Les monocytes sont des leucocytes dérivés de précurseurs de la moelle osseuse pouvant se différencier en macrophages, cellules dendritiques (CD), ou ostéoclastes (OC). Ils jouent un rôle critique dans la persistance de l'inflammation et la destruction des articulations par le biais de mécanismes encore mal connus. Les monocytes sont composés de deux grandes sous-populations chez la souris, discriminées sur la base du marqueur de surface Ly6C. Il a été suggéré que les OC pouvait être préférentiellement différenciés à partir de la sous-population monocytaire Ly6Chigh, dont l'activation excessive et prolongée est une signature clé de nombreuses pathologies inflammatoires. Parmi les acteurs moléculaires responsables de la régulation de l'expression des gènes, les miARNs jouent un rôle majeur dans de nombreux processus physiologiques, dont la réponse inflammatoire, en régulant finement les programmes génétiques au niveau post-transcriptionnel. Leur implication dans l'ostéoclastogénèse est encore mal connue. Par ailleurs, leur expression est perturbée dans de nombreuses pathologies, dont la polyarthrite rhumatoïde qui implique à la fois un dysfonctionnement de la réponse inflammatoire et de l'homéostasie osseuse. Mon projet de thèse vise à mieux comprendre l'implication des sous-populations monocytaires dans la persistance de l'inflammation et de l'activité des OC au travers de l'étude du rôle de miR-146a dans des conditions physiologiques et inflammatoires. J'ai montré que miR-146a est le miARN le plus différemment exprimé entre monocytes classiques Ly6Chigh et non-classiques Ly6Clow, et que son expression est diminuée dans les Ly6Chigh en conditions arthritiques. J'ai également montré que la perte de miR-146a augmente l'ostéoclastogénèse in vitro et l'érosion osseuse in vivo chez les souris arthritiques. Enfin, la surexpression artificielle de miR-146a dans les monocytes Ly6Chigh inhibe la différenciation osteoclastique et la perte osseuse dans l'arthrite expérimentale chez la souris. Mes résultats suggèrent que miR-146a contrôle l'hétérogénéité fonctionnelle des monocytes et qu'une diminution de son expression dans la sous-population Ly6Chigh serait responsable de l'augmentation de l'osteoclastogénèse et de l'érosion osseuse observées en conditions arthritiques. Pour finir, mes résultats montrent également qu'augmenter l'expression de miR-146a dans les monocytes Ly6Chigh présente un intérêt thérapeutique pour contrecarrer la perte osseuse associée à l'arthrite. / Introduction : Monocytes represent a prototypic cell type when investigating the interplay between immune and skeletal systems as they can give rise to different cell types including dendritic cells, macrophages and osteoclasts (OC), which play key roles in immunity and bone homeostasis. Circulating monocytes consist of at least two main functional subsets, Ly6Chigh and Ly6Clow monocytes. It has been suggested that OC might develop preferentially from the Ly6Chigh monocyte subset, which excessive and prolonged activation is a hallmark of many inflammatory diseases. Among key molecular rheostats of cell fate, micro(mi)RNAs are a class of regulatory RNAs that control basic biological functions and orchestrate inflammatory responses. Few miRNAs have been involved in osteoclastogenesis. The present study aimed at investigating the role of miRNAs in osteoclastogenesis in the context of monocyte subsets, under steady state and inflammatory conditions. Methods & Results : Using genome-wide miRNA expression study we have identified miRNAs and putative targeted pathways that are differentially expressed between Ly6Chigh and LyC6low FACS sorted mouse monocytes, and common to their human counter parts CD14+CD16- and CD14dimCD16+ monocytes, respectively. Among these, miR-146a showed higher expression in Ly6Clow monocytes when compared to Ly6Chigh monocytes. Under inflammatory arthritis conditions, expression of miR-146a in Ly6Chigh monocytes was down regulated as compared to healthy controls. Using mouse deficient for miR-146a, we showed that knockdown of miR-146a increased OC differentiation in vitro. While no bone phenotype was evidenced in miR-146a deficient mice, nor under steady state or ovariectomized conditions, arthritis-induced bone resorption and bone loss were increased in miR-146a knockout mice. Finally, using a liposomal formulation able to delivermiR-146a mimics to Ly6Chigh monocytes upon intravenous injection, we showed that enforced expression of miR-146a led to decreased number of TRAP positive cells within the synovium of arthritic mice, and efficiently reduced bone erosion in inflammatory arthritis. This effect was associated with decreased RelB expression in miR-146a-overexpressing Ly6Chigh osteoclast progenitors. Conclusion : Overall, our results show that specific over-expression of miR-146a in Ly6Chigh monocytes altered OC differentiation and decreased bone erosion in inflammatory arthritis. These data suggest a novel role for miR-146a in controlling osteoclast fate of Ly6Chigh monocyte progenitors and that reduced miR-146a expression in Ly6Chigh monocytes under arthritic conditions contributes to pathogenic bone loss. Finally, delivery of miR-146a mimics to Ly6Chigh monocytes may offer valuable therapeutic potential to interfere with pathological bone loss.

