Immune functions of human synovial cells. phenotypic and t cell regulatory properties of macrophage‐like cells that express hla–dr

Klareskog, Lars; Forsum, Urban; Kabelitz, Dieter; Plöen, L.; Sundström, Christer; Nilsson, Kenneth; Wigren, Anders; Wigzell, Hans

doi:10.1002/art.1780250502

Cited by 87 publications

(32 citation statements)

References 33 publications

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“…In agreement with prior studies by others (28)(29)(30) and by our laboratory (14), we found that the majority of synoviallining cells from RA biopsies expressed intense staining with antibodies directed against HLA-DR antigen (Fig. 1 D and Table II) and complement receptor CR3 (Fig.…”

Section: Methodssupporting

confidence: 93%

Rheumatoid arthritis synovial membrane contains a 62,000-molecular-weight protein that shares an antigenic epitope with the Epstein-Barr virus-encoded associated nuclear antigen.

Fox¹,

Sportsman²,

Rhodes³

et al. 1986

J. Clin. Invest.

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Section: Methodssupporting

confidence: 93%

Rheumatoid arthritis synovial membrane contains a 62,000-molecular-weight protein that shares an antigenic epitope with the Epstein-Barr virus-encoded associated nuclear antigen.

Fox¹,

Sportsman²,

Rhodes³

et al. 1986

J. Clin. Invest.

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“…Klareskog et al have recently demonstrated that the synovial lining cells in both RA patients and normal controls are Ia+ and O K M l + , and are capable of activating synovial or peripheral blood T cells in the presence of soluble antigen (31). While our study suggests that reactivity of the conjunctival epithelium with anti-la may reflect disease activity, studies involving larger numbers of patients will be necessary to confirm this.…”

Section: Discussionsupporting

confidence: 45%

Rheumatoid arthritis and sterile corneal ulceration

Michels

Cobo

Caldwell

et al. 1984

Arthritis & Rheumatism

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Tissue immune effector cells and epithelial surface antigens present in eye tissue of rheumatoid arthritis (RA) patients with sterile corneal ulceration were studied using a large panel of monoclonal antibodies. During periods of active corneal ulceration, conjunctivae and corneas of all RA patients studied contained numerous immune-associated (Ia) antigen-positive tissue macrophages. In 4 of 6 patients, conjunctival or corneal T cell infiltrations were present. In 2 patients, a T cell vasculitis was seen in conjunctival tissue. Conjunctival epithelial cells of all 6 RA patients expressed Ia antigens during active corneal ulceration. These data provide evidence for immune-mediated mechanisms in the pathophysiology of corneal ulceration in RA. Moreover, the expression of Ia antigens by conjunctival epithelial cells may be a useful indicator of disease activity in RA patients with sterile corneal ulceration.The pathophysiologic events in rheumatoid arthritis (RA) leading to corneal ulceration and corneal stromal loss in the absencc of scleritis are unknown (I-

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“…In addition, AMLR studies differ most profoundly from the system described in this study because they require irradiated, apoptotic APCs for induction of the T cell proliferation, which is therefore qualitatively and quantitatively different from in vitro homeostatic proliferation. Finally, mixed lymphocyte reactions were usually incubated for 7 days only (12,17,47), and the homeostatic in vitro proliferation reported to be induced by dendritic cells but not by monocytes in the mouse system was determined after 5 days of incubation (40). We saw the majority of cell divisions to take place beyond day 7 during the second week of culture.…”

Section: Cd4mentioning

confidence: 99%

Ex Vivo Homeostatic Proliferation of CD4+ T Cells in Rheumatoid Arthritis Is Dysregulated and Driven by Membrane-Anchored TNFα

Wagner

Pierer

Wahle

et al. 2004

The Journal of Immunology

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The systemic CD4+ T cell compartment in patients with rheumatoid arthritis (RA) is characterized by TCR repertoire contraction, shortened telomere lengths, and decreased numbers of recent thymic emigrants, suggesting a disturbed CD4+ T cell homeostasis. In mice, homeostatic proliferation of peripheral CD4+ T cells is regulated by TCR interaction with self peptide-MHC complexes (pMHC) and can be reproduced in vitro. We have established an ex vivo model of homeostatic proliferation, in which self-replication of human CD4+ T cells is induced by cell-cell contact with autologous monocytes. In healthy individuals, blockade of TCR-pMHC class II contact resulted in decreased CD4+ T cell division. In contrast, homeostatic proliferation in RA patients was not inhibited by pMHC blockade, but increased during the initial culture period. The anti-TNF-α Ab cA2 inhibited homeostasis-driven ex vivo proliferation in healthy controls and in RA patients. In addition, treatment of RA patients with infliximab decreased the ex vivo rate of homeostatic proliferation of CD4+ T cells. Our results suggest a disturbed regulation of CD4+ T cell homeostasis leading to the repertoire aberrations reported in RA. Membrane-anchored TNF-α appears to be a cell-cell contact-dependent stimulus of homeostatic proliferation of CD4+ T cells, possibly favoring self-replication of autoreactive CD4+ T cells in patients with RA.

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Immune functions of human synovial cells. phenotypic and t cell regulatory properties of macrophage‐like cells that express hla–dr

Cited by 87 publications

References 33 publications

Rheumatoid arthritis synovial membrane contains a 62,000-molecular-weight protein that shares an antigenic epitope with the Epstein-Barr virus-encoded associated nuclear antigen.

Rheumatoid arthritis synovial membrane contains a 62,000-molecular-weight protein that shares an antigenic epitope with the Epstein-Barr virus-encoded associated nuclear antigen.

Rheumatoid arthritis and sterile corneal ulceration

Ex Vivo Homeostatic Proliferation of CD4+ T Cells in Rheumatoid Arthritis Is Dysregulated and Driven by Membrane-Anchored TNFα

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