Autoimmunity to heterogeneous nuclear ribonucleoprotein A1 in psoriatic patients and correlation with disease severity

Guarneri, Claudio; Aguennouz, M.; Guarneri, Fabrizio; Polito, Francesca; Benvenga, Salvatore; Cannavò, Serafinella Patrizia

doi:10.1111/ddg.13631

Cited by 16 publications

(13 citation statements)

References 24 publications

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“…Previously, anti–stratum corneum autoantibodies , anti–squamous cell carcinoma antigen autoantibodies , and anti‐hsp65 autoantibodies and other autoantibodies were found in patients with psoriasis. However, the underlying mechanisms of action as well as the potential significance of those autoantibodies have yet to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…A variety of autoantibodies has been observed in patients with psoriasis, including antinuclear antibodies (ANAs), antibodies to small nuclear RNP (anti‐snRNP) and cytoplasmic RNP, antibodies to epidermal cells, or antibodies to antimicrobial peptide . Increased levels of autoantibodies against oxidized low‐density lipoprotein have been observed in patients with psoriasis .…”

Section: Introductionmentioning

confidence: 99%

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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: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Yuan

Qiu

Lin

et al. 2019

Arthritis & Rheumatology

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“…Such general inflammatory markers are accompanied by increased numbers of Th1, Th17, and Th22 cells in patients with severe psoriasis (86, 87), which provides a direct link with autoimmune (adaptive) processes. Moreover, there is an increasing number of modulating factors, such as autoimmune reactivity to ribonucleoprotein A1 (HNRNPA1) (88), which impact on the course and severity of psoriasis.…”

Section: Shades Of Gray: Crosstalk Between Adaptive and Innate Immunimentioning

confidence: 99%

Adaptive and Innate Immunity in Psoriasis and Other Inflammatory Disorders

2019

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Over the past three decades, a considerable body of evidence has highlighted T cells as pivotal culprits in the pathogenesis of psoriasis. This includes the association of psoriasis with certain MHC (HLA) alleles, oligoclonal expansion of T cells in some cases, therapeutic response to T cell-directed immunomodulation, the onset of psoriasis following bone marrow transplantation, or induction of psoriasis-like inflammation by T cells in experimental animals. There is accumulating clinical and experimental evidence suggesting that both autoimmune and autoinflammatory mechanisms lie at the core of the disease. Indeed, some studies suggested antigenic functions of structural proteins, and complexes of self-DNA with cathelicidin (LL37) or melanocytic ADAMTSL5 have been proposed more recently as actual auto-antigens in some cases of psoriasis. These findings are accompanied by various immunoregulatory mechanisms, which we increasingly understand and which connect innate and adaptive immunity. Specific adaptive autoimmune responses, together with our current view of psoriasis as a systemic inflammatory disorder, raise the question of whether psoriasis may have connections to autoimmune or autoinflammatory disorders elsewhere in the body. While such associations have been suspected for many years, compelling mechanistic evidence in support of this notion is still scant. This review sets into context the current knowledge about innate and adaptive immunological processes in psoriasis and other autoimmune or autoinflammatory diseases.

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“…Whether psoriasis should be considered a true autoimmune disease has been questioned since specific autoantigens were missing for a long time 6,10 . In 2014, cathelicidin (LL‐37) was the first autoantigen to be identified 11 and more followed rapidly in the following years (disintegrin‐like and metalloprotease domain containing thrombospondin type 1 motif‐like 5 (ADAMTSL5), phospholipase A2 group IVD (PLA2G4D), keratin 17 and heterogeneous nuclear ribonucleoprotein A1 (hnRNP‐A1) as a potential autoantigen) 9,11‐13 . Furthermore, while the role of autoreactive T cells is becoming increasingly evident, only recently autoantibodies have been observed in patients with psoriasis and PsA, including antinuclear antibodies (ANA), antibodies that bind to the antimicrobial peptide LL‐37, small nuclear RNP and cytoplasmic RNP and integrins 14‐17 .…”

Section: Introductionmentioning

confidence: 99%

Current knowledge on autoantigens and autoantibodies in psoriasis

et al. 2020

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Psoriasis is a chronic inflammatory disease of the skin, with clinically characteristic erythematous and thick scaling plaques. 1 It is now well acknowledged that in addition to psoriatic arthritis (PsA), other comorbidities such as metabolic syndrome, cardiovascular diseases, gastrointestinal diseases, psychosocial disorders, infections and malignancies may accompany psoriasis. 2 They appear to result from environmental (e.g., infection or skin trauma) and genetic factors as well as enhanced levels of various inflammatory mediators, in particular circulating lymphocytes and other peripheral blood mononuclear cells, transcription factors and cytokines like tumour necrosis factor (TNF), interleukin (IL)-12/IL-23 and IL-17. 3-5 Multiple susceptibility loci associated with innate and adaptive components of the immune system together with skin resident cell types are involved in the complex inflammatory network that drives psoriatic disease. 6 The most predominant susceptibility allele for psoriasis, the human leucocyte antigen (HLA) susceptibility locus HLA-C*06:02, is strongly associated with early onset and more severe disease. 1 To date, it has been agreed that psoriasis is

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Autoimmunity to heterogeneous nuclear ribonucleoprotein A1 in psoriatic patients and correlation with disease severity

Cited by 16 publications

References 24 publications

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Identification of Novel Autoantibodies Associated With Psoriatic Arthritis

Adaptive and Innate Immunity in Psoriasis and Other Inflammatory Disorders

Current knowledge on autoantigens and autoantibodies in psoriasis

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