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Gotowe bibliografie tematyczne / Rheumatoid arthritis Immunological aspects

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Gotowa bibliografia na temat „Rheumatoid arthritis Immunological aspects”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 31 stycznia 2023

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Artykuły w czasopismach na temat "Rheumatoid arthritis Immunological aspects"

1

Gergely, Peter. "New Immunological Aspects of Rheumatoid Arthritis". Allergy & Clinical Immunology International - Journal of the World Allergy Organization 12, nr 2 (2000): 0077–81. http://dx.doi.org/10.1027/0838-1925.12.2.77.

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YOSHINO, KAZUYA. "Immunological aspects of juvenile rheumatoid arthritis". Pediatrics International 35, nr 5 (październik 1993): 427–38. http://dx.doi.org/10.1111/j.1442-200x.1993.tb03087.x.

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Sugimoto, Masakuni, Yoshihisa Wakabayashi, Shun-Ichi Hirose i Fumimaro Takaku. "Immunological aspects of the anemia of rheumatoid arthritis". American Journal of Hematology 25, nr 1 (maj 1987): 1–11. http://dx.doi.org/10.1002/ajh.2830250102.

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Karateev, D. E. "Low activity and remission in rheumatoid arthritis. Clinical, immunological and morphological aspects". Rheumatology Science and Practice, nr 5 (15.10.2009): 4. http://dx.doi.org/10.14412/1995-4484-2009-582.

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Rodríguez, Sandra, Andrés Muñoz, Rosa-Helena Bustos i Diego Jaimes. "Pharmacovigilance of Biopharmaceuticals in Rheumatic Diseases, Adverse Events, Evolution, and Perspective: An Overview". Biomedicines 8, nr 9 (23.08.2020): 303. http://dx.doi.org/10.3390/biomedicines8090303.

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Since we have gained an understanding of the immunological pathophysiology of rheumatic diseases such as rheumatoid arthritis and systemic lupus erythematosus, treatment based on biological drugs has become a fundamental axis. These therapies are oriented towards the regulation of cytokines such as tumour necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1, and the modulation of cell-mediated immunity (B cells and T cells) by anti CD20 or anti CTAL-4 agents, and can increase the risk of associated infections or adverse events (AE). In this context, the entry of biotherapeutics represented a challenge for pharmacovigilance, risk management and approval by the main global regulatory agencies regarding biosimilars, where efficacy and safety are based on comparability exercises without being an exact copy in terms of molecular structure. The objective of this review is divided into three fundamental aspects: (i) to illustrate the evolution and focus of pharmacovigilance at the biopharmaceutical level, (ii) to describe the different approved recommendations of biopharmaceuticals (biological and biosimilars) and their use in rheumatic diseases (RDs) such as rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), systemic lupus erythematosus (SLE) and other less frequent RD like cryopyrin-associated autoinflammatory syndromes (CAPS), and (iii) to identify the main AE reported in the post-marketing phase of RD biopharmaceuticals.

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OTTEN, H. G., M. R. DAHA, M. G. J. MAARL, L. I. HOOGENDOORN, E. M. BEEM, H. H. ROOY i F. C. BREEDVELD. "IgA rheumatoid factor in mucosal fluids and serum of patients with rheumatoid arthritis: immunological aspects and clinical significance". Clinical & Experimental Immunology 90, nr 2 (28.06.2008): 256–59. http://dx.doi.org/10.1111/j.1365-2249.1992.tb07938.x.

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Pandolfi, Franco, Laura Franza, Valentina Carusi, Simona Altamura, Gloria Andriollo i Eleonora Nucera. "Interleukin-6 in Rheumatoid Arthritis". International Journal of Molecular Sciences 21, nr 15 (23.07.2020): 5238. http://dx.doi.org/10.3390/ijms21155238.

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The role of interleukin (IL)-6 in health and disease has been under a lot of scrutiny in recent years, particularly during the recent COVID-19 pandemic. The inflammatory pathways in which IL-6 is involved are also partly responsible of the development and progression of rheumatoid arthritis (RA), opening interesting perspectives in terms of therapy. Anti-IL-6 drugs are being used with variable degrees of success in other diseases and are being tested in RA. Results have been encouraging, particularly when anti-IL-6 has been used with other drugs, such as metothrexate (MTX). In this review we discuss the main immunologic aspects that make anti-IL-6 a good candidate in RA, but despite the main therapeutic options available to target IL-6, no gold standard treatment has been established so far.

