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ID PMID Title PublicationDate abstract
22389802 The contribution of four immunogenetic markers for predicting persistent activity in patie 2011 We assessed the contribution of four baseline markers-HLA-DRB1 shared epitope (SE), -308 tumor necrosis factor α gene promoter polymorphism, rheumatoid factor, and anticitrullinated peptide antibodies-for predicting persistent activity (DAS28 score ≥2.6) after one year of followup in a cohort of 201 patients with recent-onset rheumatoid arthritis (RA) or undifferentiated arthritis (UA) aged 16 years or older who had a 4-week to 12-month history of swelling of at least two joints. Patients had not been previously treated with corticosteroids or disease-modifying antirheumatic drugs (DMARD). In the best logistic regression model, only two variables were retained: SE positivity and number of DMARD administered (area under the curve = 76.4%; 95% CI: 69.2%, 84.4%; P < 0.001). The best linear regression model also included these two variables, explaining only 22.5% of the variability of DAS28 score. In this study, given an equal number of DMARD administered, the probability of persistent activity in patients with recent-onset RA or UA was significantly influenced by SE presence.
21789619 IgG RF and anti-CCP2 antibody can be positive in undifferentiated arthritis due to strepto 2012 Sep Anti-CCP2 antibody and rheumatoid (RF) tests are used for the diagnosis of rheumatoid arthritis (RA). Out of these two, anti-CCP2 antibody is supposed to be more specific for RA. Aim of the study was to present 33 cases of undifferentiated arthritis (UA) in which features of RA were not present, but anti-CCP2 antibody was positive. Out of the 33 cases of UA, 19 had well-known disease like hyperthyroidism, hypothyroidism, tubercular arthritis, traumatic arthritis, pneumonia with arthritis, varicose vein with pain in legs, cervical spondylitis and SSA. The duration of disease was more than one year in 67.86% cases. Majority of the patients were females (63.64%). Knee joint involvement was seen in maximum number (i.e. 20 cases). All 33 cases were positive for anti-CCP2 Ab. Maximum number of cases (78.78%) had involvement of one or two joints. CRP positivity was seen in 23.07% cases. Morning stiffness was present in (36.36%) cases, while swelling of the joint was present in 33.33% cases. In 16 cases, only serum sample was available for further analysis. About 62.5% cases showed IgG RF positivity. Antitubercular IgM and IgG were detected in 18.75% cases; ASO was elevated in 12.5% cases, and HBs Ag was positive in 6.25% cases. None of the controls (30 cases) were positive for these infections, anti-CCP2 antibody or RF. Thus, our study concludes that chronic infections like streptococcus, hepatitis B, tuberculosis and autoimmune thyroid diseases can produce raised levels of anti-CCP2 antibody and IgG RF.
23006786 Selective delivery of interleukine-1 receptor antagonist to inflamed joint by albumin fusi 2012 Sep 25 BACKGROUND: Interleukin-1 receptor antagonist, a cytokine that is highly therapeutic to rheumatoid arthritis and several other inflammatory diseases, exhibits rapid blood clearance and poor retention time on the target in clinical application due to its small size and lack of specificity to target tissue. Albumin has been widely employed as macromolecular carrier for drug delivery purpose to extend the plasma half-life of therapeutic molecules and has been shown to selectively accumulate and to be metabolized in the inflamed joints of patients with rheumatoid arthritis. This suggests that genetic fusion of IL-1ra to albumin can probably overcome the drawbacks of in vivo application of IL-1ra. RESULT: A recombinant protein, engineered by fusing human serum albumin (HSA) to the carboxyl terminal of IL-1ra, was produced in Pichia pastoris and purified to homogeneity. The fusion protein retained the antagonist activity of IL-1ra and had a plasma half-life of approximately 30-fold more than that of IL-1ra in healthy mice. In vivo bio-distribution studies demonstrated that the fusion protein selectively accumulated in arthritic paws for a long period of time in mice with collagen-induced arthritis, showing low uptake rates in normal organs such as liver, kidney, spleen and lung in contrast to IL-1ra alone. Moreover, this fusion protein was able to significantly improve the therapeutic efficacy of IL-1ra in collagen-induced arthritis mouse model. CONCLUSIONS: The fusion protein described here, able to selectively deliver IL-1ra to inflamed tissue, could yield important contributions for the therapy of rheumatoid arthritis and other inflammatory diseases.
