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T Cell function in untreated B cell chronic lymphocytic leukemia
Author(s) -
Fernandez L. A.,
Macsween J. M.,
Langley G. R.
Publication year - 1977
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(197703)39:3<1168::aid-cncr2820390323>3.0.co;2-g
Subject(s) - rosette (schizont appearance) , chronic lymphocytic leukemia , null cell , stimulation , leukemia , medicine , cell , rosette formation , immunology , endocrinology , receptor , biology , cell culture , biochemistry , genetics
Column separated T cells from patients with chronic lymphocytic leukemia (CLL) showed significantly greater responses to mitogens than the unseparated leukemic lymphocytes (P < 0.01). However, the mitogenic responses were significantly lower at both 4 and 8 days than controls (P < 0.01 and < 0.05). After separation, rosette forming cells were 37% in the patients with CLL and 59% in age‐matched controls, and 62% in young normal individuals. When the responses to PHA were calculated per rosette forming cell, no significant difference was observed between the leukemic patients and normal control group. This suggests that there were increased numbers of cells which have neither the characteristics of B and T cells (null cells) in patients with chronic lymphocytic leukemia, and that these cells are unresponsive to PHA. Null cells were, in fact, obtained from these patients and were found to be unresponsive to PHA. When T cells were enriched by the rosette separation technique, the responses to PHA were significantly diminished at 4 days, but not at 8 days, when compared to age‐matched and young normal control groups. These observations were unchanged when responses were calculated per rosette forming cell. The rosette forming cell in CLL appeared to respond normally to stimulation by most of the parameters measured. However, an exception noted at the short time interval (4 days) after PHA stimulation suggests that there may be a subtle intrinsic defect in rosette forming cells or that they maybe more susceptible to mechanical or chemical injury. There also appears to be an increased proportion of null cells in CLL which are unresponsive to PHA.