Displaying publications 21 - 40 of 64 in total

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  1. Palazzo L, Lindblom J, Kihlgren Olsson E, Nikiphorou E, Wincup C, Saha S, et al.
    Rheumatol Int, 2024 Oct;44(10):1923-1933.
    PMID: 39138675 DOI: 10.1007/s00296-024-05682-6
    OBJECTIVE: To determine the occurrence of breakthrough COVID-19 infections (BIs) in patients with systemic lupus erythematosus (SLE) compared with patients with other rheumatic autoimmune diseases (rAIDs), patients with non-rheumatic autoimmune diseases (nrAIDs), and healthy controls (HCs).

    METHODS: The study was based on data from 7035 fully vaccinated respondents to the online COVAD questionnaire with SLE (N = 852), rAIDs (N = 3098), or nrAIDs (N = 414), and HCs (N = 2671). BI was defined as COVID-19 infection occurring in individuals vaccinated with ≥ 2 doses (or 1 dose of J&J) ≥ 14 days after vaccination and not after 6 months since the last vaccine dose. Data were analysed using linear and logistic regression models.

    RESULTS: A total of 91/852 (10.7%) SLE patients reported at least one BI. The frequency of BIs in SLE patients was comparable to that among HCs (277/2671; p = 0.847) and patients with nrAID (39/414; p = 0.552) but higher than that among patients with other rAIDs (235/3098; p = 0.005). No demographic factors or treatments were associated with BIs in SLE patients (p ≥ 0.05 for all). Joint pain was more frequent in SLE patients than in HCs (odds ratio [OR]: 3.38; 95% confidence interval [CI]: 1.89-6.04; p 

    Matched MeSH terms: Autoimmune Diseases/epidemiology
  2. Pan SY, Chia YC, Yee HR, Fang Cheng AY, Anjum CE, Kenisi Y, et al.
    Future Sci OA, 2020 Oct 29;7(2):FSO648.
    PMID: 33437514 DOI: 10.2144/fsoa-2020-0142
    The immune system is a complex network of specialized cells and organs that recognises and reacts against foreign pathogens while remaining unresponsive to host tissues. This ability to self-tolerate is known as immunological tolerance. Autoimmune disease occurs when the immune system fails to differentiate between self and non-self antigens and releases autoantibodies to attack our own cells. Anti-idiotypic (anti-ID) antibodies are important in maintaining a balanced idiotypic regulatory network by neutralising and inhibiting the secretion of autoantibodies. Recently, anti-ID antibodies have been advanced as an alternative form of immunotherapy as they can specifically target autoantibodies, cause less toxicity and side effects, and could provide long-lasting immunity. This review article discusses the immunomodulatory potential of anti-ID antibodies for the treatment of autoimmune diseases.
    Matched MeSH terms: Autoimmune Diseases
  3. McShane CM, Murray LJ, Landgren O, O'Rorke MA, Korde N, Kunzmann AT, et al.
    Cancer Epidemiol Biomarkers Prev, 2014 Feb;23(2):332-42.
    PMID: 24451437 DOI: 10.1158/1055-9965.EPI-13-0695
    BACKGROUND: Several observational studies have investigated autoimmune disease and subsequent risk of monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma. Findings have been largely inconsistent and hindered by the rarity and heterogeneity of the autoimmune disorders investigated. A systematic review of the literature was undertaken to evaluate the strength of the evidence linking prior autoimmune disease and risk of MGUS/multiple myeloma.

    METHODS: A broad search strategy using key terms for MGUS, multiple myeloma, and 50 autoimmune diseases was used to search four electronic databases (PubMed, Medline, Embase, and Web of Science) from inception through November 2011.

