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 ◽  
...  
2002 ◽  
Vol 73 (10) ◽  
pp. 1603-1610 ◽  
Author(s):  
Fran??oise Smets ◽  
Dominique Latinne ◽  
Herv?? Bazin ◽  
Raymond Reding ◽  
Jean-Bernard Otte ◽  
...  

Author(s):  
Vaios Karanikas ◽  
Maria Zamanakou ◽  
Faye Soukou ◽  
Theodora Kerenidi ◽  
Ioannis Tsougos ◽  
...  

1994 ◽  
Vol 57 (11) ◽  
pp. 1611-1616
Author(s):  
Myat T. Kyaw-Tanner ◽  
Donald Esmore ◽  
Scott R. Burrows ◽  
Elizabeth M. Benson ◽  
Tom B. Sculley

1996 ◽  
Vol 184 (5) ◽  
pp. 1791-1800 ◽  
Author(s):  
E Scotet ◽  
J David-Ameline ◽  
M A Peyrat ◽  
A Moreau-Aubry ◽  
D Pinczon ◽  
...  

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.


2001 ◽  
Vol 55 (7) ◽  
pp. 373-380 ◽  
Author(s):  
E Houssaint ◽  
X Saulquin ◽  
E Scotet ◽  
M Bonneville

1991 ◽  
Vol 33 (4) ◽  
pp. 411-420 ◽  
Author(s):  
C. SCHMIDT ◽  
S. R. BURROWS ◽  
D. J. MOSS ◽  
T. B. SCULLEY ◽  
I. S. MISKO

2009 ◽  
Vol 83 (18) ◽  
pp. 9068-9078 ◽  
Author(s):  
Delphine Sauce ◽  
Martin Larsen ◽  
Rachel J. M. Abbott ◽  
Andrew D. Hislop ◽  
Alison M. Leese ◽  
...  

ABSTRACT In immunocompetent individuals, the stability of the herpesvirus-host balance limits opportunities to study the disappearance of a virus-specific CD8+ T-cell response. However, we noticed that in HLA-A*0201-positive infectious mononucleosis (IM) patients undergoing primary Epstein-Barr virus (EBV) infection, the initial CD8 response targets three EBV lytic antigen-derived epitopes, YVLDHLIVV (YVL), GLCTLVAML (GLC), and TLDYKPLSV (TLD), but only the YVL and GLC reactivities persist long-term; the TLD response disappears within 10 to 27 months. While present, TLD-specific cells remained largely indistinguishable from YVL and GLC reactivities in many phenotypic and functional respects but showed unique temporal changes in two markers of T-cell fate, interleukin 7 receptor alpha (IL-7Rα; CD127) and programmed death 1 (PD-1). Thus, following the antigen-driven downregulation of IL-7Rα seen on all populations in acute IM, in every case, the TLD-specific population recovered expression unusually quickly post-IM. As well, in four of six patients studied, TLD-specific cells showed very strong PD-1 upregulation in the last blood sample obtained before the cells’ disappearance. Our data suggest that the disappearance of this individual epitope reactivity from an otherwise stable EBV-specific response (i) reflects a selective loss of cognate antigen restimulation (rather than of IL-7-dependent signals) and (ii) is immediately preceded, and perhaps mediated, by PD-1 upregulation to unprecedented levels.


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