Augmentation of lymphocyte and macrophage proliferation by caprine arthritis-encephalitis virus contributes to the development of progressive arthritis

Banks, Keith L.; Jutila, Mark A.; Jacobs, Cindy; Michaels, Frank H.

doi:10.1007/bf00271868

Cited by 10 publications

(4 citation statements)

References 29 publications

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“…The erosive processes observed in the radiographic examination and SEM in the present study was also described by Bank et al () in patients with chronic inflammatory polyarthritis in humans.…”

Section: Discussionsupporting

confidence: 90%

“…Morphological approaches to joint degenerative lesions in CAE infected goats may increase understanding of its physiopathology, evolution, and disease chronicity (Bank et al, ; Leitner et al, ). Furthermore, the histopathological aspects involved in CAE were described by Wilder (), Feldmann et al (), and Carty et al () as similar to those observed in rheumatoid arthritis (RA) in humans.…”

Section: Introductionmentioning

confidence: 99%

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Comparative study by computed radiography, histology, and scanning electron microscopy of the articular cartilage of normal goats and in chronic infection with caprine arthritis‐encephalitis virus

Sousa

Filho

et al. 2013

Microscopy Res & Technique

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In the northeast of Brazil, caprine arthritis-encephalitis (CAE) is one of the key reasons for herd productivity decreasing that result in considerable economic losses. A comparative study was carried out using computed radiography (CR), histological analysis (HA), and scanning electronic microscopy (SEM) of the joints of CAE infected and normal goats. Humerus head surface of positive animals presented reduced joint space, increased bone density, and signs of degenerative joint disease (DJD). The carpal joint presented no morphological alterations in CR in any of the animals studied. Tarsus joint was the most affected, characterized by severe DJD, absence of joint space, increased periarticular soft tissue density, edema, and bone sclerosis. Histological analysis showed chronic tissue lesions, complete loss of the surface zone, absence of proteoglycans in the transition and radial zones and destruction of the cartilage surface in the CAE positive animals. Analysis by SEM showed ulcerated lesions with irregular and folded patterns on the joint surface that distinguished the limits between areas of normal and affected cartilage. The morphological study of the joints of normal and CAE positive goats deepened understanding of the alteration in the tissue bioarchitecture of the most affected joints. The SEM finding sustained previous histological reports, similar to those found for rheumatoid arthritis, suggesting that the goat infected with CAE can be considered as a potential model for research in this area.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Comparative study by computed radiography, histology, and scanning electron microscopy of the articular cartilage of normal goats and in chronic infection with caprine arthritis‐encephalitis virus

Sousa

Filho

et al. 2013

Microscopy Res & Technique

View full text Add to dashboard Cite

show abstract

“…In this regard, caprine arthritisencephalitis virus, a lentivirus in the subfamily of retroviruses, infects cells of the macrophage lineage in goats and triggers a progressive arthropathy. 86 The Lyme arthritis spirochaete, Borrelia burgdorferi, has been shown to induce both a progressive and destructive polyarthritis,87 as well as severe systemic lesions in severe combined immunodeficiency mice. 88 These studies may facilitate re-evaluation of the role of infectious agents in the pathogenesis of chronic inflammatory arthritis.…”

Section: Animal Modelsmentioning

confidence: 99%

Molecular and cellular mechanisms of joint destruction in rheumatoid arthritis: two cellular mechanisms explain joint destruction?

Gay¹,

Gay²,

Koopman³

1993

Annals of the Rheumatic Diseases

252

154

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“…The inflammatory synovitis in the early stage of this disease resembles findings in RA and other inflammatory arthritides in humans [9,10]. Also in common with findings in patients with RA, Banks et al [11] described how an elevated proportion of cells expressed molecules associated with accessory cell functions and an augmentation of CDS'*" lymphocytes in the inflamed synovium.…”

Section: Retroviruses and Rheumatoid Arthritismentioning

confidence: 53%

Retroviruses and autoimmune rheumatic diseases

Kalden

1994

Clinical and Experimental Immunology

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SUMMARYIn autoimmune rheumatic diseases, retroviruses have been repeatedly discussed as important etiologic factors. However, despite a considerable amount of indirect evidence that retroviruses might indeed be involved in triggering or perpetuating autoimmune rheumatic diseases, clear cut direct evidence is still missing. Studies on arthropathies associated with HIV-1 or HTLV-1 infection as well as new experimental animal models like the Tax transgene mice and new data from the MLKjlpr mouse model might help to answer the questions how and by what mechanisms retroviral infection may lead to autoimmune rheumatic diseases. From data obtained in the MLR//pr mouse it seems obvious that a potential link of retroviruses, apoptosis and autogenes to autoimmune diseases opens exciting new approaches to the study of rheumatic disease pathogenesis.

show abstract

Augmentation of lymphocyte and macrophage proliferation by caprine arthritis-encephalitis virus contributes to the development of progressive arthritis

Cited by 10 publications

References 29 publications

Comparative study by computed radiography, histology, and scanning electron microscopy of the articular cartilage of normal goats and in chronic infection with caprine arthritis‐encephalitis virus

Comparative study by computed radiography, histology, and scanning electron microscopy of the articular cartilage of normal goats and in chronic infection with caprine arthritis‐encephalitis virus

Molecular and cellular mechanisms of joint destruction in rheumatoid arthritis: two cellular mechanisms explain joint destruction?

Retroviruses and autoimmune rheumatic diseases

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