    RESULTS: A total of 52 studies met the inclusion criteria, of which 32 were suitably comparable to perform a meta-analysis. "Any autoimmune disorder" was associated with an increased risk of both MGUS [n = 760 patients; pooled relative risk (RR) 1.42; 95% confidence interval (CI), 1.14-1.75] and multiple myeloma (n>2,530 patients; RR 1.13, 95% CI, 1.04-1.22). This risk was disease dependent with only pernicious anemia showing an increased risk of both MGUS (RR 1.67; 95% CI, 1.21-2.31) and multiple myeloma (RR 1.50; 95% CI, 1.25-1.80).

    CONCLUSIONS: Our findings, based on the largest number of autoimmune disorders and patients with MGUS/multiple myeloma reported to date, suggest that autoimmune diseases and/or their treatment may be important in the etiology of MGUS/multiple myeloma. The strong associations observed for pernicious anemia suggest that anemia seen in plasma cell dyscrasias may be of autoimmune origin.

    IMPACT: Underlying mechanisms of autoimmune diseases, general immune dysfunction, and/or treatment of autoimmune diseases may be important in the pathogenesis of MGUS/multiple myeloma.

    Matched MeSH terms: Autoimmune Diseases/immunology*; Autoimmune Diseases/epidemiology
  4. Latiff AH, Kerr MA
    Ann. Clin. Biochem., 2007 Mar;44(Pt 2):131-9.
    PMID: 17362578 DOI: 10.1258/000456307780117993
    IgA deficiency is the most common primary immunoglobulin deficiency. The prevalence in Caucasians is around one in 500, whereas in some Asian populations it is very uncommon. Most individuals with IgA deficiency are clinically asymptomatic. Those with symptoms of immunodeficiency have predominantly sinopulmonary or gastrointestinal infections, which are more severe when associated with IgG2, IgG4 or specific antibody deficiency. IgA deficiency is believed to be one end of a spectrum of immunodeficiency with common variable immunodeficiency at the most severe end. Although primary IgA deficiency is the most commonly encountered form, secondary deficiencies due to drugs or viral infections are recognized. IgA deficiencies can be partial or transient. Primary IgA deficiency is caused by a defect of terminal lymphocyte differentiation, which leads to underproduction of serum and mucosal IgA; affected individuals have normal IgA genes. A number of non-immunoglobulin genes have been implicated in IgA deficiency. There have been many diseases reported in association with IgA deficiency, particularly autoimmune diseases. The most common association is with coeliac disease (CD), which has special significance since CD is usually diagnosed by detection of specific IgA antibodies that are obviously lacking in IgA deficiency. There is no specific treatment for patients with symptomatic IgA deficiency. Antibiotics are prescribed in those with acute infections. A significant proportion of IgA-deficient individuals are reported to have anti-IgA antibodies in their serum. Although blood or blood products given to IgA-deficient individuals can lead to severe, even fatal, transfusion reactions, such reactions are rare.
    Matched MeSH terms: Autoimmune Diseases/immunology; Autoimmune Diseases/metabolism
  5. Wah-Kheong C, Jaganathan V, Sanjiv M
    Turk J Gastroenterol, 2012;23(5):599-603.
    PMID: 23161309
    Autoimmune hepatitis is an inflammatory condition of the liver that can lead to significant morbidity and mortality. Corticosteroids with or without azathioprine have been shown to improve outcome and are the current standard of care in autoimmune hepatitis patients. However, long-term use of corticosteroids and use of azathioprine could be associated with significant adverse effects that prevent their continued use at optimal dosages or may even require complete cessation. We present a patient with autoimmune liver cirrhosis who was intolerant of corticosteroid and azathioprine, who was successfully treated with cyclosporine. To our knowledge, cyclosporine use has not been reported previously in autoimmune cirrhosis, although it has been used in autoimmune hepatitis patients with reported success and good tolerability. We conclude that cyclosporine seems to be an effective alternative to azathioprine as a steroid-sparing agent in both non-cirrhotic and cirrhotic autoimmune hepatitis.
    Matched MeSH terms: Autoimmune Diseases/drug therapy*; Autoimmune Diseases/immunology
  6. Yang Y, Li X, Li B, Mu L, Wang J, Cheng Y, et al.
    Immunol Invest, 2021 Feb;50(2-3):184-200.
    PMID: 32208776 DOI: 10.1080/08820139.2020.1718693
    BACKGROUND: Tumor necrosis factor superfamily member 4 (TNFSF4) has significant role in modulating autoimmune diseases (ADs) and single nucleotide polymorphism (SNP) is also related with the susceptibility to some diseases. So a meta-analysis aimed at systematically assessing the associations between TNFSF4 polymorphisms (rs2205960 G > A, rs704840 T > G and rs844648 G > A) and ADs risk was performed in Asians.