Background: Rheumatoid arthritis (RA) is a common complex autoimmune disorder which is influenced by both genetic and environmental factors. While multiple factors that influence susceptibility to and outcome of disease have been identified there is still a large proportion of missing heritability and limited understanding of disease pathogenesis. In recent years, biologic drug therapies have advanced treatment of RA; however good disease control is achieved in just 30% of patients, making identification of predictors of treatment response important. One area of research which is yet to be explored in relation to treatment response, and requires further evaluation in RA susceptibility, is epigenetics. Epigenetics is the study of modifications of the DNA which can influence gene expression but do not alter genetic sequence, and the most commonly studied epigenetic phenomenon, to date, is DNA methylation. Objectives: To identify DNA methylation signatures predictive of treatment response to anti-TNF biologics, to explore the role of DNA methylation in RA susceptibility using disease discordant monozygotic (MZ) twins, and to assess the effect of cryopreservation of cells on DNA methylation. Methods: Genome-wide DNA methylation levels were measured using the HumanMethylation450 BeadChip in pre-treatment whole blood DNA samples from individuals who had extremely good or extremely poor response to the anti-TNF therapies, etanercept and adalimumab, and in MZ twins discordant for RA (n=79 pairs). I also compared genome-wide methylation in cells which had been cryopreserved with fresh cells, to investigate if this technique is suitable for epigenetic investigations. Results: I identified four methylation sites which were significantly related to response to etanercept at a false discovery rate of 5%, the most significantly differentially methylated of which maps to the LRPAP1 gene (p=1.46E-8). Indeed, four other sites at the same locus also showed evidence for differential methylation indicating that this represents a differentially methylated region. No sites were significantly associated with response to adalimumab after correction for multiple testing. I identified subtle differences in DNA methylation between RA discordant twins. Although these were not statistically significant following adjustment for cell composition, one of the most differentially methylated positions mapped to the ZNF74 gene (p=4.97E-6), and replicated a methylation difference identified in the largest previous epigenome-wide association study of RA cases and unrelated healthy controls. I found that cryopreservation of cells does not significantly alter the methylome, an important observation that will impact upon design of future studies. Conclusions: In the largest studies of DNA methylation in RA treatment response and RA discordant MZ twins to date, I identified significant differential methylation in etanercept response, but not adalimumab response, and found small differences in methylation in RA discordant MZ twins. I also concluded that cryopreservation does not significantly alter the methylome.

Artrite reumatóide é uma doença auto-imune que apresenta acentuado quadro inflamatório e proliferação celular o que, provavelmente, determina a alta prevalência de doenças cardiovasculares quando comparados a população mundial. A mortalidade e a morbidade conseqüentes das doenças cardiovasculares estão 2 vezes aumentadas em pacientes com artrite reumatóide e um dos principais fatores de risco relacionados ao desenvolvimento da aterosclerose é a dislipidemia. Esse importante fator de risco vem sendo associado à artrite reumatóide e as concentrações plasmáticas de lípides são constantemente avaliadas, já que se encontra bem estabelecido a relação entre dislipidemia e alta incidência de doença cardiovascular. No entanto, o verdadeiro impacto das alterações lipídicas na artrite reumatóide não é bem conhecido, já que os resultados de perfil lipídico são contraditórios. Alterações nas concentrações plasmáticas de lípides não necessariamente acompanham distúrbios no metabolismo das lipoproteínas plasmáticas. O objetivo do presente estudo foi avaliar aspectos do metabolismo da LDL e da HDL, em pacientes com artrite reumatóide. Nesse sentido, foi avaliada a cinética plasmática de uma nanoemulsão lipídica artificial com comportamento metabólico semelhante ao da LDL em 30 pacientes com artrite reumatóide divididos