21947372 QT dispersion and cardiac involvement in patients with juvenile idiopathic arthritis. 2012 Oct Juvenile idiopathic arthritis (JIA) is the commonest cause of chronic inflammatory arthritis in childhood. Cardiac involvement as pericarditis, myocarditis and valvular disease is known to occur in patients with JIA (JIA), as it does in adults with rheumatoid arthritis. There are, however, few descriptions concerning systolic and diastolic functions of the left ventricle (LV) in children with JIA. QT dispersion (QTd) is simple noninvasive arrhythmogenic marker that can be used to assess homogeneity of cardiac repolarization and which has not been studied in JIA patients before. A recent study found that rheumatoid arthritis patients had an abnormally longer QTd and corrected QT (cQTd) dispersion, markers for ventricular arrhythmogenicity. This study assessed QTd and cQTd and their relation with systolic and diastolic function of the LV in a group of children with JIA. We performed electrocardiography and Doppler echocardiography on patients and controls. Maximum QT (QTmax), minimum QT (QTmin), QTd, corrected QT, maximum corrected QT (cQTmax), minimum corrected QT (cQTmin) and cQTd intervals were measured from standard 12-lead electrocardiography. No statistically significant differences were found between the groups in QTd and cQTd. Among the diastolic parameters, increased late flow velocity, decreased early flow velocity and prolonged isovolumic relaxation time reflected an abnormal relaxation form of diastolic dysfunction. During 12 months of follow-up, no ventricular arrhythmias were documented in either group.
22135702 Mononuclear Phagocytes in Rheumatoid Arthritis Patients and their Relatives - Family Simil 2011 The aim of this work was to study the peripheral blood monocyte functions in patients with advanced RA and their predisposed to RA relatives in comparison with those in women, not hereditary tainted with autoimmune diseases (donors). In groups comprising 24 RA patients, 24 relatives, and 24 donors the following monocyte functions were assessed: engulfment and digestion (radioisotope method); release of lysosomal glucuronidase in response to opsonized zymosan (fluorescent method); reactive oxygen species (ROS) generation (chemiluminescence), and serum levels of proinflammatory cytokines (ELISA). The monocyte specific feature in patients and their relatives is chiefly extracellular digestion due to the delayed engulfment. The digestive activity, probably inhibited in relatives, is increased in advanced RA. ROS generation by the cells and serum levels of TNF-alpha and IL-1-beta are abundant both in the patients and their relatives. High levels of pro-inflammatory cytokines, presumably, of monocyte origin, and increased levels of stimulated ROS generation may be due to the priming and prolonged activation of monocytes in relatives. CONCLUSION: We show for the first time that the functioning of circulating mononuclear phagocytes in the assumed to be healthy predisposed to RA individuals differs from that in the healthy people not hereditary tainted with autoimmune diseases and in general resembles the functioning of the cells in the patients with advanced RA.
23028409 The Therapeutic Potential for PI3K Inhibitors in Autoimmune Rheumatic Diseases. 2012 The class 1 PI3Ks are lipid kinases with key roles in cell surface receptor-triggered signal transduction pathways. Two isoforms of the catalytic subunits, p110γ and p110δ, are enriched in leucocytes in which they promote activation, cellular growth, proliferation, differentiation and survival through the generation of the second messenger PIP3. Genetic inactivation or pharmaceutical inhibition of these PI3K isoforms in mice result in impaired immune responses and reduced susceptibility to autoimmune and inflammatory conditions. We review the PI3K signal transduction pathways and the effects of inhibition of p110γ and/or p110δ on innate and adaptive immunity. Focusing on rheumatoid arthritis and systemic lupus erythematosus we discuss the preclinical evidence and prospects for small molecule inhibitors of p110γ and/or p110δ in autoimmune disease.
27790011 The role of extended scope physiotherapists in managing patients with inflammatory arthrop 2012 OBJECTIVES: To review the literature to identify whether, and how, physiotherapists working in extended scope of practice (ESP) engage with patients with inflammatory arthropathies. Measures of effectiveness of ESP were particularly sought. METHODS: A comprehensive library database search was conducted to identify English language studies published in full text in peer-reviewed journals during the years 2002-2012. Studies were allocated into the National Health and Medical Research Council hierarchy of evidence, but were not critically appraised. Data was extracted on conditions treated, ESP roles and responsibilities, and effectiveness. Data was analyzed and reported descriptively. RESULTS: We identified 123 studies, and included four. All were low hierarchy (highest being one level III_2 study). Commonly reported conditions were rheumatoid arthritis and ankylosing spondylitis. Information was provided on activities of role extension, such as triaging patients, monitoring and recommending changes to medications, referring to other health and medical professionals, and ordering and interpreting imaging. There was blurring between ESP and non-ESP roles. No study reported measures of effectiveness. CONCLUSION: There are descriptors of ESP physiotherapy activities, but no evidence of effectiveness of ESP physiotherapy in managing patients with inflammatory arthropathies.
