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Natural killer‐cell immunodeficiency in patients with chronic myelogenous leukemia. I. Analysis of the defect using the monoclonal antibodies HNK‐1 (LEU‐7) and B73.1
Author(s) -
Fujimiya Yoshiaki,
Bakke Anthony,
Chang Weng Cheng,
LinkerIsraeli Marianna,
Udis Barry,
Horwitz David,
Pattengale Paul K.
Publication year - 1986
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910370502
Subject(s) - chronic myelogenous leukemia , monoclonal antibody , immunology , peripheral blood mononuclear cell , natural killer cell , antibody , biology , monoclonal , leukemia , interferon , cytotoxic t cell , in vitro , biochemistry
Quantitative evaluation of natural killer (NK) cells using the HNK‐I (Leu‐7) and B73.1 monoclonal antibodies (MAbs) was correlated with NK activity in 13 patients with chronic myelogenous leukemia (CML) and compared to normal donor controls. A consistent observation was the presence of normal absolute numbers of B73.1 + lymphocytes as well as normal to increased absolute numbers of HNK‐I + lymphoid cells in the peripheral blood of chronic‐phase CML patients. Despite normal to increased numbers of B73.1 + and HNK‐I + lymphoid cells, these patients consistently demonstrated a significant impairment of lymphocyte‐mediated NK activity in their peripheral blood. Further experiments demonstrated that chronic‐phase CML patients, in contrast to normal controls, had significantly increased percentages of HNK‐I + , E + and B73.1 + , E + lymphoid cells and significantly decreased percentages of HNK‐I + , E − and B73.1, E − lymphoid cells, which resulted in significant reversals of the HNK‐I + , E + to HNK‐I + , E − and B73.1 + , E + to B73.1 + , E − lymphoid cell ratios. (HNK‐I + [E + /E − ] > B73.1 + E + [E + /E − ]). Furthermore, as compared to normals, both FACS‐sorted HNK‐I + and B73.1 + lymphoid cells from the E + fraction of CML patients were consistently defective in NK activity, and could not be substantially augmented with α‐interferon preparations. Although markedly defective in their ability to lyse K‐562, HNK‐I + lymphoid cells from the E + fraction of CML patients were not defective in their ability to bind to the NK‐sensitive target, K‐562. In contrast, NK‐defective B73.1 + lymphoid cells were partially defective in their ability to bind to K‐562.