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Effects of intralymphatic immunotherapy on natural killer activity in malignant melanoma patients
Author(s) -
Moy Peter M.,
Golub Sidney H.,
Calkins Edward,
Morton Donald L.
Publication year - 1985
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930290209
Subject(s) - melanoma , immunotherapy , medicine , immunology , immune system , lymphokine activated killer cell , cytolysis , natural killer cell , k562 cells , adjuvant , cell , antigen , cancer research , active immunotherapy , concomitant , cellular immunity , t cell , cytotoxicity , biology , interleukin 21 , leukemia , in vitro , biochemistry , genetics
Adjuvant immunotherapy has the theoretical attraction of augmenting the host immune response at a time when the tumor burden is low. We have previously reported that intralymphatic immunotherapy (ILI) augments the cytolytic humoral immune responses in melanoma patients. This study was undertaken to assess the effects of ILI on cell‐mediated immunity. As a model for the cellular effects of ILI, we investigated the natural killer (NK) cell activity in malignant melanoma patients. Fourteen patients were given an allogeneic cultured tumor cell vaccine (TCV) intralymphatically with concomitant administration of BCG. Natural killer cell activity was assessed sequentially using the single cell lysis and binding assay. Overall NK activity against the K562 target cell line showed a moderate increase over pretreatment levels as reflected by the increased number of target binding lymphocytes. However, the percentage of target binders mediating cell lysis remained unchanged during treatment. Assessment of NK activity against the NK‐resistant M14 melanoma cell line reflected similar findings. These results suggest the activation of NK cells by tumor antigens, BCG, and/or alloimmunization with TCV. This increase appears to be manifested by increased target recognition rather than by alterations in effector cell function.