23271168 Validation of different sets of criteria for the diagnosis of Sjögren's syndrome in Japan 2013 Mar OBJECTIVE: To validate the revised Japanese Ministry of Health criteria for the diagnosis of Sjögren's syndrome (SS) (JPN) (1999), The American-European Consensus Group classification criteria for SS (AECG) (2002), and American College of Rheumatology classification criteria for SS (ACR) (2012). METHODS: The study subjects were 694 patients with SS or suspected SS who were followed-up in June 2012 at ten hospitals that form part of the Research Team for Autoimmune Diseases, The Research Program for Intractable Disease by the Ministry of Health, Labor and Welfare (MHLW). All patients had been checked for all four criteria of the JPN (pathology, oral, ocular, anti-SS-A/SS-B antibodies). We studied the clinical diagnosis made by the physician in charge and the satisfaction of the above criteria. RESULTS: Of the 694 patients, 499 patients did not have other connective tissue diseases (CTDs). SS was diagnosed in 476 patients (primary SS in 302, secondary SS in 174), whereas non-SS was diagnosed in 218 patients (without other CTDs in 197, with other CTDs in 21) by the physician in charge. The sensitivities of JPN, AECG, and ACR in the diagnosis of all forms of SS (both primary and secondary SS) were 79.6, 78.6, and 77.5 %, respectively, with respective specificities of 90.4, 90.4, and 83.5 %. The sensitivities of the same systems in the diagnosis of primary SS were 82.1, 83.1, and 79.1 %, respectively, with specificities of 90.9, 90.9, and 84.8 %, respectively. The sensitivities of the same systems in the diagnosis of secondary SS were 75.3, 70.7, and 74.7 %, respectively, with specificities of 85.7, 85.7, and 71.4 %, respectively. CONCLUSION: The sensitivity of JPN to all forms of SS and secondary SS, the sensitivity of AECG to primary SS, and the specificities of JPN and AECG for all forms of SS, primary SS, and secondary SS were highest in the diagnosis of SS in Japanese patients. These results indicate that the JPN criteria for the diagnosis of SS in Japanese patients are superior to ACR and AECG.
23150824 Rheumatoid arthritis and primary biliary cirrhosis: cause, consequence, or coincidence? 2012 Primary biliary cirrhosis (PBC) is a progressive cholestatic liver disease characterized serologically by cholestasis and the presence of high-titre antimitochondrial antibodies and histologically by chronic nonsuppurative cholangitis and granulomata. PBC patients often have concomitant autoimmune diseases, including arthropathies. This raises the question as to whether there are shared features in the pathogenesis of those diseases with the pathogenesis of PBC. Epidemiological and large case studies have indicated that although the incidence of rheumatoid arthritis (RA) is not significantly raised in PBC patients, there appears to be a higher rate of RA in PBC patients and their relatives. Genetic studies have demonstrated that several genes implicated in PBC have also been implicated in RA. Epigenetic studies provided a wealth of data regarding RA, but the findings on epigenetic changes in PBC are very limited. As well, certain infectious agents identified in the pathogenesis of PBC may also play a role in the pathogenesis of RA. These data suggest that although RA is not significantly present in PBC, some individuals with certain genetic traits and environmental exposures may develop both conditions. This concept may also apply to other concomitant diseases found in PBC patients.
23209898 Possible influence of resistance to malaria in clinical presentation of rheumatoid arthrit 2012 Rheumatoid arthritis (RA) is a common autoimmune disease that affects all ethnic groups. Genetic factors, mainly HLA alleles, are highly associated with increased risk to develop RA. However, there are few available data about the role of these genetic polymorphisms in the prevalence or severity of RA in the Afrodescendant population, who have evolutionarily and by natural selection developed mutations that allowed them to acquire resistance to infectious diseases like malaria. Some of the mechanisms, by which this resistance was developed as a product of natural selection, are involved in different forms of immunological response, many of them of a well-known importance in the pathophysiology of RA. This paper focuses on presenting the known mechanisms of resistance to malaria and their possible contribution to the pathophysiology of RA, including "loss-of-function" mutations, lack of expression of chemokine receptors, decrease of immune complexes clearance by asplenia, or increase of immune reactivity mediated by B cells, among other mechanisms in this special group of patients.
