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Defects of class-switch recombination

Notarangelo, Luigi D. ; Lanzi, Gaetana ; Peron, Sophie ; Durandy, Anne

Journal of Allergy and Clinical Immunology, 2006-04, Vol.117 (4), p.855-864 [Periódico revisado por pares]

New York, NY: Mosby, Inc

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Título:
Defects of class-switch recombination
Autor: Notarangelo, Luigi D. ; Lanzi, Gaetana ; Peron, Sophie ; Durandy, Anne
Assuntos: Amino acids ; B-Lymphocytes - immunology ; Binding sites ; Biological and medical sciences ; CD40 Antigens - metabolism ; CD40 Ligand - genetics ; Cell adhesion & migration ; Chromosomes, Human, X - genetics ; class-switch recombination ; Cytidine Deaminase ; Cytosine Deaminase - deficiency ; Cytosine Deaminase - genetics ; Defects ; Deoxyribonucleic acid ; DNA ; DNA repair ; Enzymes ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Genes ; Human subjects ; Humans ; Hypergammaglobulinemia - genetics ; Hypergammaglobulinemia - immunology ; Immune system ; Immunodeficiencies ; Immunodeficiencies. Immunoglobulinopathies ; Immunodeficiency with hyper-IgM ; Immunoglobulin Class Switching ; Immunoglobulin M - genetics ; Immunologic Deficiency Syndromes - genetics ; Immunologic Deficiency Syndromes - immunology ; Immunopathology ; Kinases ; Lymphocytes ; Medical prognosis ; Medical sciences ; Models, Genetic ; Models, Immunological ; Mutation ; NF-kappa B - metabolism ; Proteins ; Recombination, Genetic ; Signal Transduction ; somatic hypermutation ; Somatic Hypermutation, Immunoglobulin ; Uracil-DNA Glycosidase - deficiency ; Uracil-DNA Glycosidase - genetics
É parte de: Journal of Allergy and Clinical Immunology, 2006-04, Vol.117 (4), p.855-864
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Descrição: Shaping of the secondary antibody repertoire is generated by means of class-switch recombination (CSR), which replaces IgM with other isotypes, and somatic hypermutation (SHM), which allows production of high-affinity antibodies. However, the molecular mechanisms underlying these important processes have long remained obscure. Immunodeficiency with hyper-IgM comprises a group of genetically heterogeneous defects of CSR variably associated with defects of SHM. The study of these patients has allowed us to recognize that both T-cell–B-cell interaction (resulting in CD40-mediated signaling) and intrinsic B-cell mechanisms are involved in CSR and SHM. Elucidation of the molecular defects underlying these disorders has been essential to better understand the molecular basis of Ig diversification and has offered the opportunity to define the clinical spectrum of these diseases and to prompt more accurate diagnostic and therapeutic approaches.
Editor: New York, NY: Mosby, Inc
Idioma: Inglês

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Defects of class-switch recombination

Notarangelo, Luigi D. ; Lanzi, Gaetana ; Peron, Sophie ; Durandy, Anne

New York, NY: Mosby, Inc

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