    METHODS: Total 14 eligible articles published before March 2019 involving 35 studies, of which 21 studies (16,109 cases and 26,378 controls) for rs2205960 G > A, 8 studies (2,424 cases and 3,692 controls) for rs704840 T > G, and 6 studies (3,839 cases and 5,867 controls) for rs844648 G > A were included. Effects of the three respective polymorphisms on the susceptibility to ADs were estimated by pooling the odds ratios (ORs) with their corresponding 95% confidence interval (95% CI) in allelic, dominant, recessive, heterozygous and homozygous models.

    RESULTS: The overall analysis revealed that all the rs2205960 G > A, rs704840 T > G and rs844648 G > A polymorphisms could increase the risk of ADs in allelic, dominant, recessive, heterozygous and homozygous models. Furthermore, subgroup analysis showed that both rs2205960 G > A and rs704840 T > G were significantly associated with the susceptibility to systemic lupus erythematosus (SLE). What's more, statistically significant association between rs2205960 G > A polymorphism and primary Sjögren's syndrome (pSS) susceptibility was also observed in allelic, dominant and heterozygous models.

    CONCLUSIONS: This current meta-analysis suggested that all of the three TNFSF4 polymorphisms may be associated with ADs susceptibility in Asians.

    Matched MeSH terms: Autoimmune Diseases/genetics*; Autoimmune Diseases/epidemiology
  7. Yow HY, Ikawati M, Siswanto S, Hermawan A, Rahmat AK, Tan JS, et al.
    Pharmacogenomics, 2024;25(5-6):259-288.
    PMID: 38884938 DOI: 10.1080/14622416.2024.2344430
    This scoping review explores the impact of genetic polymorphisms on the pharmacokinetics and treatment responses of mycophenolic acid (MPA), an immunosuppressant. The study includes 83 articles from 1226 original studies, focusing on transplantation (n = 80) and autoimmune disorders (n = 3). Genetic variants in uridine 5'-diphospho-glucuronosyltransferase (UGT1A9, UGT1A8 and UGT2B7) and transmembrane transporters (ABCC2, SLCO1B1, SLCO1B3 and ABCB1) significantly affected MPA's pharmacokinetics and susceptibility to its adverse effect. Whereas variants in several genes including UGT1A9, UGT2B7, IMPDH1 and IMPDH2 have been associated with a higher risk of transplant rejection. However, there is a lack of studies on MPA's impact on autoimmune disorders and limited research on the Asian population. The findings underscore the need for further research on MPA's impact across different populations and diseases, particularly among other Asian ethnic groups, to advance personalized medicine in MPA therapy.
    Matched MeSH terms: Autoimmune Diseases/drug therapy; Autoimmune Diseases/genetics
  8. Okuda K, Fu HY, Matsuzaki T, Araki R, Tsuchida S, Thanikachalam PV, et al.
    PLoS One, 2016;11(8):e0160944.
    PMID: 27501378 DOI: 10.1371/journal.pone.0160944
    Immunosuppressive agents are used for the treatment of immune-mediated myocarditis; however, the need to develop a more effective therapeutic approach remains. Nano-sized liposomes may accumulate in and selectively deliver drugs to an inflammatory lesion with enhanced vascular permeability. The aims of this study were to investigate the distribution of liposomal FK506, an immunosuppressive drug encapsulated within liposomes, and the drug's effects on cardiac function in a rat experimental autoimmune myocarditis (EAM) model. We prepared polyethylene glycol-modified liposomal FK506 (mean diameter: 109.5 ± 4.4 nm). We induced EAM by immunization with porcine myosin and assessed the tissue distribution of the nano-sized beads and liposomal FK506 in this model. After liposomal or free FK506 was administered on days 14 and 17 after immunization, the cytokine expression in the rat hearts along with the histological findings and hemodynamic parameters were determined on day 21. Ex vivo fluorescent imaging revealed that intravenously administered fluorescent-labeled nano-sized beads had accumulated in myocarditic but not normal hearts on day 14 after immunization and thereafter. Compared to the administration of free FK506, FK506 levels were increased in both the plasma and hearts of EAM rats when liposomal FK506 was administered. The administration of liposomal FK506 markedly suppressed the expression of cytokines, such as interferon-γ and tumor necrosis factor-α, and reduced inflammation and fibrosis in the myocardium on day 21 compared to free FK506. The administration of liposomal FK506 also markedly ameliorated cardiac dysfunction on day 21 compared to free FK506. Nano-sized liposomes may be a promising drug delivery system for targeting myocarditic hearts with cardioprotective agents.
    Matched MeSH terms: Autoimmune Diseases/drug therapy*; Autoimmune Diseases/metabolism
  9. Kaur A, Lee LH, Chow SC, Fang CM
    Int Rev Immunol, 2018;37(5):229-248.
    PMID: 29985675 DOI: 10.1080/08830185.2018.1469629
    Transcription factors are gene regulators that activate or repress target genes. One family of the transcription factors that have been extensively studied for their crucial role in regulating gene network in the immune system is the interferon regulatory factors (IRFs). IRFs possess a novel turn-helix turn motif that recognizes a specific DNA consensus found in the promoters of many genes that are involved in immune responses. IRF5, a member of IRFs has recently gained much attention for its role in regulating inflammatory responses and autoimmune diseases. Here, we discuss the role of IRF5 in regulating immune cells functions and how the dysregulation of IRF5 contributes to the pathogenesis of immune disorders. We also review the latest findings of potential IRF5 inhibitors that modulate IRF5 activity in the effort of developing therapeutic approaches for treating inflammatory disorders.
    Matched MeSH terms: Autoimmune Diseases
  10. Foong, Audrey Kow Siew, Nuha Fahimah Binti Wan Zahidi, Chau, Ling Tham
    MyJurnal
    Immunoglobulins are antibodies that play important roles in preserving our immune system. They have the ability to initiate humoral responses and remove antigen from the body. Out of the five major isotypes of immunoglobulins, IgG are most abundantly found in human serum. Abnormalities – deficiency or elevation in the level of IgG are found to be associated to the occurrence of several autoimmune diseases. These may include rheumatoid arthritis, Crohn’s disease, Mikulicz’s disease, Kuttner’s tumour and Hashimoto’s thyroiditis. Apart from autoimmune diseases, IgG has been found to play a role in initiating anaphylaxis, a severe and life threatening form of allergy and lately it has been discovered in cases of dengue virus infection too. It is important to acknowledge the roles of IgG on diseases