28072070 A boost in awareness. 2012 Oct 10 Every year on October 12, specialists in musculoskeletal health mark World Arthritis Day. This is an important date for raising awareness of this group of diseases, with charities invariably bumping elbows as we rush to publish research and share insights.
23257839 Lymphomatoid papulosis in a patient treated with adalimumab for juvenile rheumatoid arthri 2012 Anti-tumor necrosis factor (TNF) agents are now well regarded as highly effective treatment modalities for multiple immunologically mediated diseases, including rheumatoid arthritis, Crohn's disease and psoriasis. The mechanism of action for this particular class of medications involves the blockade of multiple intracellular signaling pathways originating from TNF-α, ultimately inducing a generalized immunosuppressed state. In fact, several cases of lymphomas have been reported in patients treated with anti-TNF-α agents, though it has been difficult to prove any degree of causality. Herein, we described a patient who developed lymphomatoid papulosis after being treated with adalimumab, whereby a clear causality could be established.
22385519 Diabetes, coeliac disease, multiple sclerosis and chronic arthritis in first-degree relati 2012 Jul AIM: To evaluate the occurrence of autoimmune diseases in first-degree relatives of children with juvenile idiopathic arthritis (JIA) and to compare the figures with published population data. MATERIALS AND METHODS: Families of the 362 children with recently diagnosed JIA admitted to Rheumatism Foundation Hospital, Finland, from 1996 to 2001 were contacted by questionnaires regarding autoimmune diseases in family members. Data were collected on type 1 diabetes, coeliac disease, multiple sclerosis and chronic arthritis, consisting mainly of JIA, rheumatoid arthritis, spondyloarthropathy or psoriatic arthritis. RESULTS: In all, 21.4% of the 355 families with a patient with JIA had members with type 1 diabetes, coeliac disease, multiple sclerosis or chronic arthritis. Thirty-three mothers and 23 fathers had type 1 diabetes, coeliac disease, multiple sclerosis or chronic arthritis in 15.2% (95% CI 11.6-19.4) of the families, and 23 mothers and 15 fathers had chronic arthritis in 10.7% (95% CI 7.7-14.5) of the families. When compared with available research data, the prevalences of rheumatoid arthritis, spondyloarthropathy, psoriatic arthritis, paediatric type 1 diabetes and JIA (in siblings) were increased in JIA families. Coeliac disease was as prevalent as in the population. CONCLUSION: Autoimmune diseases cluster in families with a child with JIA.
31643485 Interleukin Receptor Antagonists. 2012 Interleukin-1 (IL-1) and interleukin-6 (IL-6) are potent pro-inflammatory cytokines that are synthesized by many cells throughout the body and play major roles in inflammation and cell damage associated with excessive inflammation. IL-1 is increased in inflammatory conditions and appears to play a role in autoinflammatory and autoimmune diseases. Blockage of IL-1 production or inhibition of its activity decreases inflammatory responses and may be beneficial in many diseases associated with a heightened immune response such as rheumatoid arthritis, ankylosing spondylitis, gouty arthritis, osteoarthritis, juvenile idiopathic arthritis, Still disease, Familial Mediterranean fever, periodic fever and periodic syndromes. Blockage of IL-6 activity has similar clinical activity, although it has been assessed largely in inflammatory arthritidies. At least three IL-1 receptor antagonists have been approved for use in autoinflammatory conditions in the United States. In addition, a monoclonal antibody to the IL-6 receptor has been developed and shown to have beneficial effects in rheumatoid arthritis. The interleukin receptor antagonists have been associated with rare instances of clinically apparent liver injury that is generally mild and resolves with discontinuation. The interleukin receptor antagonists discussed in LiverTox include the following:
23193471 Cardiovascular disease in rheumatoid arthritis: a systematic literature review in latin am 2012 Background. Cardiovascular disease (CVD) is the major predictor of poor prognosis in rheumatoid arthritis (RA) patients. There is an increasing interest to identify "nontraditional" risk factors for this condition. Latin Americans (LA) are considered as a minority subpopulation and ethnically different due to admixture characteristics. To date, there are no systematic reviews of the literature published in LA and the Caribbean about CVD in RA patients. Methods. The systematic literature review was done by two blinded reviewers who independently assessed studies for eligibility. The search was completed through PubMed, LILACS, SciELO, and Virtual Health Library scientific databases. Results. The search retrieved 10,083 potential studies. A total of 16 articles concerning cardiovascular risk factors and measurement of any cardiovascular outcome in LA were included. The prevalence of CVD in LA patients with RA was 35.3%. Non-traditional risk factors associated to CVD in this population were HLA-DRB1 shared epitope alleles, rheumatoid factor, markers of chronic inflammation, long duration of RA, steroids, familial autoimmunity, and thrombogenic factors. Conclusions. There is limited data about CVD and RA in LA. We propose to evaluate cardiovascular risk factors comprehensively in the Latin RA patient and to generate specific public health policies in order to diminish morbi-mortality rates.
