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rdf:type |
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lifeskim:mentions |
umls-concept:C0003873,
umls-concept:C0004561,
umls-concept:C0017262,
umls-concept:C0020846,
umls-concept:C0024141,
umls-concept:C0185117,
umls-concept:C0205100,
umls-concept:C0441712,
umls-concept:C0597357,
umls-concept:C1155003,
umls-concept:C1414549,
umls-concept:C1521805,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
1990-2-27
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pubmed:abstractText |
To clarify the differential state of B cell activation in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), we investigated the expression of low-affinity receptor for IgE (Fc epsilon RII; CD23) on their peripheral B cells by a cytofluorometry using H107 (CD23) and Leu-16 (CD20) monoclonal antibodies. The percentage of CD23-negative B cells in total lymphocytes was significantly greater in both groups of patients than in normal subjects, suggesting the hyperactivity of late-phase B cells in both diseases. However, the increase of CD23-negative B cells in RA was brought about by the increased number of total B cells, although that in SLE was mainly based on the relative decrease of CD23-positive B cells. The number of IgD-positive B cells was decreased, and the number of colony-forming B cells was markedly increased in SLE patients. These observations indicate that a B cell abnormality is mainly qualitative in SLE but quantitative in RA.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-1079727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-2426355,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-2523867,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-2525911,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-2942602,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-2953844,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-3033649,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-3038527,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-3041491,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-3260102,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-3358796,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-412774,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-5309797,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-6232028,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-6259207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-6259211,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-6429035,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-6971105,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-6976374,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-7138600,
http://linkedlifedata.com/resource/pubmed/commentcorrection/2532990-789096
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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 |
Dec
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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 |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
348-53
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2532990-Adult,
pubmed-meshheading:2532990-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:2532990-Arthritis, Rheumatoid,
pubmed-meshheading:2532990-B-Lymphocytes,
pubmed-meshheading:2532990-Humans,
pubmed-meshheading:2532990-Immunoglobulin E,
pubmed-meshheading:2532990-Lupus Erythematosus, Systemic,
pubmed-meshheading:2532990-Lymphocyte Activation,
pubmed-meshheading:2532990-Middle Aged,
pubmed-meshheading:2532990-Receptors, Fc,
pubmed-meshheading:2532990-Receptors, IgE
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pubmed:year |
1989
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pubmed:articleTitle |
Possible different mechanisms of B cell activation in systemic lupus erythematosus and rheumatoid arthritis: opposite expression of low-affinity receptors for IgE (CD23) on their peripheral B cells.
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pubmed:affiliation |
Second Division of Internal Medicine, Kyoto University Medical School, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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