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RJ Ford, J Tsao, NM Kouttab, CG Sahasrabuddhe and SR Mehta
The cellular immune defect in untreated Hodgkin's disease (HD) has long
been recognized. This defect appears to be responsible for at least some of
the morbidity and ultimately the mortality associated with the disease. In
recent years, many studies have shown that the T cell component of the
immune response is the apparent site where the defect in HD exists and
where the immunoregulatory abnormalities that may account for the deficit
are observed. The discovery of the lymphokines and monokines, comprising
the human interleukin system, has elucidated some aspects of the regulatory
control of the functional pathways involved in T lymphocyte activation and
proliferation. The interleukin system can therefore provide the framework
to dissect immunodeficiency states, such as that seen in HD. The present
study indicates that HD patients' interleukin 1 (IL1) response appears to
be normal, as is their T cell proliferative response to exogenous IL2.
Interleukin 2 production by HD patients' peripheral blood mononuclear
cells, however, is decreased when compared with age/sex-matched controls.
The inability to generate IL2 after appropriate stimulation may reflect
either a primary cellular defect or a regulatory defect, such as excessive
immunosuppression, giving rise to the characteristic T cell
hyporesponsiveness seen in HD.
This article has been cited by other articles:
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| Copyright © 1984 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
