[CANCER RESEARCH 54, 4430-4435, August 15, 1994]
Abnormal Cytokine Expression in Sézary and Adult T-Cell Leukemia Cells
Correlates with the Functional Diversity between
These T-Cell Malignancies1
Craig L. Tendier,2 Jack D. Burton, Jonathan Jatte, David Danielpour, Michael Charley, J. Philip McCoy,
Mark R. Pittelkow, and Thomas A. Waldmann
Division of Pediatrie Oncology, Mount Sinai School of Medicine, New York, New York 10029-6574 /C. L. T./; Metabolism Branch ¡J.D. B., T. A. W.] and Laboratory of
Chemoprevention [D. D.], National Cancer Institute, NIH, Bethesda, Maryland 20892; Division of Allergy and Pulmonary Medicine, Hahnemann University, Philadelphia, PA
19102 [J. J.¡; Department of Dermatology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260 fM. C, J. P. M.]; and Department of Dermatology,
Mayo Clinic, Rochester, Minnesota 55905 [M. R. W.]
ABSTRACT
TheSézarysyndrome (SzS) and adult T-cell leukemia (ATL) are malig
nant proliferations of mature T-lymphocytes that possess distinct func
tions. Sézarycells function as helper cells, whereas ATL cells are usually
suppressor effectors. Although phenotypically similar (CD4+/CD7-/
CDS—), these functional differences between the T-cell lymphoprolifera-
tive disorders suggest different patterns of cytokine expression. We wished
to delineate the cytokine mechanisms potentially underlying the diverse
functional characteristics of SzS and ATL. Therefore, we analyzed the
expression of interleukins (IL) 2, 4, and 5, y-interferon, and transforming
growth factor /!, in the highly purified leukemic T-cells from 5 SzS and 5
ATL patients. Decreased inKNA and protein levels of IL-2, y-interferon,
and 11-5 were detected in mitogen-stimulated ATL and SzS cells when
compared to similarly cultured normal CD4+ cells. In contrast, IL-4
production was markedly up-regulated in the leukemic cells of 4/5 SzS
patients as compared to ATL and normal controls. Finally, fresh ATL
cells secreted higher levels of transforming growth factor ß,into the
culture medium than the malignant T-cells from SzS patients. Collectively
these results suggest that, similar to the murine CD4-expressing T-cell
subsets Thl and I h2, different cytokine profiles exist in a human popu
lation of CD4+ T-cells. Moreover, the distinct patterns of IL-4 and
transforming growth factor ß,expression by SzS and ATL cells, respec
tively, are most consistent with the functional differences (i.e., helper
versus suppressor activity) between these T-cell malignancies and thus
may play important roles in the pathogenesis of the paraneoplastic fea
tures associated with these two leukemias.
INTRODUCTION
The malignant expansion of mature CD4+ T-cells is represented
clinically by two distinct human leukemias known as the SzS3 and
ATL. SzS is a cutaneous T-cell lymphoma associated with diffuse
skin involvement known as erythroderma, generalized lymphadenop-
athy, and circulating malignant cells in the blood (1, 2). ATL occurs
in patients infected with the retrovirus HTLV-I and is also character
ized by infiltration of the skin with malignant T-cells (3). However, it
tends to have a more aggressive course than SzS and is often com
plicated by hepatosplenomegaly, hypercalcemia, and an extremely
high incidence of opportunistic infections (4, 5).
The circulating leukemic cells in SzS and ATL patients share the
Received 3/31/94; accepted 6/13/94.
The costs of publication of this article were defrayed in part by the payment of page
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1 Supported in part by a Young Investigator Award from the Mount Sinai Children's
Health Research Center. NICHD Grant, 5P30 HD28822 (C. L. T.).
2 To whom requests for reprints should be addressed, at PédiatrieHematology/Oncol-
ogy, Mount Sinai Medical Center, Box 1208, One Gustave Levy Place, New York, NY
10029.
3 The abbreviations used are: SzS, Sézary syndrome; ATL, adult T-cell leukemia; IL-2,
interleukin 2; IFN-7, -y-interferon; TGF-/3,, transforming growth factor ß,;PHA, phyto-
hemagglutinin; PMA, phorbol 12-myristate 13-acetate; PCR, polymerase chain reaction;
ELISA, enzyme-linked immunosorbent assay; HTLV-I, human T-cell leukemia virus type
I; PBMC, peripheral blood mononuclear cell; cDNA, complementary DNA.
identical mature T-cell phenotype, CD4+, but lack CD7 and CDS
antigen expression (6, 7). Although phenotypically similar, biological
differences between these T-lymphoproliferative disorders suggest an
altered pattern of cytokine expression. For example, in immunoglobulin
biosynthesis assays the neoplastic T-cells from SzS patients function as
helper cells when cocultured with stimulated normal B-cells, whereas in
the same assay ATL cells effectively suppress normal immunoglobulin
production (8). Moreover, peripheral blood lymphocytes from ATL pa
tients have impaired proliferative responses to T-cell mitogens (5). This
in vitro immunosuppressor activity of ATL cells is paralleled clinically
by the uniform finding of cutaneous anergy, failure to make antibody to
infused murine monoclonal antibodies, and increased incidence of op
portunistic infections in ATL patients (5, 9-10). In contrast, lack of
anergy, elevated levels of IgE, and the production of antibodies following
antigenic stimulation have all been demonstrated in patients with SzS (1,
2). These functional and clinical immunological differences between the
CD4+ leukemic T-cells from SzS and ATL patients suggest that, similar
to the murine T-helper cell populations designated Th 1 and Th2, distinc
tive cytokine profiles exist among human CD4-expressing T-cell subsets
as well.
Recently, mitogen-activated peripheral blood mononuclear cells
isolated from SzS patients were shown to produce significantly higher
protein levels of IL-4 and lower levels of IL-2 and IFN-y than did
similarly cultured cells from normal controls (11). However, this
study did not provide direct evidence that it is the malignant Sézary
cell which is responsible for the abnormal immune response since
enriched CD4+ leukemic populations from SzS patients were not
analyzed. Moreover, there has been no investigation comparing the
cytokine profile in SzS with respective levels of cytokine expression
in ATL to better define their relevance to the pathogenesis of the
immunological abnormalities associated with these T-cell malignan
cies. Therefore, we have examined the expression of IL-2, IFN-y,
IL-4, IL-5, and TGF-ß, in highly purified populations of leukemic
T-cells isolated from SzS and ATL patients to determine which
cytokines are potential mediators of the diverse immune abnormalities
observed in these T-cell lymphoproliferative disorders and to gain
insight into the regulatory network of cells that control the human
immune response.
MATERIALS AND METHODS
Patients. Five patients with SzS and five with ATL were studied. Healthy
blood bank donors, all males with a mean age of 46 years (range, 25-70),
served as normal controls. Informed consent was obtained from all patient
and volunteer blood donors. The SzS group consisted of four males and one
female from the United States with a mean age of 64 years (range, 50-71).
This patient population was characterized by the presence of erythroderma,
lymphadenopathy, and a circulating pool of abnormal lymphocytes with cere-
briform nuclei and a predominant CD4+/CD7-/CD8- T-cell phenotype.
Except for one SzS patient with a total WBC of 7,100/mm3, leukocytosis was
a consistent finding in this group ranging from 18,100 to 45,800 cells/mm3. All
4430
Research.
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