The psoriasis‐associated antigen, pso p27, participates in the formation of complement activating immune‐complexes in psoriatic scale

Åsbakk, Kjetil; Bergh, Kåre; Iversen, Ole‐Jan

doi:10.1111/j.1699-0463.1990.tb01014.x

Cited by 22 publications

(7 citation statements)

References 20 publications

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“…In psoriatic skin lesions, a proteolytically cleaved product of SERPINB3, Pso p27, was identified in mast cells [55, 56]. Pso p27 can complex with IgG as well as complement factor C1q and form large aggregates in skin scale lesions and serum in psoriasis patients, suggesting an immunogenic role of Pso p27 [57]. High concentrations of Pso p27 specific antibodies can be extracted from psoriatic scales, suggesting Pso p27 is an immunogen [58].…”

Section: Serpinb3/b4 In Inflammatory Diseasesmentioning

confidence: 99%

SERPINB3 and B4: From biochemistry to biology

Sun

Sheshadri

Zong

2017

Seminars in Cell & Developmental Biology

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Human SERPINB3 and SERPINB4 are evolutionary duplicated serine/cysteine protease inhibitors. Genomic analysis indicates that these paralogous genes were encoded from independent loci arising from tandem gene duplication. Although the two molecules share 92% identity of their amino acid sequences, they are distinct in the Reactive Center Loop (RCL) including a hinge region and catalytic sequences which accounts for altered substrate specificity. Elevated expression of the two molecules have been reported to contribute to numerous pathological conditions such as inflammatory diseases and cancer. In this review, we focus on summarizing the biochemical features of SERPINB3/B4 and discussing the mechanistic basis for their biological functions and implications in human diseases.

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Section: Serpinb3/b4 In Inflammatory Diseasesmentioning

confidence: 99%

SERPINB3 and B4: From biochemistry to biology

Sun

Sheshadri

Zong

2017

Seminars in Cell & Developmental Biology

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“…This indicates that the particles were not infectious agents, but may have been ERVs. Subsequently, using monoclonal antibodies against the retroviral p27 protein (Asbakk & Iversen 1988), Asbakk et al (1990) purified an antigen, designated pso p27, from psoriasis lesions. As both antigens had a similar molecular weight they suggested that they were probably identical.…”

Section: Retrovirus Particles In Autoimmune Diseasesmentioning

confidence: 99%

The Potential Roles of Endogenous Retroviruses in Autoimmunity

Nakagawa

Harrison²

1996

Immunological Reviews

115

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Endogenous retroviruses (ERVs) are estimated to comprise up to 1% of human DNA. While the genome of many ERVs is interrupted by termination codons, deletions or frame shift mutations, some ERVs are transcriptionally active and recent studies reveal protein expression or particle formation by human ERVs. ERVs have been implicated as aetiological agents of autoimmune disease, because of their structural and sequence similarities to exogenous retroviruses associated with immune dysregulation and their tissue-specific or differentiation-dependent expression. In fact, retrovirus-like particles distinct from those of known exogenous retroviruses and immune responses to ERV proteins have been observed in autoimmune disease. Quantitatively or structurally aberrant expression of normally cryptic ERVs, induced by environmental or endogenous factors, could initiate autoimmunity through direct or indirect mechanisms. ERVs may lead to immune dysregulation as insertional mutagens or cis-regulatory elements of cellular genes involved in immune function. ERVs may also encode elements like tax in human T-lymphotrophic virus type I (HTLV-I) or tat in human immunodeficiency virus-I (HIV-I) that are capable of transactivating cellular genes. More directly, human ERV gene products themselves may be immunologically active, by analogy with the superantigen activity in the long terminal repeat (LTR) of mouse mammary tumour viruses (MMTV) and the non-specific immunosuppressive activity in mammalian type C retrovirus env protein. Alternatively, increased expression of an ERV protein, or expression of a novel ERV protein not expressed in the thymus during acquisition of immune tolerance, may lead to its perception as a neoantigen. Paraneoplastic syndromes raise the possibility that novel ERV-encoded epitopes expressed by a tumour elicit immunity to cross-reactive epitopes in normal tissues. Recombination events between different but related ERVs, to whose products the host is immunologically tolerant, may also generate new antigenic determinants. Frequently reported humoral immunity to exogenous retrovirus proteins in autoimmune disease could be elicited by cross-reactive ERV proteins. A review of the evidence implicating ERVs in immune dysfunction leads to the conclusion that direct molecular studies are likely to establish a pathogenic role for ERVs in autoimmune disease.

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“…Immunological analyses have shown that a protein present in psoriatic scale, Pso p27, participates in the generation of complexes, both in the psoriatic plaques and in synovial fluid in patients with psoriasis arthritis (Asbakk et al, 1990;Rødahl et al, 1988). We have presented evidence that the Pso p27 antigen is expressed by mast cells in the skin lesions (Iversen et al, 1995).…”

Section: Discussionmentioning

confidence: 88%