em 2 grupos de acordo com a atividade da doença, alta atividade (n=14) e remissão (n=16) e 30 indivíduos controle. A nanoemulsão marcada com éster de colesterol 14EC (EC-14C) e colesterol livre 3H (CL-3H) foi injetada endovenosamente após 12 horas de jejum. As amostras de sangue foram coletadas em tempos pré-determinados (5 min, 1, 2, 4, 6, 8 e 24 horas) após a injeção, para determinação das curvas de decaimento plasmático e da taxa fracional de remoção (TFR) dos lípides marcados, por análise compartimental. As TFR-EC-14C e TFR-CL-3H foram maiores no grupo AR quando comparado ao grupo controle (49%, p<0,05 e 44%, p<0,05, respectivamente), não havendo diferença entre os subgrupos de artrite reumatóide. No grupo artrite reumatóide e em seus subgrupos, as concentrações de HDL-C e apo E foram maiores quando comparados ao grupo controle (33%, p<0,0001 e 20%, p<0,01, respectivamente), enquanto os níveis de apo B foram menores na artrite reumatóide quando comparados ao grupo controle (16%, p<0,05). A transferência de colesterol esterificado radioativo da nanoemulsão para a HDL foi menor na artrite reumatóide, comparando-se com o grupo controle. A transferência dos outros lípides foi similar nos dois grupos. A HDL dos pacientes com artrite reumatóide foi menor do que a dos controles. Esses resultados podem contribuir com a melhor compreensão de possíveis mecanismos relacionados a uma maior incidência de doenças cardiovasculares em pacientes com artrite reumatóide / Mortality and morbidity, as a consequence of cardiovascular diseases, is twice as high in patients with rheumatoid arthritis than in the general worldwide population. This autoimmune disease has predominant inflammatory and cell proliferation background probably explains the high prevalence of cardiovascular disease. Dyslipidemias are important risk factors for cardiovascular disease. This study investigated the link between RA and plasma lipids as a predisposition to this high cardiovascular disease incidence. However, the impact of lipids on cardiovascular risk in rheumatoid arthritis is unclear. So much so, that lipid profiles in patients with rheumatoid arthritis in published studies is contradictory. The events of intravascular lipoprotein metabolism do not necessarily produce altered levels of plasma lipids. In an attempt to unravel novel dysfunctional mechanisms that could trigger pro-atherogenic processes beyond the concentration of the plasma lipids, plasma clearance of a lipidic nanoemulsion that resembles the LDL metabolic behavior were investigated in rheumatoid arthritis patients and compared to control subjects without the disease. 30 patients with rheumatoid arthritis divided into 2 groups according to disease activity, high activity (n=14) and remission (n=16), and 30 controls were studied. A nanoemulsion labeled with 14C-cholesteryl esther (14C-CE) and 3H-free cholesterol (3H-FC) were endovenously injected after which blood samples were collected at pre-determined periods (5 min, 1, 2, 4, 6, 8 and 24 hours), in order to determine the radioactivity of the plasma decay curves and calculate the fractional clearance rate (FCR) of the labeled lipids for compartmental analysis. In the rheumatoid arthritis group and subgroups the HDL-C and apo E concentration were higher when compared to control group (33%, p<0,0001 e 20%, p<0,01, respectively) while apo B concentration was lower (16%, p<0,05). The 14-CE-FCR and 3H-FC-FCR were greater in rheumatoid arthritis group and subgroups when compared to controls (49%, p<0,05 e 44%, p<0,05, respectively). There were no differences between the rheumatoid arthritis subgroups. Therefore, rheumatoid arthritis accelerates the LDL plasma removal, as indicated by a higher 14-CE-FCR and 3H-FC-FCR. The transfer of other lipids was also similar in both groups. The HDL of the rheumatoid arthritis patients was lower than that of the control group. These results could clarify possible mechanisms that can be related to a higher cardiovascular incidence in patients with rheumatoid arthritis

