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Blood, 1 May 2002, Vol. 99, No. 9, pp. 3272-3279
IMMUNOBIOLOGY
Humoral immune responses against Wilms tumor gene WT1
product in patients with hematopoietic malignancies
Olga A. Elisseeva,
Yoshihiro Oka,
Akihiro Tsuboi,
Kiyoyuki Ogata,
Fei Wu,
Eui Ho Kim,
Toshihiro Soma,
Hiroya Tamaki,
Manabu Kawakami,
Yusuke Oji,
Naoki Hosen,
Takeshi Kubota,
Masashi Nakagawa,
Tamotsu Yamagami,
Akira Hiraoka,
Machiko Tsukaguchi,
Keiko Udaka,
Hiroyasu Ogawa,
Tadamitsu Kishimoto,
Taisei Nomura, and
Haruo Sugiyama
From the Departments of Radiation Biology, of Molecular
Medicine, and of Clinical Laboratory Science, Osaka University Medical
School; Third Department of Internal Medicine, Nippon Medical School,
Tokyo; Department of Medicine, Osaka Minami National Hospital; Nissay
Hospital, Nippon Life Saiseikai Foundation, Osaka; Center for Adult
Diseases, Osaka; Sakai Municipal Hospital, Osaka; Department of
Biophysics, Kyoto University; and Osaka University, Japan.
Wilms tumor gene WT1 is expressed at high
levels in hematopoietic malignancies, such as leukemias and
myelodysplastic syndromes (MDS), and in various kinds of solid tumors,
including lung cancer, and it exerts an oncogenic function in these
malignancies. IgM and IgG WT1 antibodies were measured by means of dot
blot assay in 73 patients with hematopoietic malignancies (16 acute
myeloid leukemia [AML], 11 acute lymphoid leukemia [ALL], 13 chronic myeloid leukemia [CML], and 33 MDS) and 43 healthy
volunteers. Immunoglobulin IgM, IgG, and IgM+IgG WT1 antibodies were
detected in 40 (54.8%), 40 (54.8%), and 24 (32.8%), respectively, of
the 73 patients with hematopoietic malignancies, whereas 7 (16.2%), 2 (4.7%), and none of the 43 healthy volunteers had IgM, IgG, or IgM+IgG
WT1 antibodies, respectively. Furthermore, immunoglobulin isotype class
switching of WT1 antibodies from IgM to IgG occurred in conjunction
with disease progression from refractory anemia (RA) to RA with excess of blasts (RAEB), and further to RAEB in transformation (RAEB-t) in MDS
patients. These results showed that humoral immune responses against
the WT1 protein could be elicited in patients with WT1-expressing hematopoietic malignancies, and they suggested that the helper T-cell
responses needed to induce humoral immune responses and immunoglobulin
isotype class switching from IgM to IgG were also generated in these
patients. Our findings may provide new insight into the rationale for
elicitation of cytotoxic T-cell responses against the WT1 protein in
cancer immunotherapy using the WT1 vaccine.
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