TY - JOUR
T1 - Multivariate analysis of T‐cell functional defects and circulating serum factors in hodgkin's disease
AU - Schulof, Richard S.
AU - Bockman, Richard S.
AU - Garofalo, John A.
AU - Cirrincione, Constance
AU - Cunningham‐Rundles, Susanna
AU - Fernandes, Gabriel
AU - Day, Noorbibi K.
AU - Pinsky, Carl M.
AU - Incefy, Genevieve S.
AU - Thaler, Howard T.
AU - Good, Robert A.
AU - Gupta, Sudhir
PY - 1981/8/15
Y1 - 1981/8/15
N2 - A comprehensive immunologic and serologic analysis was performed on 31 untreated patients with Hodgkin's disease. Immune evaluations stressed T‐cell functional activity and included traditional parameters (PHA responsiveness and delayed hypersensitivity skin reactivity), as well as newer functional assays (T‐cell colony formation, chemotaxis, spontaneous and antibody‐dependent cytotoxicity, and concanavalin A‐induced suppressor cell activity (CISA)). Serum factors included ferritin, prostaglandins, zinc, copper, immune complexes, and thymic hormone activity. Every patient exhibited at least one T‐cell or serum abnormality. The greatest percentage of patients exhibited T‐cell defects in chemotaxis (85%), colony formation (81%), and PHA reactivity (64%). Immune defects were more common with advanced disease but were not related to absolute T‐cell or monocyte count, skin test anergy, or abnormalities of Tμ/Tγ cell proportions. Linear relationships were identified among abnormalities in the three assays employing mononuclear cells (PHA, colony formation, CISA) which may have reflected the inhibitory influence of monocytes present in the mononuclear cell preparations. Low serum zinc correlated with marked impairment of T‐cell chemotaxis. Elevated prostaglandins were associated with high PHA reactivity and with depressed colony formation. Our results indicate that many complex factors, including intrinsic T‐cell defects, contribute to the impaired immunity associated with Hodgkin's disease.
AB - A comprehensive immunologic and serologic analysis was performed on 31 untreated patients with Hodgkin's disease. Immune evaluations stressed T‐cell functional activity and included traditional parameters (PHA responsiveness and delayed hypersensitivity skin reactivity), as well as newer functional assays (T‐cell colony formation, chemotaxis, spontaneous and antibody‐dependent cytotoxicity, and concanavalin A‐induced suppressor cell activity (CISA)). Serum factors included ferritin, prostaglandins, zinc, copper, immune complexes, and thymic hormone activity. Every patient exhibited at least one T‐cell or serum abnormality. The greatest percentage of patients exhibited T‐cell defects in chemotaxis (85%), colony formation (81%), and PHA reactivity (64%). Immune defects were more common with advanced disease but were not related to absolute T‐cell or monocyte count, skin test anergy, or abnormalities of Tμ/Tγ cell proportions. Linear relationships were identified among abnormalities in the three assays employing mononuclear cells (PHA, colony formation, CISA) which may have reflected the inhibitory influence of monocytes present in the mononuclear cell preparations. Low serum zinc correlated with marked impairment of T‐cell chemotaxis. Elevated prostaglandins were associated with high PHA reactivity and with depressed colony formation. Our results indicate that many complex factors, including intrinsic T‐cell defects, contribute to the impaired immunity associated with Hodgkin's disease.
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U2 - 10.1002/1097-0142(19810815)48:4<964::AID-CNCR2820480419>3.0.CO;2-B
DO - 10.1002/1097-0142(19810815)48:4<964::AID-CNCR2820480419>3.0.CO;2-B
M3 - Article
C2 - 6456060
AN - SCOPUS:0019506822
VL - 48
SP - 964
EP - 973
JO - Cancer
JF - Cancer
SN - 0008-543X
IS - 4
ER -