IL4 production and increased CD30 expression by a unique CD8+ T‐cell subset in B‐cell chronic lymphocytic leukaemia

Phenotypic and functional abnormalities within the residual non‐B‐cell compartment of B‐cell chronic lymphocytic leukaemia (CLL) suggest an interaction between tumour cells and host immune effectors. To explore the possibility of a polarized Th1/Th2 response we have studied CD30 antigen expression a...

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Published in:British journal of haematology Vol. 104; no. 3; pp. 589 - 599
Main Authors: De TOTERO, DANIELA, REATO, GIGLIOLA, MAURO, FRANCESCA, CIGNETTI, ALESSANDRO, FERRINI, SILVANO, GUARINI, ANNA, GOBBI, MARCO, GROSSI, CARLOENRICO, FOA, ROBERT
Format: Journal Article
Language:English
Published: Oxford, U.K. and Cambridge, USA Blackwell Science Ltd 01-03-1999
Blackwell
Blackwell Publishing Ltd
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Summary:Phenotypic and functional abnormalities within the residual non‐B‐cell compartment of B‐cell chronic lymphocytic leukaemia (CLL) suggest an interaction between tumour cells and host immune effectors. To explore the possibility of a polarized Th1/Th2 response we have studied CD30 antigen expression and the pattern of cytokine production by purified CLL T cells. Activated T cells from CLL patients showed a significant increase in the expression of CD30 compared to normal controls. Accordingly, high levels of soluble CD30 were detected in supernatants from activated T‐cell cultures, as well as in CLL serum samples. Messenger RNA for IL4 was found in both resting and, to a greater extent, in activated CLL T lymphocytes. The latter cells were also capable of releasing IL4. Three‐colour immunofluorescence analyses revealed a strong CD30 expression in the CD3+/CD8+/CD28− large granular lymphocyte subset, which is considerably expanded in CLL. Production of IL4, as well as expression and release of CD30 by these T cells, was conclusively demonstrated at the clonal level. These findings document an expansion of a peculiar subset of ‘Th2‐like’ cells in CLL, with an increased IL4 production and CD30 expression and release, that are likely to contribute to both the B‐cell accumulation and immune‐defects characteristic of this disease.
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ISSN:0007-1048
1365-2141
DOI:10.1046/j.1365-2141.1999.01219.x