SUB-POPULATIONS OF HUMAN LYMPHOCYTES-T .6. MALDISTRIBUTION OF T-CELL SUBSETS ASSOCIATED WITH ABNORMAL LOCOMOTION OF T-CELLS IN UNTREATED ADULT PATIENTS WITH HODGKINS-DISEASE

  • 1 January 1980
    • journal article
    • research article
    • Vol. 42  (1) , 186-195
Abstract
Peripheral blood and splenic T cells from adult patients with Hodgkin''s disease were examined for the proportions and numbers of T cells with receptors for IgM (T.mu.) or IgG (T.gamma.) and their locomotor responses to chemotactic stimuli of casein and [Escherichia coli] endotoxin-activated serum (EAS). Of the patients, 30% had absolute lymphopenia in the peripheral blood. The proportion of T.mu. cells was comparable but the proportion of T.gamma. cells was significantly increased (P < 0.001), resulting in an abnormally low ratio of T.mu./T.gamma. cells when compared to those for age- and sex-matched controls. In the spleens, the proportions of T cells and T.mu. cells were significantly increased (P < 0.001) and T.gamma. cells significantly decreased (P < 0.001), resulting in an abnormally high ratio of T.mu./T.gamma. cells when compared with normal spleens. In the peripheral blood T.mu. and T.gamma. cells were increased and T cells lacking either receptor (T.vphi.) were significantly decreased in patients in whom spleens were involved by the tumor when compared to those in whom spleens were not involved by the tumor. Peripheral blood T cells from patients with Hodgkin''s disease responded poorly to the chemotactic stimuli when compared to T cells from normal controls or T cells from the spleens of the same patients. T.mu. cell proportions in patients with combined stages III and IV were significantly lower (P < 0.025) than those in the peripheral blood of patients in combined stages I and II. No correlation was observed between the above parameters and histopathological types of Hodgkin''s disease. An abnormal distribution of T cell subsets and abnormality of locomotion of T cells between peripheral blood and spleens in patients with Hodgkin''s disease was demonstrated. This might explain the cellular basis of at least certain immunodeficiencies so commonly associated with Hodgkin''s disease.