especially subclass IgG4 which the elevation has been tied to numerous diseases such as Kuttner’s tumour and Hashimoto’s thyroiditis hence termed IgG4-related diseases. In addition, the roles of IgG in anaphylaxis are of importance, too, as IgG has been used in allergy immunotherapy. Hence, this review is a mini compilation of effects of IgG abnormalities based on their subclasses. Hopefully it will provide insightful understanding on the development of diagnostic and therapeutic courses for the aforementioned IgG abnormalities in the future.
    Matched MeSH terms: Autoimmune Diseases
  11. Panirselvam RR, Ramly SS, Harun NA
    MyJurnal
    Systemic lupus erythematosus (SLE) is a debilitating and chronic autoimmune disease which strikes insidiously. The disease currently has a prevalence of 43/ 100 000 individuals in Malaysia. The presentation of the disease is varied resulting in delay in diagnosis and onset of complications prior to management. The disease commonly presents as joint pain and cutaneous manifestations. Neuropsychiatric presentation accounts for 24% of symptoms during onset of illness. This case report highlights that we encountered a patient who presented with neuropsychiatric manifestations, whereby the patient was managed for the psychiatric symptoms prior to the organic diagnosis being made.
    Matched MeSH terms: Autoimmune Diseases
  12. Stephen SE, Loong JLX, Hoong CK, Lim SM, Botross NP
    Am J Case Rep, 2018 Jul 23;19:858-863.
    PMID: 30033442 DOI: 10.12659/AJCR.909228
    BACKGROUND Acquired hemophilia is a rare but potentially dangerous bleeding disorder caused by autoantibodies against coagulation factors. It affects 1 to 1.5 per 1 million people each year. While 50% of cases could be idiopathic, other causes include malignancies, diabetes, pregnancy, infection, and autoimmune disorders. CASE REPORT We report a case of a 90-year-old male who developed a spontaneous hematoma on the dorsum of his right hand, with no prior history of trauma or any other mucosal bleeding. His activated partial thromboplastin time (aPTT) was found to be prolonged (>180 seconds) with a very low level of factor VIII (0.1%). CONCLUSIONS As workups did not identify the source, including malignancy and autoimmune diseases, of his acquired hemophilia, it is believed to be idiopathic. He was started on intravenous recombinant factor VIIa (NovoSeven) to control the bleeding in combination with an immunosuppressive therapy of cyclophosphamide and prednisolone. In approximately 10% of patients with acquired hemophilia, underlying malignancy, such as squamous cell cancer, chronic lymphocytic leukemia, non-Hodgkin lymphoma, and multiple myeloma can present and commonly develop in elderly patients. Therefore, patients diagnosed with idiopathic acquired hemophilia should be given long-term follow up.
    Matched MeSH terms: Autoimmune Diseases/diagnosis; Autoimmune Diseases/drug therapy; Autoimmune Diseases/etiology
  13. Lim JA, Lee ST, Moon J, Jun JS, Kim TJ, Shin YW, et al.
    Ann Neurol, 2019 03;85(3):352-358.
    PMID: 30675918 DOI: 10.1002/ana.25421
    OBJECTIVE: There is no scale for rating the severity of autoimmune encephalitis (AE). In this study, we aimed to develop a novel scale for rating severity in patients with diverse AE syndromes and to verify the reliability and validity of the developed scale.

