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Binding of Leukaemic Blasts to Various Subpopulations of Lymphokine‐Activated Killer Cells
Author(s) -
PALUCKA A. K.,
PORWIT A.,
REIZENSTEIN P.
Publication year - 1993
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1993.tb01754.x
Subject(s) - lymphokine activated killer cell , cd16 , k562 cells , lymphokine , transferrin receptor , cytotoxic t cell , microbiology and biotechnology , biology , natural killer cell , cd3 , immunology , chemistry , antigen , cd8 , interleukin 21 , receptor , leukemia , in vitro , biochemistry
Conjugate formation by natural killer (NK)‐resistant and N K‐sensitive leukaemic cell lines with fresh and IL‐2‐stimulated (lymphokine‐activated killer, LAK) peripheral blood lymphocytes (PBL) was studied by a flow cytofluorometry method with double staining, A significant difference in binding of NK‐resistant T‐cell lymphoma (HuT 78) and NK‐sensitive myeloid (K562) blasts to fresh PBL was observed ( P <0.01). Activation of lymphocytes with IL‐2 resulted in a significant increase of binding and killing of both K562 and HuT 78. However, in the case of blasts from NK‐resistant cell line Daudi a similar conjugate formation with fresh PBL and LAK effectors was observed, despite a significant increase in killing. Various subpopulalions of LAK effectors (CD3, CD16 and CD56 positive) displayed similar binding activity towards myeloid (K562) and lymphoid (Raji) blasts, which shows that conjugate formation occurs not only with NK‐cell‐derived. but also with T‐cell‐derived LAK cells. The blocking of CD71 antigen (transferrin receptor) on K562 blasts inhibited binding of cytotoxic lymphocytes, which was mostly due to the blocking of binding of CD56 + subpopulation. Our results indicate that the resistance of leukaemic blasts to cell‐mediated cytotoxicity may depend on different (and probably several) steps of this process.