La polyarthrite rhumatoïde (PR) est une maladie auto-immune (MAI) dans laquelle des anticorps anti-peptides citrullinés (ACPA) sont un outil diagnostique très spécifique. L’un des traitements clé de la PR est le méthotrexate (MTX). En plus de son action directe sur la maladie il renforce l’effet des anti-TNF alpha (aTNF). Ceci pourrait passer par une prévention de la formation d’anticorps anti-médicaments dirigés contre les aTNF ce qui leur fait perdre leur efficacité.Nous avons développé un modèle macaque pour reproduire la maladie humaine par immunisation avec des peptides citrullinés dans le contexte d’un facteur génétique favorisant la PR : l’épitope HLA partagé. L’immunisation de macaques avec divers peptides citrullinés en utilisant un boost intra-articulaire a déclenché une réponse T et B anti-citrulline et a entraîné une mono-arthrite chronique.Le rôle du MTX sur l’immunogénicité des aTNF a été étudié sur un modèle de souris autoimmunes, les souris BAFF transgéniques (tg) qui présentent une MAI. L’utilisation du MTX juste avant l’injection d’aTNF a permis de prévenir l’immunisation contre ce médicament uniquement chez ces souris BAFFtg et pas chez des souris sauvages ou chez des macaques. Nous avons démontré que ces souris BAFFtg surexprimaient CD73, ce qui permettait une sécrétion accrue d’adénosine et de cellules B régulatrices sous l’effet du MTX. L’interaction entre BAFF et le méthotrexate a été confirmée chez l’homme dans la cohorte ABIRISK : le MTX prévient plus efficacement l’immunogénicité chez les patients avec des taux de BAFF élevés.En conclusion, nous avons mis au point deux nouveaux modèles animaux permettant de mieux comprendre la physiopathologie de la PR et d’optimiser l’utilisation des traitements biologiques qui s’étend dans tous les domaines de la médecine. / Title : Development of new animal models to study the pathophysiology of RA and the role of methotrexate-induced tolerance.Keywords : Rheumatoid arthritis, shared epitope, ACPA, immunogenicity, methotrexate, TNF inhibitorsAbstract: Rheumatoid arthritis (RA) is an autoimmune disease (AID) where antibodies directed against citrullinated peptides (ACPA) are highly specific for the diagnosis. One of the key treatments of RA is methotrexate. It has an action on both the disease and reinforces the effect of second line TNF inhibitors (TNFi). MTX might act via prevention of anti-drug antibodies (ADAb) directed against TNFi that are implicated in loss of efficacy of TNFi. We have developed a macaque model to recapitulate the human disease by immunization with citrullinated peptides in the context of a genetic factor favoring RA: the shared epitope on the HLA. Immunization of macaques with citrullinated peptides and intra-articular boost cause an anti-citrulline T and B cell response and a chronic monoarthritis.The role of MTX-induced tolerance against TNFI has been studied in autoimmune BAFF transgenic (tg) mice using MTX just before treatment with TNFi we were able to prevent ADAb formation in BAFFtg mice and not wild type mice or macaques. We identified that BAFFtg mice expressed elevated CD73 leading to more adenosine and regulatory B cells as actors in MTX-induced tolerance. This MTX-BAFF interaction was further confirmed in humans in the ABIRISK cohort where MTX was more efficient to prevent ADAb formation in RA patients with elevated BAFF levels.Setting up two new animal models allows better understanding of RA pathophysiology and better use of biologics that extend to other domains of medicine.

Background: MicroRNAs (miRNAs) are small non-coding single-stranded RNAs involved in the posttranscriptional inhibition of gene expression and thereby regulating all cellular functions. Their dysregulation contributes to the pathophysiology of many diseases, including rheumatic diseases. MiRNAs can also be found extracellularly in body fluids and represent promising diagnostic and prognostic biomarkers. Our study aimed to investigate miRNAs as biomarkers of stage and activity and predictors of therapeutic response of two most common inflammatory rheumatic diseases: spondyloarthritis (SpA) and rheumatic arthritis (RA). Results: We found several circulating miRNAs differentially expressed in SpA patients reflecting the severity of axial involvement and/or disease activity. The decrease in circulating miR-145 in plasma of patients with ankylosing spondylitis 3 months of anti-TNF therapy predicted a good therapeutic response and low disease activity after a year of therapy. Circulating and intracellular expression of miR-125b in peripheral blood mononuclear cells (PBMC) was lower in treatment-naïve patients with early RA than in healthy controls. Baseline expression of miR-125 in PBMC predicted a (non)adequate therapeutic response. We also found the increased expression of miR-451 in PBMC in...