    METHODS: The key items were generated by a panel of experts and selected according to content validity ratios. The developed scale was initially applied to 50 patients with AE (development cohort) to evaluate its acceptability, reproducibility, internal consistency, and construct validity. Then, the scale was applied to another independent cohort (validation cohort, n = 38).

    RESULTS: A new scale consisting of 9 items (seizure, memory dysfunction, psychiatric symptoms, consciousness, language problems, dyskinesia/dystonia, gait instability and ataxia, brainstem dysfunction, and weakness) was developed. Each item was assigned a value of up to 3 points. The total score could therefore range from 0 to 27. We named the scale the Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The new scale showed excellent interobserver (intraclass correlation coefficient [ICC] = 0.97) and intraobserver (ICC = 0.96) reliability for total scores, was highly correlated with modified Rankin scale (r = 0.86, p

    Matched MeSH terms: Autoimmune Diseases/complications; Autoimmune Diseases/physiopathology; Autoimmune Diseases/psychology; Autoimmune Diseases of the Nervous System/complications; Autoimmune Diseases of the Nervous System/physiopathology*; Autoimmune Diseases of the Nervous System/psychology*
  14. Miyaji K, Paul F, Shahrizaila N, Umapathi T, Yuki N
    J Neuroimmunol, 2014 Nov 15;276(1-2):172-4.
    PMID: 25156074 DOI: 10.1016/j.jneuroim.2014.08.004
    Given their localization and important role in regulating complement, complement regulatory proteins may act as target antigens and their antibodies as biomarkers in demyelinating neuropathies. We investigated the binding of autoantibodies to complement regulatory proteins (CD46, 55 and 59) in demyelinating diseases. In 42 acute inflammatory demyelinating polyneuropathy, 23 chronic inflammatory demyelinating polyneuropathy, 13 acute motor axonal neuropathy, 71 multiple sclerosis, and 19 neuromyelitis optica patients as well as 55 healthy controls, we were unable to detect significant titers of antibodies to CD46, CD55 and CD59. These autoantibodies are unlikely to be biomarkers in acute and chronic inflammatory demyelinating polyneuropathies.
    Matched MeSH terms: Autoimmune Diseases of the Nervous System/pathology*
  15. Abdullah S, Fadzli F, Ramli N, Tan CT
    Mult Scler Relat Disord, 2017 Feb;12:34-38.
    PMID: 28283103 DOI: 10.1016/j.msard.2016.12.011
    BACKGROUND AND OBJECTIVE: The recently introduced International Consensus diagnostic criteria for diagnosis of neuromyelitis spectrum disorder include patients who are seronegative for AQP4 antibody. The criteria are dependent on typical MRI changes in the spinal cord, optic nerve and brain. This study aims to determine whether there are significant differences in the MRI brain images between AQP4 positive and negative patients with IIDDs.

    METHOD: MRI brain of patients with a diagnosis of IIDDs presented to the Hospital from 2010 to 2015 was analysed. The MRI was assessed by 2 radiologists blinded to the AQP4 status, on features said to be typical of NMOSD and MS.

    RESULTS: Thirty nine patients fulfilled the criteria and were included in the study. They consisted of 19 AQP4 seropositive and 20 AQP4 seronegative patients. The mean age was older (37.0 vs. 28.8 years) among the AQP4 positive group. The majority of the patients were ethnic Chinese (72%), followed by the Malays and Indians. Those with AQP4 seropositive status generally has less brain lesions, and significantly less fulfilling the McDonald DIS criteria as compared to those with AQP4 seronegative status (15.8% vs. 60.0%, p=0.005). None of the seven cerebral MRI features highlighted in NMOSD 2015 diagnostic criteria, said to be characteristic of NMOSD was more common among the AQP4 positive patients. These features were in fact seen less frequently among the AQP4 seropositive patients. An example was the extensive hemispheric lesion seen in 10.5% of AQP4 seropositive patients vs. 45% of that AQP4 seronegative group.

    CONCLUSION: There was no characteristic MRI brain features in the Malaysian AQP4 seropositive IIDD patients versus those who are seronegative. This could be a reflection of ethnical difference.

