| pubmed-article:12723978 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12723978 | lifeskim:mentions | umls-concept:C0004364 | lld:lifeskim |
| pubmed-article:12723978 | lifeskim:mentions | umls-concept:C0004561 | lld:lifeskim |
| pubmed-article:12723978 | lifeskim:mentions | umls-concept:C0302350 | lld:lifeskim |
| pubmed-article:12723978 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:12723978 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:12723978 | pubmed:dateCreated | 2003-5-1 | lld:pubmed |
| pubmed-article:12723978 | pubmed:abstractText | Depleting B cells with anti-CD20 monoclonal antibodies emerges as a new therapeutic strategy in autoimmune diseases. Preliminary clinical studies suggest therapeutic benefits in patients with classic autoantibody-mediated syndromes, such as autoimmune cytopenias. Treatment responses in rheumatoid arthritis have opened the discussion about whether mechanisms beyond the removal of potentially pathogenic antibodies are effective in B-cell depletion. B cells may modulate T-cell activity through capturing and presenting antigens or may participate in the neogenesis of lymphoid microstructures that amplify and deviate immune responses. Studies exploring which mechanisms are functional in which subset of patients hold the promise of providing new and rational treatment approaches for autoimmune syndromes. | lld:pubmed |
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| pubmed-article:12723978 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12723978 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12723978 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12723978 | pubmed:issn | 1478-6362 | lld:pubmed |
| pubmed-article:12723978 | pubmed:author | pubmed-author:WeyandCorneli... | lld:pubmed |
| pubmed-article:12723978 | pubmed:author | pubmed-author:GoronzyJörg... | lld:pubmed |
| pubmed-article:12723978 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12723978 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:12723978 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12723978 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12723978 | pubmed:pagination | 131-5 | lld:pubmed |
| pubmed-article:12723978 | pubmed:dateRevised | 2010-7-19 | lld:pubmed |
| pubmed-article:12723978 | pubmed:meshHeading | pubmed-meshheading:12723978... | lld:pubmed |
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| pubmed-article:12723978 | pubmed:meshHeading | pubmed-meshheading:12723978... | lld:pubmed |
| pubmed-article:12723978 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12723978 | pubmed:articleTitle | B cells as a therapeutic target in autoimmune disease. | lld:pubmed |
| pubmed-article:12723978 | pubmed:affiliation | Departments of Medicine and Immunology, Mayo Clinic, Rochester, MN, USA. goronzy.jorg@mayo.edu | lld:pubmed |
| pubmed-article:12723978 | pubmed:publicationType | Editorial | lld:pubmed |
| pubmed-article:12723978 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12723978 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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