Tackling the autoimmune side in Spondyloarthritis: A systematic review

Chimenti, Maria Sole; Perricone, Carlo; Conigliaro, Paola; Triggianese, Paola; D’Antonio, Arianna; Martino, Erica De; Fonti, Giulia Lavinia; Caso, Francesco; Costa, Luisa; Perricone, Roberto

doi:10.1016/j.autrev.2020.102648

Cited by 14 publications

(17 citation statements)

References 128 publications

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“…The inhibition of this cytokine, whose signaling pathway uses the protein gp130 as a common signal transducer, could impair the host capacity for generating acute phase responses, including Th17 differentiation and long-lived plasma cell generation [36,42,43]. In fact, some clinical data derived from RCTs supports the notion that IL-6-targeting agents increase the risk of infection to a degree similar to TNFis [36,40,52,53]. On the other hand, neutropenia induced by IL-6 inhibition would frequently occur, due to a margination of neutrophils rather than peripheral sequestration.…”

Section: Risk Of Infections In Rmds and Autoinflammatory Disordersmentioning

confidence: 99%

“…RA and SpA are chronic inflammatory diseases, mainly affecting the joint, mediated by autoimmune and inflammatory process [52,53].…”

Section: Incidence and Outcomes Of Covid-19 In Arthritis Patientsmentioning

confidence: 99%

“…More specifically, whereas RA is characterized by predominant peripheral synovial inflammation sustained by autoantibodies and B-and T-lymphocytes mechanisms, SpAs provide a main innate-immunity mediated pathogenesis leading to inflammation of synovial-entheseal structures and axial skeleton. SpA group includes ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis (ReA), enteropathic, and undifferentiated spondylarthritis (uSpA) [52,53]. In patients with RA and SpA, it is recognized that the immunosuppressive therapy and the presence of comorbidities are associated with an increased risk of infections [54][55][56][57].…”

Section: Incidence and Outcomes Of Covid-19 In Arthritis Patientsmentioning

confidence: 99%

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Pathogenic implications, incidence, and outcomes of COVID-19 in autoimmune inflammatory joint diseases and autoinflammatory disorders

et al. 2021

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As the coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to spread rapidly, there are still many unresolved questions of how this virus would impact on autoimmune inflammatory joint diseases and autoinflammatory disorders. The main aim of this paper is to describe the main studies focusing their attention on COVID-19 incidence and outcomes of rheumatoid arthritis (RA), spondylarthritis (SpA), and autoinflammatory disease cohorts. We also revised possible pathogenic mechanisms associated with. Available data suggest that, in patients with RA and SpA, the immunosuppressive therapy, older age, male sex, and the presence of comorbidities (hypertension, lung disease, diabetes, CVD, and chronic renal insufficiency/end-stage renal disease) could be associated with an increased risk of infections and high rate of hospitalization. Other studies have shown that lower odds of hospitalization were associated with bDMARD or tsDMARDs monotherapy, driven largely by anti-TNF therapies. For autoinflammatory diseases, considering the possibility that COVID-19 could be associated with a cytokine storm syndrome, the question of the susceptibility and severity of SARS-CoV-2 infection in patients displaying innate immunity disorders has been raised. In this context, data are very scarce and studies available did not clarify if having an autoinflammatory disorder could be or not a risk factor to develop a more severe COVID-19. Taking together these observations, further studies are likely to be needed to fully characterize these specific patient groups and associated SARS-CoV-2 infection.

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Section: Risk Of Infections In Rmds and Autoinflammatory Disordersmentioning

confidence: 99%

“…RA and SpA are chronic inflammatory diseases, mainly affecting the joint, mediated by autoimmune and inflammatory process [52,53].…”

Section: Incidence and Outcomes Of Covid-19 In Arthritis Patientsmentioning

confidence: 99%

Section: Incidence and Outcomes Of Covid-19 In Arthritis Patientsmentioning

confidence: 99%

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Pathogenic implications, incidence, and outcomes of COVID-19 in autoimmune inflammatory joint diseases and autoinflammatory disorders

et al. 2021

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“…Spondyloarthritis (SpA) is a heterogeneous group of inflammatory chronic diseases characterized by common clinical features, as inflammatory back pain, peripheral joint involvement, dactylitis and enthesitis ( Chimenti et al, 2020b ). SpA can be divided into predominantly axial or predominantly peripheral form, with or without psoriasis (PsO), inflammatory bowel disease (IBD) or previous associated infection.…”

