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Persistent Hypogammaglobulinemia after Receiving Rituximab Post-HSCT Is Not Caused by an Intrinsic B Cell Defect

International journal of molecular sciences, 2023-11, Vol.24 (21), p.16012

2023

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Cysteine and hydrophobic residues in CDR3 serve as distinct T-cell self-reactivity indices

Journal of allergy and clinical immunology, 2019-07, Vol.144 (1), p.333-336

2019

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Novel Genome-Editing Tools to Model and Correct Primary Immunodeficiencies

Frontiers in immunology, 2015-05, Vol.6, p.250-250

2015

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Partial correction of immunodeficiency by lentiviral vector gene therapy in mouse models carrying Rag1 hypomorphic mutations

Frontiers in immunology, 2023, Vol.14, p.1268620-1268620

2023

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Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56bright NKG2A+++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Frontiers in immunology, 2017-07, Vol.8, p.798-798

2017

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Corrigendum: Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56 bright NKG2A +++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Frontiers in immunology, 2017, Vol.8, p.1244

2017

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Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56 bright NKG2A +++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Frontiers in immunology, 2017, Vol.8, p.798

2017

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Corrigendum: Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56bright NKG2A+++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Frontiers in immunology, 2017-01, Vol.8, p.1244-1244

2017

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EXTL3 mutations cause skeletal dysplasia, immune deficiency, and developmental delay

The Journal of experimental medicine, 2017-03, Vol.214 (3), p.623-637

2017

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Abnormalities of T-cell receptor repertoire in CD4+ regulatory and conventional T cells in patients with RAG mutations: Implications for autoimmunity

Journal of allergy and clinical immunology, 2017-12, Vol.140 (6), p.1739-1743.e7

2017

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Persistent Hypogammaglobulinemia after Receiving Rituximab Post-HSCT Is Not Caused by an Intrinsic B Cell Defect

Cysteine and hydrophobic residues in CDR3 serve as distinct T-cell self-reactivity indices

Novel Genome-Editing Tools to Model and Correct Primary Immunodeficiencies

Partial correction of immunodeficiency by lentiviral vector gene therapy in mouse models carrying Rag1 hypomorphic mutations

Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56bright NKG2A+++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Corrigendum: Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56 bright NKG2A +++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56 bright NKG2A +++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

Corrigendum: Natural Killer Cells from Patients with Recombinase-Activating Gene and Non-Homologous End Joining Gene Defects Comprise a Higher Frequency of CD56bright NKG2A+++ Cells, and Yet Display Increased Degranulation and Higher Perforin Content

EXTL3 mutations cause skeletal dysplasia, immune deficiency, and developmental delay

Abnormalities of T-cell receptor repertoire in CD4+ regulatory and conventional T cells in patients with RAG mutations: Implications for autoimmunity

Modeling altered T-cell development with induced pluripotent stem cells from patients with RAG1-dependent immune deficiencies

Human JAK1 gain of function causes dysregulated myelopoeisis and severe allergic inflammation

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