Detection of HIV-I related antigens in rheumatoid synovial tissues.

Ziegler, Benedikt L.; Thomas, Christian A.

doi:10.1267/ahc.24.1

Cited by 17 publications

(6 citation statements)

References 26 publications

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“…On tbe other hand, synovial specimens from osteoarthritis, juvenile rheumatoid arthritis, psoriatic arthritis, Dupuytren's contracture and limb gangrene patients were negative. Similarly, Ziegler & Thomas (1991) demonstrated with HIV-specific monoclonal antibodies that more than 50% of 23 RA specimens had immunoreactivity for pl7 and p24 gag proteins. However, antibodies against HTLV-I and HIV-I were not detected in RA sera that corresponded to the fresh synovial specimens.…”

Section: Immune Responses To Human Exogenous or Endogenous Retrovirusmentioning

confidence: 84%

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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Section: Immune Responses To Human Exogenous or Endogenous Retrovirusmentioning

confidence: 84%

The Potential Roles of Endogenous Retroviruses in Autoimmunity

Nakagawa

Harrison²

1996

Immunological Reviews

115

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“…Remarkably, the sera from such patients lacked antibodies to HTLV-1. In a similar study, Ziegler and Thomas (210) used monoclonal antisera to p17 and p24 of HIV-1 to detect antigens in synovial specimens obtained from patients with rheumatoid arthritis. Approximately 55% of 33 patients had p17 and p24 antigens in rheumatoid synovial tissues.…”

Section: Hervs and Autoimmune Diseasementioning

confidence: 99%

Human endogenous retroviruses: nature, occurrence, and clinical implications in human disease.

Urnovitz¹,

Murphy²

1996

Clinical Microbiology Reviews

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“…In a pivotal study of 23 patients it was demonstrated that 45% of synovial tissues obtained from patients with RA were positive for HTLV-1 p19 and p24 antigens but, intriguingly, no antibodies to HTLV-1 were detected in the sera [35]. In addition, another study showed 55% of patients with RA had p17 and p24 HIV antigens in synovial tissues but, yet again, their sera tested negative for antibodies to HIV [36]. It was therefore likely that an alternative retrovirus, with sequence homology to HTLV-1 (in the former) or HIV-1 (in the latter), was the cause of the immune response.…”

Section: Role Of Hervs In Diseasementioning

confidence: 99%

Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?

Tugnet¹,

Rylance²,

Roden³

et al. 2013

TORJ

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Autoimmune rheumatic diseases, such as RA and SLE, are caused by genetic, hormonal and environmental factors. Human Endogenous Retroviruses (HERVs) may be triggers of autoimmune rheumatic disease. HERVs are fossil viruses that began to be integrated into the human genome some 30-40 million years ago and now make up 8% of the genome. Evidence suggests HERVs may cause RA and SLE, among other rheumatic diseases. The key mechanisms by which HERVS are postulated to cause disease include molecular mimicry and immune dysregulation. Identification of HERVs in RA and SLE could lead to novel treatments for these chronic conditions. This review summarises the evidence for HERVs as contributors to autoimmune rheumatic disease and the clinical implications and mechanisms of pathogenesis are discussed.

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Detection of HIV-I related antigens in rheumatoid synovial tissues.

Cited by 17 publications

References 26 publications

The Potential Roles of Endogenous Retroviruses in Autoimmunity

The Potential Roles of Endogenous Retroviruses in Autoimmunity

Human endogenous retroviruses: nature, occurrence, and clinical implications in human disease.

Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?

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