci, V. Orru, P. Zavattari, et al.
Autoimmune-associated lymphoid tyrosine phosphatase is a gain-of-function variant.
Nat Genet, 37 (2005), pp. 1317-1319
[75.]
N. Sakaguchi, T. Takahashi, H. Hata, T. Nomura, T. Tagami, S. Yamazaki, et al.
Altered thymic T-cell selection due to a mutation of the ZAP-70 gene causes autoimmune arthritis in mice.
Nature, 426 (2003), pp. 454-460
[76.]
D.M. Soper, D.J. Kasprowicz, S.F. Ziegler.
IL-2Rbeta links IL-2R signaling with Foxp3 expression.
Eur J Immunol, 37 (2007), pp. 1817-1826
[77.]
T.R. Malek, A.L. Bayer.
Tolerance not immunity, crucially depends on IL-2.
Nat Rev Immunol, 4 (2004), pp. 665-674
[79.]
M. Ota, Y. Katsuyama, A. Kimura, K. Tsuchiya, M. Kondo, T. Naruse, et al.
A second susceptibility gene for developing rheumatoid arthritis in the human MHC is localized within a 70-kb interval telomeric of the TNF genes in the HLA class III region.
Genomics, 71 (2001), pp. 263-270
[80.]
D.M. Lee, D.S. Friend, M.F. Gurish, C. Benoist, D. Mathis, M.B. Brenner.
Mast cells: a cellular link between autoantibodies and inflammatory arthritis.
Science, 297 (2002), pp. 1689-1692
[81.]
I. Matsumoto, M. Maccioni, D.M. Lee, M. Maurice, B. Simmons, M. Brenner, et al.
How antibodies to a ubiquitous cytoplasmic enzyme may provoke jointspecific autoimmune disease.
Nat Immunol, 3 (2002), pp. 360-365
[82.]
I. Matsumoto, A. Staub, C. Benoist, D. Mathis.
Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme.
Science, 286 (1999), pp. 1732-1735
[83.]
K. Tilleman, B.K. van, A. Dhondt, I. Hoffman, K.F. de, E. Veys, et al.
Chronically inflamed synovium from spondyloarthropathy and rheumatoid arthritis investigated by protein expression profiling followed by tandem mass spectrometry.
Proteomics, 5 (2005), pp. 2247-2257
[84.]
R. Gobezie, P.J. Millett, D.S. Sarracino, C. Evans, T.S. Thornhill.
Proteomics: applications to the study of rheumatoid arthritis and osteoarthritis.
J Am Acad Orthop Surg, 14 (2006), pp. 325-332
[85.]
P.R. Thompson, W. Fast.
Histone citrullination by protein arginine deiminase: is arginine methylation a green light or a roadblock?.
ACS Chem Biol, 1 (2006), pp. 433-441
[86.]
W.H. Robinson, H. Garren, P.J. Utz, L. Steinman.
Millennium Award. Proteomics for the development of DNA tolerizing vaccines to treat autoimmune disease.
Clin Immunol, 103 (2002), pp. 7-12
[87.]
A. Sinz, M. Bantscheff, S. Mikkat, B. Ringel, S. Drynda, J. Kekow, et al.
Mass spectrometric proteome analyses of synovial fluids and plasmas from patients suffering from rheumatoid arthritis and comparison to reactive arthritis or osteoarthritis.
Electrophoresis, 23 (2002), pp. 3445-3456
[88.]
H. Dotzlaw, M. Schulz, M. Eggert, G. Neeck.
A pattern of protein expression in peripheral blood mononuclear cells distinguishes rheumatoid arthritis patients from healthy individuals.
Biochim Biophys Acta, 1696 (2004), pp. 121-129
[89.]
H. Liao, J. Wu, E. Kuhn, W. Chin, B. Chang, M.D. Jones, et al.
Use of mass spectrometry to identify protein biomarkers of disease severity in the synovial fluid and serum of patients with rheumatoid arthritis.
Arthritis Rheum, 50 (2004), pp. 3792-3803
[90.]
E. Kuhn, J. Wu, J. Karl, H. Liao, W. Zolg, B. Guild.
Quantification of C-reactive protein in the serum of patients with rheumatoid arthritis using multiple reaction monitoring mass spectrometry and 13C-labeled peptide standards.
Proteomics, 4 (2004), pp. 1175-1186
[91.]
P.K. Petrow, K.M. Hummel, J. Schedel, J.K. Franz, C.L. Klein, U. Muller-Ladner, et al.
Expression of osteopontin messenger RNA and protein in rheumatoid arthritis: effects of osteopontin on the release of collagenase 1 from articular chondrocytes and synovial fibroblasts.
Arthritis Rheum, 43 (2000), pp. 1597-1605
[92.]
R.H. Scofield.
Autoantibodies as predictors of disease.
Lancet, 363 (2004), pp. 1544-1546
Copyright © 2008. Sociedad Española de Reumatología and Colegio Mexicano de Reumatología
