Autoantibodies in inflammatory arthritis

Conigliaro, Paola; Chimenti, Maria Sole; Triggianese, Paola; Sunzini, Flavia; Novelli, Lucia; Perricone, Carlo; Perricone, Roberto

doi:10.1016/j.autrev.2016.03.003

Cited by 102 publications

(67 citation statements)

References 180 publications

(216 reference statements)

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“…Importantly, we found that the levels of both anti–ADAMTS‐L5 and anti–LL‐37 autoantibodies were significantly elevated in patients with PsA compared to non‐PsA controls, suggesting that these molecules may be involved in the pathogenesis of PsA. This is consistent with previous findings showing that autoantibodies may be associated with PsA . Furthermore, the autoantibodies against ADAMTS‐L5 or LL‐37 could be used as biomarkers to discriminate PsA from non‐PsA.…”

Section: Discussionsupporting

confidence: 91%

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Yuan

Qiu

Lin

et al. 2019

Arthritis & Rheumatology

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Objective. The autoimmune etiology in psoriasis remains to be clarified. We therefore undertook this study to identify novel pathogenic autoantigens and autoantibodies in patients with psoriasis, with the aim of shedding light on the molecular and cellular basis of the pathogenesis of psoriasis and psoriatic arthritis (PsA).Methods. In this study, we developed an autoantigen array system that harbors a variety of antigens, including typical autoantigens in rheumatic diseases as well as skin antigens, inflammatory mediators, and putative autoantigens in psoriasis. Serum samples from patients with psoriasis (n = 73) were used to interrogate the antigens on the array. In addition, enzyme-linked immunosorbent assays of individual autoantibodies were used in validation studies.Results. Levels of several autoantibodies were found to be elevated in the serum of patients with psoriasis compared to healthy controls; in particular, IgG autoantibodies against 2 novel antigens, LL-37 and ADAMTS-L5, were significantly increased in patients with psoriasis. Importantly, serum levels of IgG autoantibodies against LL-37 and ADAMTS-L5 were correlated with the Psoriasis Area and Severity Index, and reflected disease progression in longitudinally collected serum samples from patients with psoriasis. Importantly, both anti-ADAMTS-L5 and anti-LL-37 autoantibody levels were also significantly elevated in psoriasis patients with PsA compared to those without PsA, suggesting that these molecules may be involved in the pathogenesis of PsA.Conclusion. Our findings indicate that these identified autoantibodies may be useful biomarkers and may serve as therapeutic targets in psoriasis and PsA.

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Section: Discussionsupporting

confidence: 91%

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Yuan

Qiu

Lin

et al. 2019

Arthritis & Rheumatology

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“…This thinning might also be due to HCQ treatment or apoptosis of retinal ganglion cells induced by anti-Ro antibodies. It is well known that autoantibodies may exert a pathogenic role in autoinflammatory/autoimmune diseases [46, 47]. Data from the literature suggest that anti-Ro antibodies could play a role in mediating or potentiating vascular injury in the central nervous system [48].…”

Section: Discussionmentioning

confidence: 99%

Evidence for the Detection of Subclinical Retinal Involvement in Systemic Lupus Erythematosus and Sjögren Syndrome: A Potential Association with Therapies

Conigliaro

Triggianese

Draghessi

et al. 2018

Int Arch Allergy Immunol

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Background: Retinal involvement in systemic lupus erythematosus (SLE) and Sjögren syndrome (SS) may be subclinical and thus underdiagnosed. Objectives: We aimed at evaluating morphological and functional visual abnormalities in a cohort of SLE and SS patients in the absence of an overt clinical visual impairment. We also investigated potential associations between retinal disorders and disease activity, organ involvement, and treatment with steroid and/or hydroxychloroquine. Methods: The study comprised 42 SLE and 36 primary SS patients and 76 healthy controls (HC). Ophthalmological examination, standard automated perimetry, spectral-domain optical coherence tomography, and fundus perimetry were performed. Results: Retinal thickness of the posterior pole was not different between SLE and HC groups, but it was reduced in the SS group compared with both the HC and the SLE group. In SLE and SS patients, mean defect and pattern standard deviation by standard automated perimetry were higher than in HC. Visual field index values were lower in both SLE and SS patients than in HC. SLE patients with nephritis displayed increased mean defect and pattern standard deviation and reduced visual field index values compared to patients without nephritis. In SLE and SS patients, fundus perimetry differential sensitivity was reduced, and mean defect values were higher than in HC. Disturbances in fundus perimetry in the SLE group were more prevalent in steroid-naïve patients and in SS patients who received a cumulative hydroxychloroquine dose > 1,000 g. Conclusions: Functional eye impairment was demonstrated in SLE patients, possibly associated with kidney involvement. In SLE, corticosteroids might exert a protective role. Morphological alterations and functional impairment were detected in SS patients, which may be linked to hydroxychloroquine toxicity.

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“…The pathology of RA involves components of innate and adaptive immunity (1). Although the pathogenesis of RA remains poorly understood, production of autoantibodies along with infiltration of synovial fluid and tissues by inflammatory cells have been identified as key events (2)(3)(4). Collageninduced arthritis (CIA) is a murine model that closely mimics RA (5).…”

mentioning

confidence: 99%

ICOS Signaling Controls Induction and Maintenance of Collagen-Induced Arthritis

Panneton

Yazdchi

Witalis

et al. 2018

The Journal of Immunology

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ICOS is a key costimulatory receptor facilitating differentiation and function of follicular helper T cells and inflammatory T cells. Rheumatoid arthritis patients were shown to have elevated levels of ICOS T cells in the synovial fluid, suggesting a potential role of ICOS-mediated T cell costimulation in autoimmune joint inflammation. In this study, using ICOS knockout and knockin mouse models, we found that ICOS signaling is required for the induction and maintenance of collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis. For the initiation of CIA, the Tyr-based SH2-binding motif of ICOS that is known to activate PI3K was critical for Ab production and expansion of inflammatory T cells. Furthermore, we found that Tyr-dependent ICOS signaling is important for maintenance of CIA in an Ab-independent manner. Importantly, we found that a small molecule inhibitor of glycolysis, 3-bromopyruvate, ameliorates established CIA, suggesting an overlap between ICOS signaling, PI3K signaling, and glucose metabolism. Thus, we identified ICOS as a key costimulatory pathway that controls induction and maintenance of CIA and provide evidence that T cell glycolytic pathways can be potential therapeutic targets for rheumatoid arthritis.

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Autoantibodies in inflammatory arthritis

Cited by 102 publications

References 180 publications

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Evidence for the Detection of Subclinical Retinal Involvement in Systemic Lupus Erythematosus and Sjögren Syndrome: A Potential Association with Therapies

ICOS Signaling Controls Induction and Maintenance of Collagen-Induced Arthritis

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