scholarly journals Demonstration of impaired T cell regulation of Epstein-Barr virus stimulated B lymphocytes in rheumatoid arthritis with HLA identical, disease discordant sibling pairs.

1988 ◽  
Vol 47 (5) ◽  
pp. 372-376 ◽  
Author(s):  
M C Fawcett ◽  
D J Walker ◽  
I D Griffiths
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cell ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Cell Regulation ◽  
Sibling Pairs ◽  
Barr Virus ◽  
T Cell Regulation ◽  
Epstein Barr

A Mechanism of T Cell Regulation of Epstein-Barr Virus Latency

1993 ◽  
Vol 147 (2) ◽  
pp. 256-266 ◽  
Author(s):  
Patrizia Frugoni ◽  
Sandra E. Pike ◽  
Giovanna Tosato
Keyword(s):  
T Cell ◽  
Epstein Barr Virus ◽  
Cell Regulation ◽  
Barr Virus ◽  
Virus Latency ◽  
T Cell Regulation ◽  
Epstein Barr

scholarly journals Effect of methotrexate and anti-TNF on Epstein-Barr virus T-cell response and viral load in patients with rheumatoid arthritis or spondylarthropathies

2009 ◽  
Vol 11 (3) ◽  
pp. R77 ◽  
Author(s):  
Corinne Miceli-Richard ◽  
Nicolas Gestermann ◽  
Corinne Amiel ◽  
Jérémie Sellam ◽  
Marc Ittah ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Viral Load ◽  
T Cell ◽  
Cell Response ◽  
Epstein Barr Virus ◽  
T Cell Response ◽  
Barr Virus ◽  
Epstein Barr

Frequencies of epstein-barr virus—inducible IgM anti-IgG B lymphocytes in normal children and children with juvenile rheumatoid arthritis

1982 ◽  
Vol 25 (8) ◽  
pp. 959-965 ◽  
Author(s):  
Sherman Fong ◽  
John J. Miller ◽  
Terry L. Moore ◽  
Constantine D. Tsoukas ◽  
John H. Vaughan ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Juvenile Rheumatoid Arthritis ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
Normal Children ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals T cell response to Epstein-Barr virus transactivators in chronic rheumatoid arthritis.

1996 ◽  
Vol 184 (5) ◽  
pp. 1791-1800 ◽  
Author(s):  
E Scotet ◽  
J David-Ameline ◽  
M A Peyrat ◽  
A Moreau-Aubry ◽  
D Pinczon ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
T Cell ◽  
Epstein Barr Virus ◽  
Large Fraction ◽  
T Cell Response ◽  
Unknown Etiology ◽  
Rheumatoid Arthritis Pathogenesis ◽  
Chronic Rheumatoid Arthritis ◽  
Barr Virus ◽  
Epstein Barr

Rheumatoid arthritis is a multistep disorder associated with autoimmune features of yet unknown etiology. Implication of viruses such as Epstein-Barr virus (EBV) in rheumatoid arthritis pathogenesis has been suspected on the basis of several indirect observations, but thus far, a direct link between EBV and rheumatoid arthritis has not been provided. Here we show that a large fraction of T cells infiltrating affected joints from a patient with chronic rheumatoid arthritis recognizes two EBV transactivators (BZLF1 and BMLF1) in a major histocompatibility complex-restricted fashion. Responses to these EBV antigens by synovial lymphocytes from several other chronic rheumatoid arthritis patients were readily detectable. Thus these results suggest a direct contribution of EBV to chronic rheumatoid arthritis pathogenesis. They also demonstrate for the first time the occurrence of T cell responses against EBV transactivating factors, which might be central in the control of virus reactivation.

scholarly journals Analysis of the defects responsible for the impaired regulation of Epstein-Barr virus-induced B cell proliferation by rheumatoid arthritis lymphocytes. I. Diminished gamma interferon production in response to autologous stimulation.

1983 ◽  
Vol 157 (1) ◽  
pp. 173-188 ◽  
Author(s):  
F Hasler ◽  
H G Bluestein ◽  
N J Zvaifler ◽  
L B Epstein
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Gamma Interferon ◽  
Barr Virus ◽  
T Cell Regulation ◽  
Epstein Barr

T cells of patients with rheumatoid arthritis (RA) do not control the rate of B lymphoblast transformation induced by Epstein-Barr virus (EBV) as efficiently as T cells from healthy individuals; thus, lymphoblast cell lines are established more readily in RA lymphocytes in vitro after EBV infection. In the present experiments, we have asked whether this T cell regulation can be reproduced by lymphocytes. We found that normal T cells, activated in allogeneic or autologous mixed leukocyte reactions (MLR), produce lymphokines that inhibit in vitro EBV-induced B cell proliferation. Allogeneic MLR supernatants inhibited EBV-induced DNA synthesis 62 +/- 4% (mean +/- SE) at 10 d post-infection, whereas autologous MLR supernatants suppressed it 50 +/- 3%. RA T cell supernatants produced in an allogeneic MLR suppressed as well as normal T cell supernatants (64 +/- 5% inhibition). In contrast, supernatants from RA autologous MLR had little inhibitory activity. EBV-induced DNA synthesis at 10 d was reduced only 8 +/- 3%, compared with the 50 +/- 3% suppressive activity of normal autologous MLR supernatants. The magnitude of the proliferative responses in the autologous MLR regenerating the lymphokines was similar in the normal and RA populations. After depletion of adherent cells from the RA auto-MLR stimulators, supernatant inhibitory activities increased to normal levels (from 11 +/- 6 [SE] to 52 +/- 6% [SE]). The inhibitory factor involved in the regulation of in vitro EBV infection is a protein with a molecular weight of approximately 50,000. Its activity is eliminated by hearing at 56 degrees C and by exposure to acid at pH 2. The inhibitory activity is blocked by mixing the MLR supernatants with a polyvalent antisera or monoclonal antibodies specific for human gamma interferon. Gamma interferon produced by activating T cells in allo- or auto-MLR can reproduce T cell-mediated regulation of EBV-induced B cell proliferation, and the failure of RA auto-MLR to generate that lymphokine parallels the defective T cell regulation of EBV-induced B cell proliferation characteristic of RA lymphoid cells.

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