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Reyes-Castillo, Zyanya, José Francisco Muñoz-Valle i Mara A. Llamas-Covarrubias. "Clinical and immunological aspects of anti-peptidylarginine deiminase type 4 (anti-PAD4) autoantibodies in rheumatoid arthritis". Autoimmunity Reviews 17, nr 2 (luty 2018): 94–102. http://dx.doi.org/10.1016/j.autrev.2017.11.023.

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Skovsgaard Itenov, K., N. Søe, E. M. Bartels, H. Bliddal i M. Andersen. "AB0103 SITE SPECIFICITY OF RHEUMATOID ARTHRITIS INFLAMMATION: A SECONDARY ANALYSIS OF BIOPSIES FROM RADIAL AND ULNAR ASPECTS OF MCP JOINTS". Annals of the Rheumatic Diseases 81, Suppl 1 (23.05.2022): 1182.2–1182. http://dx.doi.org/10.1136/annrheumdis-2022-eular.5196.

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BackgroundUlnar drift is a common complication of Rheumatoid Arthritis (RA) (1,2). There is no clear consensus regarding the etiology of the hand deformity. Observations from corrective hand surgery and other studies have noted more pronounced inflammation in the radial site of the MCP-joints (3,4). This could partly explain the pathophysiology behind the ulnar deviation.ObjectivesTo determine if there is more pronounced inflammation, measured by increased CD-68 expression (5) and Krenn-synovitis score (6), at the radial side of the MCP joints when compared to the ulnar side, in patients with verified RA.MethodsWe included RA patients from a previous study who had biopsies taken from the most affected joints based on clinical examination and ultrasound (7). Twenty-nine PIP-, MCP- and wrist-joints were biopsied. Biopsies from the MCP-joints were taken from the dorso-ulnar and dorso-radial concavity. Inflammation was graded by the Krenn-synovitis score (0-9) and the density of CD-68-positive cells (%). The difference between radial and ulnar joint inflammation was calculated by paired t-test. P-value <0.05 was considered statistically significant.ResultsIn 8 patients biopsies were taken from both the ulnar and the radial site of the same MCP-joint. The mean difference in inflammation on the radial and ulnar site of MCP-joints was based on differences in CD-68 density: 0,67% (95%-CI -4,77 to 6,10; P = 0,77) (Figure 1) and Krenn-score: 0,83 (95%-CI -1,31 to 2,98; P = 0,36), respectively.Figure 1.Paired data on CD-68 percentage in radial and ulnar sitesConclusionThere was no difference in concentration of inflammatory cells or overall synovial pathology between the radial and ulnar site of MCP-joints in RA patients. The impression of a more pronounced inflamed synovium on the radial site of MCP joints, as observed during surgery, does not seem to arise from an immunological preference, but rather to be linked to a larger synovial volume.References[1]Wise KS: The anatomy of the metacarpo-phalangeal joints, with observations of the aetiology of ulnar drift. J. Bone Joint Surg. Br. 1975; 57:485–90[2]Johnsson PM, Eberhardt K: Hand deformities are important signs of disease severity in patients with early rheumatoid arthritis. Rheumatology 2009; 48:1398–1401[3]Philpott H.T. Synovial tissue perivascular edema is associated with altered gait patterns in patients with knee osteoarthritis, Osteoarthritis and Cartilage. 2022; 30(1): 42-51[4]Tan AL, Tanner SF, Conaghan PG, et al.: Role of metacarpophalangeal joint anatomic factors in the distribution of synovitis and bone erosion in early rheumatoid arthritis. Arthritis Rheum. 2003; 48:1214–22[5]Zhang X.-P: Addition of Fibroblast-Stromal Cell Markers to Immune Synovium Pathotypes Better Predicts Radiographic Progression at 1 Year in Active Rheumatoid Arthritis, Frontiers in Immunology 2021; 12: 778480[6]Krenn V, Morawietz L, Burmester G-R, et al.: Synovitis score: discrimination between chronic low-grade and high-grade synovitis. Histopathology 2006; 49:358–364[7]Andersen M, Ellegaard K, Hebsgaard JB, et al.: Ultrasound colour Doppler is associated with synovial pathology in biopsies from hand joints in rheumatoid arthritis patients: a cross-sectional study. Ann. Rheum. Dis. 2014; 73:678–683AcknowledgementsThe authors would like to thank the study participants as well as Inger Wätjen, Eva Littrup Andersen, Mette Okkels, Jette Møller Frøsig and Suzi Høeg Madsen for technical assistance. I have no acknowledgements to declare.Disclosure of InterestsKatrine Skovsgaard Itenov: None declared, Niels Søe: None declared, Else Marie Bartels: None declared, Henning Bliddal: None declared, Martin Andersen Grant/research support from: The primary study was supported by unrestricted grants from Novo Nordisk, Employee of: Was employed at Novo Nordisk A/S during the conduction of the study.