BACKGROUND: Juvenile idiopathic arthritis (JIA) is the most prevalent childhood rheumatic disease and significantly impacts a child’s well-being by potentially leading to disability and long-lasting effects. It consists of all forms of arthritis developing before the age of 16, therefore managing this disease is not simple. JIA can lead to a host of different medical problems over time and requires early attention and adequate treatment to prevent these long-term consequences. However, many children still experience pain after traditional treatment, indicating a need for alternative treatment modalities. Exercise therapy is one form of treatment that can potentially enhance a child’s quality of life. LITERATURE REVIEW FINDINGS: Multiple forms of exercise therapy have been shown to improve quality of life, functional ability and pain in patients with JIA. Exercise does not worsen disease activity, including the number of joints affected. While there are a limited number of studies in the JIA population, studies on patients with rheumatoid arthritis, a rheumatic disease diagnosed in adulthood, demonstrate the potential for exercise therapy to alter the pathophysiology of the disease and lead to better immune function. Exercise may have the ability to affect children with JIA in the same way as the two diseases share a similar pathophysiology. PROPOSED PROJECT: The goal of the proposed randomized control trial is to measure the impact of an exercise intervention on the quality of life of children with JIA, the effect exercise on participant immune function and variations in response between each subtype of JIA. Children will either complete high intensity interval walking training three times a week or no exercise intervention for 10 weeks. Various outcomes including quality of life, functional status, pain and fitness level will be measured before and after the intervention. Blood analysis to assess changes in immune function and further analysis between subtypes will also be conducted. CONCLUSIONS: The use of exercise therapy as a management tool for JIA should be considered earlier on in the disease course. It has not been found to worsen the disease and has produced increases in quality of life, functional status and pain. The benefits of this therapy are widespread and are not limited to healthy individuals. SIGNIFICANCE: This will be the first time these analyses will be performed and, if improvement is seen, this could help guide a physician’s disease management plan. Data from this study could provide information on how exercise modifies the disease and how to design more structured exercise programs appropriate to each subtype of JIA. Exercise may begin to be incorporated into the treatment plan for these children to increase disease remission rates, reduce the amount and severity of disease flares and provide both physical and psychological benefits.

Background: Osteoblasts participating in the inflammation regulation gradually obtain concerns. However, its role in joint inflammation of rheumatoid arthritis (RA) is largely unknown. Here, we investigated the role of osteoblastic pleckstrin homology domain-containing family O member 1 (PLEKHO1), a negative regulator of osteogenic lineage activity, in regulating joint inflammation in RA. Methods: The level of osteoblastic PLEKHO1 in RA patients and collagen-induced arthritis (CIA) mice was examined. The role of osteoblastic PLEKHO1 in joint inflammation was evaluated by a CIA mice model which was induced in osteoblast-specific Plekho1 conditional knockout mice and mice expressing high Plekho1 exclusively in osteoblasts, respectively. The effect of osteoblastic PLEKHO1 inhibition was explored in a CIA mice model. The mechanism of osteoblastic PLEKHO1 in regulating joint inflammation was performed by a series of in vitro studies. Results: PLEKHO1 was highly expressed in osteoblasts from RA patients and CIA mice. Osteoblastic Plekho1 deletion ameliorated joint inflammation, whereas overexpressing Plekho1 only within osteoblasts exacerbated local inflammation in CIA mice. PLEKHO1 was required for TNF receptor-associated factor 2 (TRAF2)-mediated the ubiquitination of receptor-interacting serine/threonine-protein kinase 1 (RIP1) to activate nuclear factor kappa-light-chain-enhancer of activated B (NF-kB) pathway for inducing inflammatory cytokines production in osteoblasts. Moreover, osteoblastic PLEKHO1 inhibition improved joint inflammation and attenuated bone formation reduction in CIA mice. Conclusions: These data strongly suggest that highly expressed PLEKHO1 in osteoblasts mediates joint inflammation in RA. Targeting osteoblastic PLEKHO1 may exert dual therapeutic action of alleviating joint inflammation and promoting bone repair in RA.

No description available.

