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rdf:type |
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lifeskim:mentions |
umls-concept:C0002880,
umls-concept:C0003241,
umls-concept:C0004561,
umls-concept:C0026336,
umls-concept:C0027651,
umls-concept:C0205463,
umls-concept:C0301625,
umls-concept:C0699748,
umls-concept:C0870509,
umls-concept:C1510411,
umls-concept:C2347946
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pubmed:issue |
2
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pubmed:dateCreated |
1993-9-10
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pubmed:abstractText |
We showed previously that broadly reactive IgG anti-immunoglobulin autoantibodies produced by rats during the immune response suppress the B cell response. We report here on the effect of a similar human antibody on self-reactive human B cells. IgG anti-F(ab')2 was added to cultures of anti-erythrocyte autoantibody-producing B cells derived from healthy donors. A dose-dependent suppression of the antibody response was obtained (maximum at 1.3 ng IgG/10(6) cells). This effect was competitively inhibited by F(ab')2 gamma. Autoimmune haemolytic anaemia can be caused by chronic monoclonal B cell proliferation. To reproduce this condition in vitro we immortalized B cells with Epstein-Barr virus (EBV) and raised a B cell population with anti-erythrocyte autoantibody activity. These cells were electrically fused with CB-F7 tumour cells and an IgG1 cold-reactive anti-erythrocyte autoantibody-producing B cell line was established. Surprisingly, the tumour cells were not suppressed by IgG anti-F(ab')2. It is known that anti-immunoglobulins selectively suppress antigen-receptor (AgR)-occupied B cells by a Fc gamma-receptor (Fc gamma R)-mediated mechanism. To occupy their AgR, we preincubated the tumour cells with anti-AgR antibody. In spite of this, their susceptibility to suppression was not restored. As shown by rabbit IgG-sensitized ox erythrocyte (EA)-rosetting, this refractoriness was not due to a loss of Fc gamma R. Our experiments delineate a mechanism of peripheral B cell suppression to autoantigens, and show a way of escape from control relevant for the pathogenesis of autoimmune haemolytic anaemia.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-13940587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-1631951,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-1631952,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-1703209,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-1830923,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-1944535,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-1956380,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-2356469,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-2389476,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-2526369,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-2586604,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-2586609,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-2788981,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-3261841,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-3480535,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4121353,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4125922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4131540,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4158463,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4546876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4630646,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4875623,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4900673,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-4976105,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-6210096,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-6300689,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-6350525,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-6435121,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-6601551,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-6970643,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-7021394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8394233-7021396
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
93
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
253-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8394233-Anemia, Hemolytic, Autoimmune,
pubmed-meshheading:8394233-Antibodies, Anti-Idiotypic,
pubmed-meshheading:8394233-Autoantibodies,
pubmed-meshheading:8394233-B-Lymphocytes,
pubmed-meshheading:8394233-Cell Line, Transformed,
pubmed-meshheading:8394233-Cell Transformation, Neoplastic,
pubmed-meshheading:8394233-Cells, Cultured,
pubmed-meshheading:8394233-Erythrocytes,
pubmed-meshheading:8394233-Herpesvirus 4, Human,
pubmed-meshheading:8394233-Humans,
pubmed-meshheading:8394233-Immunoglobulin Fab Fragments,
pubmed-meshheading:8394233-Immunoglobulin G
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pubmed:year |
1993
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pubmed:articleTitle |
Suppression of anti-erythrocyte autoantibody-producing B cells by a physiological IgG-anti-F(ab')2 antibody and escape from suppression by tumour transformation; a model relevant for the pathogenesis of autoimmune haemolytic anaemia.
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pubmed:affiliation |
Blood Bank, University of Heidelberg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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