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Dekhtiarenko, N. О., L. M. Panchenko, M. P. Hrytsai, O. M. Linenko, V. I. Sabadosh i K. M. Salmanova. "Analysis of Some Immunological Aspects of Joint Infections Developed as a Result of Intra-Articular Glucocorticoid Injection". Visnyk Ortopedii Travmatologii Protezuvannia, nr 4(111) (20.12.2021): 21–27. http://dx.doi.org/10.37647/0132-2486-2021-111-4-21-27.

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Summary. The work is devoted to the studies of immune status of patients with infectious complications after local glucocorticoid injections. Objective: to assess the state of the immune system of patients with infectious complications after local glucocorticoid injections, to monitor the dynamics of immunological parameters before and after sanitizing surgical treatment, and to reveal factors that are important for predicting the course of the disease and treatment results. Materials and Methods. The immune status of 26 patients with purulent inflammatory processes after local glucocorticoid injections in rheumatoid arthritis, deforming osteoarthritis, and chronic synovitis was studied. Immunological, hematological, and statistical research methods were used. Results. Changes of immunity factors as well as hematological parameters were revealed: a decrease in the content of T-lymphocytes (CD3+), T-helpers (CD4+), T-suppressors / cytotoxic lymphocytes (CD8+), immunoglobulins of classes A, M, and G; an increase in the levels of circulating immune complexes (СIC), the number of thrombocytes, erythrocyte sedimentation rate (ESR), and the reaction of the neutrophil leukocytes. It has been shown that the improvement of the immune status and the decrease in the level of inflammatory reactions after the sanitizing surgical intervention occurs slowly, which requires the inclusion of immunocorrective therapy in the treatment of such patients. Conclusions. Primary examination of patients before surgery for the purpose of sanitizing the infection showed that the local inflammatory process in the bones and joints occurs against the background of altered immunological and hematological parameters. Dynamic follow-up showed that we are dealing not only with a local process, but also with a systemic inflammatory response. A variant of the laboratory criterion for the course of infectious complications and the effectiveness of the treatment can be the determination in the dynamics of the content of T-lymphocytes and their subpopulations, the levels of the CIC, platelets and ESR.

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Rozprawy doktorskie na temat "Rheumatoid arthritis Immunological aspects"

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Sverdrup, Berit. "Aspects of the role of mineral oil as immunological adjuvant in rheumatoid arthritis /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-112-8/.

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Effertz, Bernard Stephen. "The humoral immune response to streptococcal cell wall-induced arthritis in the rat". Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184877.

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I investigated the humoral immune response to streptococcal cell walls (SCW) in arthritis susceptible Lewis and resistant Fisher rats. All rats were given a single intraperitoneal injection of either SCW or saline (controls). Rats were sacrificed, three rats per time point, over an eleven week period and serum was collected for ELISA. SCW injected Lewis rats produced anti-SCW antibody, whereas control rats did not. Anti-SCW antibody was significantly elevated over controls between days 14-28 (post injection). Both saline and SCW injected Fisher rats produced anti-SCW antibody, but with different kinetics. Anti-SCW antibody increased by day 7 and remained elevated over controls till day 21, after which there was no difference. ELISA were designed to determine the SCW epitope(s) recognized by anti-SCW antibody. Formamide extracts of SCW, peptidoglycan and polysaccharide, were investigated along with the terminal epitope of polysaccharide, N-acetyl-D-glucosamine, and the peptidoglycan precursor peptide. The data revealed that anti-SCW antibody was directed against a combined SCW epitope, given the lack of significant binding to any of the SCW epitopes tested. Isotype analysis of anti-SCW antibody revealed that the Lewis response was composed primarily of IgG2a whereas the Fisher response was composed primarily of IgM. Binding of rat IgG isotypes to whole streptococcus, SCW, peptidoglycan, and polysaccharide was investigated, given the possibility of background binding by the streptococcal Fc-receptor. Streptococcal binding of rat IgG was specific for IgG2c and the polysaccharide portion of SCW was necessary for binding. Passive immunization of naive Lewis rats with antibody from rats with active arthritis was ineffective at transferring the disease. However, subcutaneous injection of affinity purified anti-SCW antibody or IgG into Lewis rats, followed twenty-four hours later by a single intraperitoneal injection of SCW, suppressed the acute phase and inhibited the chronic disease. IgM rheumatoid factor (RF) was present in the serum of both saline and SCW injected Lewis and Fisher rats. However, SCW injection only induced a significant increase in IgM RF (between days 3-7) in Lewis rats. Passive immunization of Fisher rats with affinity purified IgM RF (from Lewis serum), three days post SCW injection, was ineffective at inducing arthritis.

