Abstract
MALT1 mutations impair normal NF-κB activation and paracaspase activity to cause a novel combined immunodeficiency. The clinical and immunological phenotype of MALT1 deficiency can be successfully treated with hematopoietic stem cell transplantation following reduced intensity conditioning.
Keywords:
CARD11–BCL10–MALT1 (CBM) signalosome complex; Combined immunodeficiency; Hematopoietic stem cell transplantation (HSCT); MALT1 mutations; NF-κB; Paracaspase.
Copyright © 2016 Elsevier Inc. All rights reserved.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Caspases / deficiency
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Caspases / genetics*
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Caspases / metabolism
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Cells, Cultured
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Hematopoietic Stem Cell Transplantation / methods*
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Humans
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Immunologic Deficiency Syndromes / genetics
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Immunologic Deficiency Syndromes / metabolism
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Immunologic Deficiency Syndromes / therapy*
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Leukocytes, Mononuclear / metabolism
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Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
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Mutation*
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NF-kappa B / metabolism
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Neoplasm Proteins / deficiency
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Neoplasm Proteins / genetics*
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Neoplasm Proteins / metabolism
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Signal Transduction
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Treatment Outcome
Substances
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NF-kappa B
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Neoplasm Proteins
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Caspases
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MALT1 protein, human
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Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein