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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
1976-10-2
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pubmed:abstractText |
Investigation of the cell S--Ig in acute lymphocytic leukaemia (ALL), at the onset of relapse of the disease, shows quite marked differences from patient to patient according to the extent of the immunofluorescent-positive cells. They may vary from 0.5 to 25% or more. When these Ig-positive cells are treated with trypsin and then incubated "in vitro" for six hours, many of them are no longer Ig-positive, i.e. they do not synthesize Ig. It might be possible, that the membrane-Ig observed before trypsinization does not represent true Ig-determinants of mature B-cells (antibodies attached to leukaemia-specific determinants?). The extent of these features decrease in remission until their disappearance. Relationship between the cell immunological patterns and the treatment response in ALL could exist. In a group of ALL-patients under the same treatment, that is, vincristine and prednisone, the correlation between the course of the disease after the above-mentioned therapy showed quick and complete remission in patients with low percentage of Ig-positive cells (below 10%) and poor improvement (often without complete remission) in patients with higher percentage of Ig-positive cells. Among the most important B-lymphocyte abnormalities in chronic lymphocytic leukaemia (CLL) are the following: (a) fluorescence intensity may vary not only from patient to patient, but also from cell to cell in the same patient; (b) the Fc-receptor can be lacking; (c) the C3b-receptor is not always present, or it is from 2 to 20-folds less frequent than the C3d-receptor, whereas normal human lymphocytes do not show any outstanding differences between the number of EAC rosette-forming cells either when tested with mouse complement (C3d-receptor) or with human complement C3b-receptor); (d) the traffic capacity of peripheral-blood B-lymphocytes in CLL is quite defective. Results of the observations on lymphocytes in CLL, taken as a whole, suggest that CLL is in general given by the expansion of an abnormal clone of cells of B origin, arrested in their maturative development, non-responsive to the mitogen stimulation, accumulating in the peripheral-blood for a traffic deficiency. On the contrary, the T-cells class is apparently normal, and the T-cell extent in CLL-peripheral blood can be even greater than normal when taken as absolute value.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0017-6559
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
21-33
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:780227-B-Lymphocytes,
pubmed-meshheading:780227-Humans,
pubmed-meshheading:780227-Leukemia, Lymphoid,
pubmed-meshheading:780227-Lymphocytes,
pubmed-meshheading:780227-Radiation Effects,
pubmed-meshheading:780227-Receptors, Antigen, B-Cell,
pubmed-meshheading:780227-Spleen,
pubmed-meshheading:780227-T-Lymphocytes,
pubmed-meshheading:780227-X-Rays
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pubmed:year |
1975
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pubmed:articleTitle |
Lymphocyte immunological patterns in leukaemia: a review.
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pubmed:publicationType |
Journal Article,
Review
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