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Nordström, Dan C. E. "Cellular inflammation in arthritis a study of clinical, histological, and immunological aspects in rheumatoid and reactive arthritis /". Hki : Societas scientiarum Fennica, 1989. http://catalog.hathitrust.org/api/volumes/oclc/58508848.html.

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Lacey, Derek. "NFκB independent pathway activation of rheumatoid arthritis FLS by macrophage migration inhibitory factor (MIF)". Monash University, Faculty of Medicine, 2003. http://arrow.monash.edu.au/hdl/1959.1/9457.

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Penglis, Peter Savas. "The relationships between eicosanoid production and pro-inflammatory cytokines". Title page, contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09php3985.pdf.

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Includes bibliographical references (leaves 182-240). Explores alternate strategies that may alter inflammatory cytokine production, particularly tumour necrosis factor đ [tumor necrosis factor-alpha], and therefore provide a possible treatment for rheumatoid arthritis.

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Duke, O. L. "Immunological observations in rheumatoid arthritis". Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598674.

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Bedwell, A. E. "Immunological abnormalities of rheumatoid arthritis". Thesis, University of Bristol, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372005.

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Pritchard, M. L. "Psychological aspects of rheumatoid arthritis". Thesis, University of Exeter, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381050.

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Milicic, Anita. "Studies of the genetic and immunological basis of rheumatoid arthritis". Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.275411.

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Brink, Mikael. "Presence of immunological markers preceding the onset of rheumatoid arthritis". Doctoral thesis, Umeå universitet, Reumatologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-102589.

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Rheumatoid arthritis (RA) is a chronic inflammatory disease with an unknown aetiology characterized by joint destruction. Both genetic and environmental factors contribute to the disease development with HLA-DRB1* alleles and smoking identified as most important. The disease is characterized by the presence of autoantibodies, originally by rheumatoid factor (RF) and more recently by anti citrullinated protein/peptide antibodies (ACPA) and antibodies against carbamylated peptides (CarP). These autoantibodies are present, not only after the onset of disease, but also prior to the onset of symptoms. The development of RA is a gradual process lasting several years before the onset of any joint symptom, but when and if there is a temporal difference in the development both between and within the different antibody systems is currently unknown. B-cells produce the antibodies, and a subset of B-cells, i.e., B-regulatory (Breg) cells, produces interleukin-10, and thus have the ability to down-regulate pro-inflammatory cytokines. Whether the Breg cells are involved in the pathogenesis of RA is, as yet, unknown. The aim of this thesis was to increase knowledge of the pathophysiological processes in the development of RA through identification of factors involved. The analyses involved detection of autoantibodies to post-translationally modified peptides/proteins in addition to RF isotypes, cell surface markers on immune cells in asymptomatic individuals, who have an increased risk of developing RA. In a co-analysis of the registers of patients with RA attending the Department of Rheumatology, with the registers from population based screening programmes within the Biobank of Northern Sweden, blood samples collected from individuals prior to the onset of symptoms were identified, as were those from population control subjects. A cohort of pre-symptomatic individuals also donated samples at the time of receiving a diagnosis of RA. First-degree relatives (FDR) of patients with RA were also identified and included for analyses. The levels of ten different ACPAs, i.e., (fibrinogen (Fib) α563-583(573), Fibα580-600(591), Fibβ62-81a(72), Fibβ62-81b(74), Fibβ36-52, a-enolase (CEP-1), triple helical collagen type II (citC1III), filaggrin (Fil307-324), vimentin (Vim) 2-17, and Vim60-75) were measured using the ImmunoCAP ISAC system (Phadia/ThermoFischer, Uppsala, Sweden) in blood samples from individuals before the onset of symptoms and when diagnosed with RA in comparison with those in population based controls. In a subset of samples, the levels of anti-CarP antibodies were measured using ELISA coated with anti-CarP-FCS, as well as analysis of RF of IgM, IgG and IgA isotype using the EliA assay (Phadia, Uppsala, Sweden). Breg cells were analysed both with and without stimulation ex vivo along with other cell types using flow cytometry in samples from patients with RA, their first degree relatives (FDR) and healthy controls. In paper I it was shown that levels of ACPA were initially restricted to a few antibodies but disseminated over time to involve additional different antibodies. The levels of antibodies to CEP-1, Fibß36-52, and filaggrin were significantly increased. In paper II, anti-CarP antibodies were positive in 5-13% of the individuals negative for the various ACPA studied. The presence of anti-CarP antibodies was significantly related to radiological destruction of joints at baseline, at follow-up after 24 months and to the radiological progress between baseline and 24months. In paper III, the relationships between the frequencies of RF isotypes, the ten different ACPA, anti-CCP2 and anti-CarP antibodies before the onset of any symptoms and the presence of certain combinations of antibodies were associated with a very high risk of developing RA. In paper IV Breg cells from patients with RA are functionally impaired and FDR showed a similar pattern by responding less to stimulation ex vivo than cells from healthy controls. In conclusion, individuals who subsequently develop RA have an increased number and amount of ACPAs, anti-CarP antibodies and RF of IgM, IgG and IgA isotype, several years before symptom onset. Most of the different antibodies analysed remain associated with disease development after adjustments for each separate antibody. In FDRs, Breg cells were functionally altered in that they produce less IL-10 and consequently contribute to a more inflammation-prone status, as in their relatives with RA. These findings contribute to information about the development of RA as well as a given individual’s risk(s) of developing RA and its progression.

