Lectin-dependent cell-mediated cytotoxicity and blastogenesis by large granular-enriched and depleted lymphocytes

• Published in: Clinical and experimental immunology Vol. 63; no. 1; pp. 171 - 178
• Main Authors: PERL, A, GONZALEZ-CABELLO, R, LASKAY, T, BENCZUR, M, LANG, I, ONODY, K, NEKAM, K, GERGELY, P, FEHER, J
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell 1986
• Subjects: Biological and medical sciences; Cell Line; Concanavalin A - pharmacology; Cytotoxic reactions (adcc reaction, cell-mediated lympholysis, complement-dependent cytotoxicity and others); Cytotoxicity, Immunologic; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immunobiology; Immunological reactions in vitro; Interferon Type I - immunology; Killer Cells, Natural - immunology; Lymphocyte Activation; Lymphocytes - immunology; Nasopharyngeal Neoplasms - immunology; Human; Cell proliferation; Cell culture; Lectin; Cytotoxicity; Cellular immunity; Blast transformation; Concanavalin A; Large granular lymphocyte; Cell subpopulation; Natural killer cell; Mitogen; Lymphocyte
• ISSN: 0009-9104; 1365-2249

The role of larger granular-enriched and depleted lymphocytes was studied in lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 human epipharynx carcinoma target cells. LDCC was evaluated by detachment from the monolayer of 3H-thymidine-prelabelled HEp-2 cells in a 24 h assay at effector-target cell ratios of 25:1 and 50:1 in the presence of 25 micrograms/ml concanavalin A (Con A). Under the aforementioned conditions but in the absence of Con A natural cell-mediated cytotoxicity (NCMC) was not found. However, cytotoxicity was significantly augmented in the presence of Con A (= LDCC) using human peripheral blood mononuclear cells (PBMC) as effectors. Large granular lymphocytes (LGL), which show high natural killer (NK) activity to K 562 target cells, failed to be cytotoxic against HEp-2 targets similar to large granular depleted lymphocytes (LGL-DL). On the other hand, LGL caused only a slight LDCC; whilst LGL-DL induced strong LDCC activity towards HEp-2 targets. In comparison to LDCC using LGL-DL as effector cells, LGL and LGL-DL mixed at a ratio of 1:2, and added to target cells, had no major effect on LDCC, while a lower level of LDCC was observed at LGL/LGL-DL ratios of 1:1, and 2:1, suggesting the dilution of LGL-DL, potential effectors of LDCC to HEp-2 cells, rather than a specific regulatory role of LGL in LDCC. In parallel studies, the proliferation of LGL-DL in response to Con A was less than that observed with PBMC or LGL. The response could be restored by replacing half of LGL-DL per culture with an equal number of LGL, or by the addition of 10% monocytes. Significant functional differences between LGL and LGL-DL in LDCC as well as in Con A-induced blastogenesis are suggested.