The purpose of this project was to examine the effect of hypnosis as a treatment in the control of pain in a population of rheumatoid arthritic patients and further to examine any associated change in emotionality. Three groups of patients suffering from the pain of rheumatoid arthritis were selected. One group served as a control group. The other two groups served as a modified control group and as a treatment group, respectively. All three groups were pre, mid, and post-tested using the McGill Pah Questionnaire, the Minnesota Multiphasic Personality Inventory, the California Personality Inventory Well-Being scale items, and a check of their medication intake. The testing periods were before any treatment procedures were introduced, after a 6 week therapy involvement period for the modified control group and treatment group, and after another 6 week period with no further interaction of the patients with the therapists. The treatment group received hypnosis instruction for the treatment of pain, the modified control group received a ventilation or talk therapy, and the control group was not seen by any therapist. It was fond that self-hypnosis offers a viable and practical treatment technique to individuals in the control of their pain. individuals were not only able to reduce their perception of pain and its effect on their lives, but they were also able to be the ones in control of the process. Both the treatment group and the modified control group were able to achieve positive change in several emotional factors. The treatment group was able to achieve a more significant change and one that persisted after the therapy sessions were terminated. The members of the treatment group were thus able to increase their emotional functioning and decrease their dependency on medications. The treatment group was the only group able to decrease medication intake significantly thus gain indicating the importance of learning self-help procedure for controlling pain. It would seem from the results of this study that using self-hypnosis for pain control is useful and practical.

Bakgrund: Reumatoid artrit (RA) är en autoimmun sjukdom som påverkar leder, senor och skelettvävnad genom att den orsakar inflammation. Det finns evidens för ärftlighet och även immunologiska faktorer spelar en roll men varför sjukdomen utvecklas är ännu inte känd. Omvårdnad sker främst i form av utbildning om egenvård och träning samt medicinering. Syfte: Syftet var att beskriva vilka faktorer som påverkar livskvaliteten hos personer med Reumatoid Artrit. Metod: Arbetet är en litteraturöversikt. Urvalskriterierna var att artiklarna ska vara på engelska, publicerade inom de senaste fem åren (2016–2021), peer-reviewed och deltagare ska vara vuxna. De valda databaserna var PubMed och Cinahl complete. Databasernas fokusområden är omvårdnadsforskning och medicin vilket är relevant för det som eftersöks i arbetet. Sökmetoden var boolesk och sökorden var rheumatoid arthritis och quality of life. Artiklar som bedömts relevanta för att besvara syftet valdes ut. Resultat: Resultatet visar att de faktorer som kan påverka den mentala och fysiska livskvaliteten negativt hos personer med RA var smärta, depression, trötthet, sjukdomsaktivitet, övervikt, brist på sömn samt hög ålder. Kunskap om sjukdomen, inställning, stark identitet, hög motståndskraft samt psykologisk rådgivning, socialt stöd, träning, goda relationer, god ekonomi, hög utbildning och arbete sågs kunna påverka livskvaliteten positivt. Sammanfattning: RA påverkar personers livskvalitet i olika dimensioner på flera olika sätt. Sjukdomsaktivitet, information om sjukdomen och socialt stöd sågs vara några av de mest avgörande faktorerna för livskvaliteten. Som sjuksköterskor och omvårdnadsledare är det viktigt att undersöka faktorer som bidrar till bättre/sämre livskvalitet för att kunna främja patientens förmåga till egenvård. Sjuksköterskan bär ett ansvar för att säkra varje patients enskilda rätt till vård, vilket är en förutsättning för ett jämlikt samhälle. / Background: Rheumatoid arthritis (RA) is an autoimmune disease that affects joints, tendons and tissues by causing inflammation in them. There is evidence of the disease having hereditary and immunological factors that contribute to the emergence of Rheumatoid Arthritis, but the cause behind it is still unknown. Care is primarily focused on information about selfcare and exercise as well as medication. Aim: The aim was to describe the factors influencing the quality of life for people with Rheumatoid Arthritis. Method: This paper is a literature review. The inclusion criterias are that the articles are in English, published within the last five years (2016–2021), they are peer-reviewed and participants in studies are adults. The chosen databases were PubMed and Cinahl complete which both focus on nursing and medicine which are relevant for this review. The search method was boolean, and search words were rheumatoid arthritis and quality of life. The articles used for the assignment were chosen based on their abstract, how well the article could serve to answer the aim. Results: The results found that factors that can decrease the quality in life in people with Rheumatoid Arthritis is pain, depression, fatigue, disease activity, overweight, lack of sleep and old age. Knowledge about the disease, positive attitude, clear sense of identity, high resilience as well as therapy, social support, physical activity, marriage, good financial health, high education and employment was seen to improve the quality of life. Conclusion: RA affects people's quality of life in different dimensions and ways. Disease-activity, information about the disease and social support were seen as some of the most crucial factors in determining the quality of life. As nurses and leading care-givers it is important to know what factors can contribute a better/worse quality of life in order to encourage selfcare. Nurses carry a responsibility to ensure every patient’s right to medical treatment and care which is a prerequisite for an equal society.