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Książki na temat "Rheumatoid arthritis Immunological aspects"

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Radboud J. E. M. Dolhain. T cells in the inflamed joints of patients with rheumatoid arthritis. [Leiden: University of Leiden, 1998.

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David, Isenberg, i Rademacher T. W, red. Abnormalities of IgG glycosylation and immunological disorders. Chichester: Wiley, 1996.

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S, Panayi Gabriel, red. Immunology of the connective tissue diseases. Dordrecht: Kluwer Academic Publishers, 1994.

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M, Cutolo, i New York Academy of Sciences., red. Basic and clinical aspects of neuroendocrine immunology in rheumatic diseases. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2006.

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Coping with rheumatoid arthritis. Garden City Park, N.Y: Avery Pub. Group, 1988.

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Psychological aspects of rheumatoid arthritis. New York: Springer-Verlag, 1989.

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Pritchard, Mary L. Psychological Aspects of Rheumatoid Arthritis. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-9666-6.

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Leitch, Michael. Living with arthritis: People with arthritis talk about coping from day to day. Bath: Chivers, 1988.

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C, Singleton Mary, i Branch Eleanor F, red. Physical therapy and the arthritis patient: Clinical aspects and approaches to management. New York: Haworth Press, 1988.

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Ronday, H. K. Aspects of proteolytic joint destruction in rheumatoid arthritis. Leiden: University of Leiden, 1998.

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Części książek na temat "Rheumatoid arthritis Immunological aspects"

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Hashimoto, Toshihide. "Rheumatoid Arthritis: Psychosocial Aspects". W Encyclopedia of Behavioral Medicine, 1914–17. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_427.

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Molina, Kristine M., Kristine M. Molina, Heather Honoré Goltz, Marc A. Kowalkouski, Stacey L. Hart, David Latini, J. Rick Turner i in. "Rheumatoid Arthritis: Psychosocial Aspects". W Encyclopedia of Behavioral Medicine, 1679–81. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_427.

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Hashimoto, Toshihide. "Rheumatoid Arthritis: Psychosocial Aspects". W Encyclopedia of Behavioral Medicine, 1–3. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-6439-6_427-2.

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Grabiec, Aleksander M., Paul P. Tak i Kris A. Reedquist. "Epigenetics of Rheumatoid Arthritis". W Epigenetic Aspects of Chronic Diseases, 107–19. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-644-1_7.

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van Vollenhoven, Ronald F. "General Treatment Aspects". W Biologics for the Treatment of Rheumatoid Arthritis, 9–27. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-13108-5_2.

