Abstract
We previously showed that a specific antileukemia T-cytotoxic response is spontaneously elicited in acute lymphoblastic leukemia (ALL) patients and might contribute to host antileukemia defense, even though it is insufficient for tumor growth control. In this study, we report that multifactorial factors account for some of the acquired immune defects seen in ALL patients. In bone marrow of ALL patients, T cells do not express CD40L and CD25 markers, their apoptosis rate is increased, and a predominance of a CD4 cell subset expressing a Th2 phenotype is detected. A lack of expression of B7-1 molecules and other activation molecules is observed on all ALL blasts. These different parameters combined lead to in vivo dysfunction of T-cell proliferative and cytotoxic activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis
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B7-1 Antigen / analysis
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Bone Marrow / pathology
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CD40 Ligand
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Calcium Signaling
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Cell Cycle
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Child
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Child, Preschool
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Female
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Humans
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Immunologic Deficiency Syndromes / etiology*
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Immunologic Deficiency Syndromes / pathology
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Lymphocyte Activation
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Lymphokines / metabolism
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Male
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Membrane Glycoproteins / analysis
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology*
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Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology
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Receptors, Interleukin-2 / analysis
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T-Lymphocyte Subsets / immunology*
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T-Lymphocyte Subsets / metabolism
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T-Lymphocyte Subsets / pathology
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T-Lymphocytes, Cytotoxic / immunology
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T-Lymphocytes, Cytotoxic / pathology
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Th2 Cells / immunology
Substances
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B7-1 Antigen
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Lymphokines
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Membrane Glycoproteins
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Receptors, Interleukin-2
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CD40 Ligand