23320137 Potential of (18)F-FDG-PET as a valuable adjunct to clinical and response assessment in rh 2012 Dec 28 AIM: To evaluate the role of fluorine-18-labeled fluorodeoxyglucose positron emission tomography ((18)F-FDG PET) in various rheumatic diseases and its potential in the early assessment of treatment response in a limited number of patients. METHODS: This study involved 28 newly diagnosed patients, of these 17 had rheumatoid arthritis (RA) and 11 had seronegative spondyloarthropathy (SSA). In the SSA group, 7 patients had ankylosing spondylitis, 3 had psoriatic arthritis, and one had non-specific SSA. Patients with RA were selected as per the American College of Rheumatology criteria. One hour after FDG injection, a whole body PET scan was performed from the skull vertex to below the knee joints using a GE Advance dedicated PET scanner. Separate scans were acquired for both upper and lower limbs. Post-treatment scans were performed in 9 patients in the RA group (at 6-9 wk from baseline) and in 1 patient with psoriatic arthropathy. The pattern of FDG uptake was analysed visually and quantified as maximum standardized uptake value (SUVmax) in a standard region of interest. Metabolic response on the scan was assessed qualitatively and quantitatively and was correlated with clinical assessment. RESULTS: The qualitative FDG uptake was in agreement with the clinically involved joints, erythrocyte sedimentation rate, C-reactive protein values and the clinical assessment by the rheumatologist. All 17 patients in the RA group showed the highest FDG avidity in painful/swollen/tender joints. The uptake pattern was homogeneous, intense and poly-articular in distribution. Hypermetabolism in the regional nodes (axillary nodes in the case of upper limb joint involvement and inguinal nodes in lower limb joints) was a constant feature in patients with RA. Multiple other extra-articular lesions were also observed including thyroid glands (in associated thyroiditis) and in the subcutaneous nodules. Treatment response was better appreciated using SUVmax values than visual interpretation, when compared with clinical evaluation. Four patients showed a favourable response, while 3 had stable disease and 2 showed disease progression. The resolution of regional nodal uptake (axillary or inguinal nodes based on site of joint involvement) in RA following disease modifying anti-rheumatoid drugs was noteworthy, which could be regarded as an additional parameter for identifying responding patients. In the SSA group, uptake in the affected joint was heterogeneous, low grade and non-symmetrical. In particular, there was intense tendon and muscular uptake corresponding to symptomatic joints. The patients with psoriatic arthritis showed intense FDG uptake in the joints and soft tissue. CONCLUSION: (18)F-FDG PET accurately delineates the ongoing inflammatory activity in various rheumatic diseases (both at articular and extra-articular sites) and relates well to clinical symptoms. Different metabolic patterns on FDG-PET scanning in RA and SSA can have important implications for their diagnosis and management in the future with the support of larger studies. FDG-PET molecular imaging is also a sensitive tool in the early assessment of treatment response, especially when using quantitative information. With these benefits, FDG-PET could play a pivotal clinical role in the management of inflammatory joint disorders in the future.
20035333 The effects of PDL-Ig on collagen-induced arthritis. 2011 Apr Programmed death ligand (PDL) is a new member of the B7 family of costimulatory molecules that specifically interacts with programmed death 1 (PD-1) expressed on activated T cells, B cells, and myeloid cells. Collagen II (CII)-induced arthritis (CIA) is an experimental model of arthritis that has been used to dissect the pathogenesis of human rheumatoid arthritis. In this study, we have investigated the effects of PDL-Ig on CIA. Administration of PDL-Ig significantly ameliorated the disease as assessed by clinical arthritis score and histology in the joints. Expression of proinflammatory cytokines, such as IL-17 and IL-23, in the serum was reduced by PDL-Ig treatment. These results showed a beneficial effect of PDL-Ig on CIA through anti-inflammatory actions and inhibition of cell proliferation in response to CII, suggesting that the PD-1-PDL pathway may be involved in the pathogenesis of CIA, and thus PDL-Ig may be a useful therapy for the improvement of human rheumatoid arthritis.