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Gay, S., i R. E. Gay. "Pathology of Rheumatoid Arthritis: Molecular and Inflammatory Aspects". W Symposium in Immunology VIII, 199–203. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59947-7_13.

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Situnayake, R. D., i B. McConkey. "Clinical aspects and side-effects of sulphasalazine in the treatment of rheumatoid arthritis". W Side-Effects of Anti-Inflammatory Drugs, 209–21. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-010-9775-8_23.

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Panayi, G. S. "Immunological and Immune-Mediated Toxic Effects of Gold Compounds Used in the Treatment of Rheumatoid Arthritis". W Immunotoxicity of Metals and Immunotoxicology, 155–61. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-8443-4_14.

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Lafyatis, Robert, i André Capron. "Expression cloning using antibodies from a patient with rheumatoid arthritis of an autoantigen homologous to the Drosophila splicing regulator, suppressor-of-white-apricot". W Autoimmunity: Experimental Aspects, 59–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78779-9_7.

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Kremer, Joel M., David A. Lawrence i William Jubiz. "Different Doses of Fish — Oil Fatty Acid Ingestion in Active Rheumatoid Arthritis: A Prospective Study of Clinical and Immunological Parameters". W Dietary ω3 and ω6 Fatty Acids, 343–50. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-2043-3_31.

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Streszczenia konferencji na temat "Rheumatoid arthritis Immunological aspects"

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Hamar, A., A. Pusztai, E. Végh, Á. Horváth, K. Gulyás, S. Szamosi, Z. Pethő i in. "P133 Clinical and immunological effects of tofacitinib therapy in rheumatoid arthritis". W 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.120.

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Bazarniy, VV, NS Petrovich, SV Tsvirenko i GA Tsaur. "AB0011 The estimation of synovial fluid immunological parameters in rheumatoid arthritis". W Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.810.

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Silva, CA, MJ Quartilho, JA Da Silva, A. Malcata i A. Porto. "SAT0143 Psychosomatic aspects of fibromyalgia versus rheumatoid arthritis". W Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.602.

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Murata, O., K. Suzuki, H. Sugiura, Y. Kondo, M. Takeshita, H. Yasuoka, K. Yamaoka i in. "SAT0652 Clinical and immunological significance of radiographic thymic alterations in patients with rheumatoid arthritis". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3933.

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Urban, M., J. Olson, J. Vega i G. Harris. "Juvenile rheumatoid arthritis: clinical aspects and new rehabilitation treatment options". W Pediatric Gait: A New Millennium in Clinical Care and Motion Analysis Technology. IEEE, 2000. http://dx.doi.org/10.1109/pg.2000.858874.

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Kanjana, Korawit, Parawee Chevaisrakul, Ponpan Matangkasombut, Karan Paisooksantivatana i Putthapoom Lumjiaktase. "SAT0007 THE SUPPRESSIVE ACTIVITY OF PERIPHERAL BLOOD TREG REPRESENTS IMMUNOLOGICAL REMISSION IN RHEUMATOID ARTHRITIS PATIENTS". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.1487.

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Julià, Antonio, Maria Lopez Lasanta, Antonio Gómez, Raimon Sanmarti, Carlos Marras Fernandez Cid, José Manuel Pina Salvador, Susana Romero-Yuste i in. "SAT0020 BLOOD RNA SEQUENCING REVEALS IMMUNOLOGICAL PROCESSES ASSOCIATED WITH THE RESPONSE TO ABATACEPT IN RHEUMATOID ARTHRITIS". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5389.

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Rosas-Gómez de Salazar, J., M. Martín-López, T. Oton, L. Carmona, A. Balsa, J. Calvo-Alén, R. Sanmarti i J. Tornero. "AB1318 Practical aspects of biological-drug monitoring in rheumatoid arthritis and spondyloarthritis". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4611.

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Gontar, IP, EV Baranov, LA Maslakova, AS Trofimenko i OV Paramonova. "AB0228 Immunological approach to the diagnosis of lesions of the nervous system in patients with rheumatoid arthritis". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.3123.

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Sanz, S. Castañeda, MA Gonzalez-Gay, EF Vicente, C. Alegre de Miguel, M. De la Hera, V. Torrente-Segarra, L. Merino-Meléndez i in. "AB1192 National barometer to assess the emotional aspects of patients with rheumatoid arthritis. opinar project". W Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5336.

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