Regulation of autoreactive anti-IgG (Rheumatoid Factor) B cells in normal and autoimmune mice

1999 ◽  
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Mark J. Shlomchik
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Ann Marshak-Rothstein ◽  
Liliana Busconi ◽  
Christina M. Lau ◽  
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Elizabeth A. Leadbetter ◽  
...  

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M. Corr ◽  
W. O. Weigle ◽  
...  
Keyword(s):  
B Cells ◽  

2015 ◽  
Vol 98 (2) ◽  
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Ying Yi Zheng ◽  
Seung-Chul Choi ◽  
Leilani Zeumer ◽  
Laurence Morel

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Jacqueline William ◽  
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Mark J. Shlomchik

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Jean-Claude Garaud ◽  
...  
Keyword(s):  
B Cells ◽  

1991 ◽  
Vol 173 (2) ◽  
pp. 487-489 ◽  
Author(s):  
E Roosnek ◽  
A Lanzavecchia

Using Epstein-Barr virus B cell clones and antigen-specific T cell clones, we asked how antigen-antibody complexes are handled by B cells. We found that the only B cells capable of efficient presentation of antigen-antibody complexes are those that bind the complexes via membrane immunoglobulin, i.e., rheumatoid factor-producing B cells and, to a lower extent, antigen-specific B cells. On the contrary, nonspecific B cells, although capable of binding antigen-antibody complexes, fail to present them to T cells. Thus, rheumatoid factor B cells can present any antigen in the context of an immune complex and be triggered by T cells specific for a variety of foreign antigens. These results demonstrate a mechanism of intermolecular help that may be responsible for the production of rheumatoid factor and possibly of other types of autoantibodies.


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