Cutaneous delayed hypersensitivity responses to tumor‐associated and other antigens in acute leukemia
- 15 September 1973
- journal article
- research article
- Published by Wiley in International Journal of Cancer
- Vol. 12 (2) , 409-419
- https://doi.org/10.1002/ijc.2910120212
Abstract
Fifty‐three patients with ALL (acute lymphocytic leukemia), twenty‐five patients with AML (acute myelogenous leukemia), and thirty‐eight healthy persons were tested for cutaneous delayed hypersensitivity with a standard battery of recall antigens and membrane extracts of normal white cells. The leukemic patients were also tested with membrane extracts of autologous and allogeneic blast and remission cells. There was not a significant difference between normals and leukemics in their response to PPD, mumps or SKSD. Positive results were elicited in the leukemia patients by blast cell extracts and not by extracts of remission or normal cells. In both AML and ALL patients, there was a statistically significant difference in the percentage of positive responses to autologous (and in ALL, allogeneic) blast extracts in remission and relapse. Serial responses of patients to autologous blast material were usually related to clinical status, being positive in remission and negative when a patient relapsed. There was a slight increase in remission length for patients who had positive responses to autologous material. A small group of ALL patients on an immunotherapy protocol, receiving BCG and allogeneic blast cells, was studied. There was no increase in incidence of positive reactions to the immunizing or other allogeneic blast cells after being on this protocol as compared with the reactions prior to receiving the cells. On different ALL treatment protocols there were different percentages of positive responses to autologous blast material. The pattern of responses seen in leukemia patients to autologous and allogeneic blast cells as compared with their responses to normal cells, remission cells, and other leukemia type cells provides evidence for cell‐mediated immunity to tumor‐associated antigens on human acute leukemia cells.Keywords
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