    Matched MeSH terms: Demyelinating Autoimmune Diseases, CNS/blood*
  16. Abd Rahman AN, Tett SE, Staatz CE
    Clin Pharmacokinet, 2014 Mar;53(3):227-245.
    PMID: 24327238 DOI: 10.1007/s40262-013-0124-z
    Mycophenolic acid (MPA) is a potent immunosuppressant agent, which is increasingly being used in the treatment of patients with various autoimmune diseases. Dosing to achieve a specific target MPA area under the concentration-time curve from 0 to 12 h post-dose (AUC12) is likely to lead to better treatment outcomes in patients with autoimmune disease than a standard fixed-dose strategy. This review summarizes the available published data around concentration monitoring strategies for MPA in patients with autoimmune disease and examines the accuracy and precision of methods reported to date using limited concentration-time points to estimate MPA AUC12. A total of 13 studies were identified that assessed the correlation between single time points and MPA AUC12 and/or examined the predictive performance of limited sampling strategies in estimating MPA AUC12. The majority of studies investigated mycophenolate mofetil (MMF) rather than the enteric-coated mycophenolate sodium (EC-MPS) formulation of MPA. Correlations between MPA trough concentrations and MPA AUC12 estimated by full concentration-time profiling ranged from 0.13 to 0.94 across ten studies, with the highest associations (r (2) = 0.90-0.94) observed in lupus nephritis patients. Correlations were generally higher in autoimmune disease patients compared with renal allograft recipients and higher after MMF compared with EC-MPS intake. Four studies investigated use of a limited sampling strategy to predict MPA AUC12 determined by full concentration-time profiling. Three studies used a limited sampling strategy consisting of a maximum combination of three sampling time points with the latest sample drawn 3-6 h after MMF intake, whereas the remaining study tested all combinations of sampling times. MPA AUC12 was best predicted when three samples were taken at pre-dose and at 1 and 3 h post-dose with a mean bias and imprecision of 0.8 and 22.6 % for multiple linear regression analysis and of -5.5 and 23.0 % for maximum a posteriori (MAP) Bayesian analysis. Although mean bias was less when data were analysed using multiple linear regression, MAP Bayesian analysis is preferable because of its flexibility with respect to sample timing. Estimation of MPA AUC12 following EC-MPS administration using a limited sampling strategy with samples drawn within 3 h post-dose resulted in biased and imprecise results, likely due to a longer time to reach a peak MPA concentration (t max) with this formulation and more variable pharmacokinetic profiles. Inclusion of later sampling time points that capture enterohepatic recirculation and t max improved the predictive performance of strategies to predict EC-MPS exposure. Given the considerable pharmacokinetic variability associated with mycophenolate therapy, limited sampling strategies may potentially help in individualizing patient dosing. However, a compromise needs to be made between the predictive performance of the strategy and its clinical feasibility. An opportunity exists to combine research efforts globally to create an open-source database for MPA (AUC, concentrations and outcomes) that can be used and prospectively evaluated for AUC target-controlled dosing of MPA in autoimmune diseases.
    Matched MeSH terms: Autoimmune Diseases/metabolism*
  17. LIE-INJOLUAN EN, PILLAY RP
    Acta Haematol., 1964 May;31:282-8.
    PMID: 14172696
    Matched MeSH terms: Autoimmune Diseases*
  18. STEIN J, STEIN B, YU M, CHEE M, CHEW BK
    Med J Malaysia, 1963 Dec;18:116-21.
    PMID: 14117279
    Matched MeSH terms: Autoimmune Diseases*
  19. Bello RO, Chin VK, Abd Rachman Isnadi MF, Abd Majid R, Atmadini Abdullah M, Lee TY, et al.
    Int J Mol Sci, 2018 Apr 11;19(4).
    PMID: 29641433 DOI: 10.3390/ijms19041149
    The recently identified cytokines-interleukin (IL)-35 and interleukin (IL)-37-have been described for their anti-inflammatory and immune-modulating actions in numerous inflammatory diseases, auto-immune disorders, malignancies, infectious diseases and sepsis. Either cytokine has been reported to be reduced and in some cases elevated and consequently contributed towards disease pathogenesis. In view of the recent advances in utilizing cytokine profiles for the development of biological macromolecules, beneficial in the management of certain intractable immune-mediated disorders, these recently characterized cytokines (IL-35 and IL-37) offer potential as reasonable targets for the discovery of novel immune-modulating anti-inflammatory therapies. A detailed comprehension of their sophisticated regulatory mechanisms and patterns of expression may provide unique opportunities for clinical application as highly selective and target specific therapeutic agents. This review seeks to summarize the recent advancements in discerning the dynamics, mechanisms, immunoregulatory and anti-inflammatory actions of IL-35 and IL-37 as they relate to disease pathogenesis.
    Matched MeSH terms: Autoimmune Diseases/etiology*
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