Section: Introductionmentioning

confidence: 99%

Genetics, Epigenetics, and Gender Impact in Axial-Spondyloarthritis Susceptibility: An Update on Genetic Polymorphisms and Their Sex Related Associations

et al. 2021

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Spondyloarthritis (SpA) is a group of chronic inflammatory rheumatic disease that can be divided into predominantly axial or predominantly peripheral involvement, with or without associated psoriasis, inflammatory bowel disease or previous infection. Axial SpA (axSpA) encompasses ankylosing spondylitis (AS) with radiological sacroiliitis, and a type without radiographic sacroiliitis, called “non-radiographic axial SpA” (nr-axSpA). Males and females show large differences in their susceptibility to SpA, such as distinctions in clinical patterns, phenotypes and in therapeutical response, particularly to TNF inhibitors (TNFi). Several studies indicate that AS women have doubled risk to failure TNFi compared with males. This diversity in drugs’ efficacy among women and men may be caused by differences in the balance of sex hormones and in gene-specific expression likely triggered by X-chromosome instability and gene-specific epigenetic modifications. Evidence reported that polymorphisms in microRNAs on X- and other chromosomes, such as miR-146a, miR-155, miR-125a-5p, miR-151a-3p and miR-22-3p, miR-199a-5p could be involved in the different clinical presentation of SpA, as well as disease activity. In addition, association with non−response to TNFi treatment and presence of IRAK3 and CHUCK genes in SpA patients was recently detected. Finally, polymorphisms in genes involved in IL-23/IL-17 pathway, such as in drug pharmacodynamics and pharmacokinetics may have a role in response to TNFi, IL17i, and IL23i. A major understanding of genomic variability could help in the development of new therapeutic targets or in taking advantages of different mechanisms of action of biological drugs. Moving from the multifactorial etiology of disease, the present review aims at evaluating genetic and epigenetic factors and their relationship with sex and bDMARDs response, helping to investigate the different expression among males and females of genes on X- and other chromosomes, as well as mi-RNA, to highlight relationships between sex and occurrence of specific phenotypes and symptoms of the disease. Moreover, the role of the epigenetic modification in relation to immune-regulatory mechanisms will be evaluated.

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“…In this attempt, knowledge gained from in vitro studies, which have demonstrated both direct or indirect effects of IL-23 on osteoblasts and osteoclasts is valuable 20 . While one study demonstrated that IL-23 can promote osteoclast formation by upregulation of RANK on bone marrow (BM)-derived osteoclast precursors 21 , another study demonstrated inhibitory effects of IL-23 on osteoclast formation through induction of GM-CSF in T cells 17 .…”

Section: Introductionmentioning

confidence: 99%

IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation

Razawy

Alves

Koedam

et al. 2021

Sci Rep

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The IL-23 receptor (IL-23R) signaling pathway has pleiotropic effects on the differentiation of osteoclasts and osteoblasts, since it can inhibit or stimulate these processes via different pathways. However, the potential role of this pathway in the regulation of bone homeostasis remains elusive. Therefore, we studied the role of IL-23R signaling in physiological bone remodeling using IL-23R deficient mice. Using µCT, we demonstrate that 7-week-old IL-23R−/− mice have similar bone mass as age matched littermate control mice. In contrast, 12-week-old IL-23R−/− mice have significantly lower trabecular and cortical bone mass, shorter femurs and more fragile bones. At the age of 26 weeks, there were no differences in trabecular bone mass and femur length, but most of cortical bone mass parameters remain significantly lower in IL-23R−/− mice. In vitro osteoclast differentiation and resorption capacity of 7- and 12-week-old IL-23R−/− mice are similar to WT. However, serum levels of the bone formation marker, PINP, are significantly lower in 12-week-old IL-23R−/− mice, but similar to WT at 7 and 26 weeks. Interestingly, Il23r gene expression was not detected in in vitro cultured osteoblasts, suggesting an indirect effect of IL-23R. In conclusion, IL-23R deficiency results in temporal and long-term changes in bone growth via regulation of bone formation.

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Tackling the autoimmune side in Spondyloarthritis: A systematic review

Cited by 14 publications

References 128 publications

Pathogenic implications, incidence, and outcomes of COVID-19 in autoimmune inflammatory joint diseases and autoinflammatory disorders

Pathogenic implications, incidence, and outcomes of COVID-19 in autoimmune inflammatory joint diseases and autoinflammatory disorders

Genetics, Epigenetics, and Gender Impact in Axial-Spondyloarthritis Susceptibility: An Update on Genetic Polymorphisms and Their Sex Related Associations

IL-23 receptor deficiency results in lower bone mass via indirect regulation of bone formation

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