22906101 Cartilage oligomeric matrix protein specific antibodies are pathogenic. 2012 Aug 20 INTRODUCTION: Cartilage oligomeric matrix protein (COMP) is a major non-collagenous component of cartilage. Earlier, we developed a new mouse model for rheumatoid arthritis using COMP. This study was undertaken to investigate the epitope specificity and immunopathogenicity of COMP-specific monoclonal antibodies (mAbs). METHODS: B cell immunodominant regions on the COMP molecule were measured with a novel enzyme-linked immunosorbent assay using mammalian expressed full-length mouse COMP as well as a panel of recombinant mouse COMP fragments. 18 mAbs specific to COMP were generated and the pathogenicity of mAbs was investigated by passive transfer experiments. RESULTS: B cell immunodominant epitopes were localized within 4 antigenic domains of the COMP but with preferential response to the epidermal growth factor (EGF)-like domain. Some of our anti-COMP mAbs showed interactions with the native form of COMP, which is present in cartilage and synovium. Passive transfer of COMP-specific mAbs enhanced arthritis when co-administrated with a sub-arthritogenic dose of a mAb specific to collagen type II. Interestingly, we found that a combination of 5 COMP mAbs was capable of inducing arthritis in naive mice. CONCLUSIONS: We have identified the specificities of mAbs to COMP and their contribution to the development of arthritis. These findings will further improve our understanding of the autoantibody mediated immunopathologies occurring widely in rheumatoid arthritis (RA), as well as in other autoimmune disorders.
23264777 Combined anti-tumor necrosis factor-α therapy and DMARD therapy in rheumatoid arthritis p 2012 Periodic assessment of gene expression for diagnosis and monitoring in rheumatoid arthritis (RA) may provide a readily available and useful method to detect subclinical disease progression and follow responses to therapy with disease modifying anti-rheumatic agents (DMARDs) or anti-TNF-α therapy. We used quantitative real-time PCR to compare peripheral blood gene expression profiles in active ("unstable") RA patients on DMARDs, stable RA patients on DMARDs, and stable RA patients treated with a combination of a disease-modifying anti-rheumatoid drug (DMARD) and an anti-TNF-α agent (infliximab or etanercept) to healthy human controls. The expression of 48 inflammatory genes were compared between healthy controls (N = 122), unstable DMARD patients (N = 18), stable DMARD patients (N = 26), and stable patients on combination therapy (N = 20). Expression of 13 genes was very low or undetectable in all study groups. Compared to healthy controls, patients with unstable RA on DMARDs exhibited increased expression of 25 genes, stable DMARD patients exhibited increased expression of 14 genes and decreased expression of five genes, and combined therapy patients exhibited increased expression of six genes and decreased expression of 10 genes. These findings demonstrate that active RA is associated with increased expression of circulating inflammatory markers whereas increases in inflammatory gene expression are diminished in patients with stable disease on either DMARD or anti-TNF-α therapy. Furthermore, combination DMARD and anti-TNF-α therapy is associated with greater reductions in circulating inflammatory gene expression compared to DMARD therapy alone. These results suggest that assessment of peripheral blood gene expression may prove useful to monitor disease progression and response to therapy.
22105703 Animal models in autoimmune diseases: lessons learned from mouse models for Sjögren's syn 2012 Feb The mouse model is the one of the most frequently used and well-established animal models, and is currently used in many research areas. To date, various mouse models have been utilized to elucidate underlying causes of multifactorial autoimmune conditions, including pathological immune components and specific signaling pathways. This review summarizes the more recent mouse models for Sjögren's syndrome, a systemic autoimmune disease characterized by lymphocytic infiltration in the exocrine glands, such as the salivary and lacrimal glands, and loss of secretory function, resulting in dry mouth and dry eyes in patients. Although every Sjögren's syndrome mouse model resembles the major symptoms or phenotypes of Sjögren's syndrome conditions in humans, the characteristics of each model are variable. Moreover, to date, there is no single mouse model that can completely replicate the human conditions. However, unique features of each mouse model provide insights into the roles of potential etiological and immunological factors in the development and progression of Sjögren's syndrome. Here, we will overview the Sjögren's syndrome mouse models. Lessons from these mouse models will aid us to understand underlying immune dysregulation in autoimmune diseases in general, and will guide us to direct future research towards appropriate diagnostic and therapeutic strategies.