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We began analyzing https://link.springer.com/article/10.1007/s10875-014-0106-4, but it redirected us to https://link.springer.com/article/10.1007/s10875-014-0106-4. The analysis below is for the second page.

Title[redir]:
Germline CARD11 Mutation in a Patient with Severe Congenital B Cell Lymphocytosis | Journal of Clinical Immunology
Description:
Purpose Activating germline mutations in CARD11 have recently been linked to a rare genetic disorder associated with congenital B cell lymphocytosis. We describe a patient with a similar clinical phenotype who had a de novo germline G123D CARD11 mutation. Methods Whole exome sequencing was performed on DNA from the patient and his biological parents. Laboratory studies examined characteristics of the patient’s B and T lymphocytes. A CARD11 cDNA containing the mutation was transfected into a lymphocyte cell line to gain an understanding of its function. RNA sequencing was performed on samples from the patient and from patients with alternate germline CARD11 mutations and differential gene expression analysis was performed. Results The patient had a decade-long history of severe polyclonal B lymphocytosis in the 20,000–90,000 lymphocytes/mm3 range, which was markedly exacerbated by EBV infection and splenectomy at different times. He had a heterozygous germline CARD11 mutation causing a G123D amino acid substitution, which was demonstrated to induce NF-κB activation in unstimulated lymphocytes. In contrast to previous patients with CARD11 mutations, this patient’s B cells exhibited higher expression of several cell cycle progression genes, as well as enhanced proliferation and improved survival following B cell receptor stimulation. Conclusions This is the third reported germline and first de novo CARD11 mutation shown to cause congenital B cell lymphocytosis. The mutation was associated with a dramatically greater lymphocytosis than in previously described cases, disproportionate to the level of constitutive NF-κB activation. However, comparative review of the patient’s clinical history, combined with additional genomic and functional analyses, underscore other important variables that may affect pathophysiology or regulate mutant CARD11 function in B cell proliferation and disease. We now refer to these patients as having BENTA disease (B cell Expansion with NF-κB and T cell Anergy).

Matching Content Categories {📚}

  • Telecommunications
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Content Management System {📝}

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Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

pubmed, article, google, scholar, cell, cas, card, central, germline, mutation, mutations, lymphocytosis, patient, national, usa, research, congenital, andrew, snow, gene, bcell, lymphoma, immunol, clinical, jeffrey, patients, human, biol, health, university, privacy, cookies, content, journal, severe, stinson, expression, proliferation, disease, access, med, nature, cyclin, allergy, institute, bethesda, function, information, publish, search,

Topics {✒️}

ikappab-nf-kappab signaling module month download article/chapter constitutive nf-κb activation epstein-barr virus induce nf-κb activation cd40 signaling-mediated induction b-cell lymphoproliferative disorders pkc-responsive inhibitory domain death receptor-induced apoptosis benta disease rap1-binding protein rapl sivasish sindiri anti-ig antibodies coupled antibody-secreting plasma cells cell cycle-regulated expression b-cell expansion card11 germline mutation germline card11 mutation germline card11 mutations hiv-infected viremic individuals lela kardava & susan moir oncogenic card11 mutations snow contributed equally cell receptor stimulation full article pdf extensive antigen-induced hematopoietic cell cycle author information authors cell lymphocytosis explained nf-κb human diffuse large human bcl6 gene nuclear factor kappa da silva ys tumor suppressor gene privacy choices/manage cookies clinical immunology aims similar clinical phenotype van der burg mol cell biol selective gene activation bcl-3-binding protein lymphocyte cell line cell lymphoma van dongen jj dramatically greater lymphocytosis protein kinase pkr il-21 induces differentiation severe combined immunodeficiency t-cell anergy

Schema {🗺️}

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         headline:Germline CARD11 Mutation in a Patient with Severe Congenital B Cell Lymphocytosis
         description:Activating germline mutations in CARD11 have recently been linked to a rare genetic disorder associated with congenital B cell lymphocytosis. We describe a patient with a similar clinical phenotype who had a de novo germline G123D CARD11 mutation. Whole exome sequencing was performed on DNA from the patient and his biological parents. Laboratory studies examined characteristics of the patient’s B and T lymphocytes. A CARD11 cDNA containing the mutation was transfected into a lymphocyte cell line to gain an understanding of its function. RNA sequencing was performed on samples from the patient and from patients with alternate germline CARD11 mutations and differential gene expression analysis was performed. The patient had a decade-long history of severe polyclonal B lymphocytosis in the 20,000–90,000 lymphocytes/mm3 range, which was markedly exacerbated by EBV infection and splenectomy at different times. He had a heterozygous germline CARD11 mutation causing a G123D amino acid substitution, which was demonstrated to induce NF-κB activation in unstimulated lymphocytes. In contrast to previous patients with CARD11 mutations, this patient’s B cells exhibited higher expression of several cell cycle progression genes, as well as enhanced proliferation and improved survival following B cell receptor stimulation. This is the third reported germline and first de novo CARD11 mutation shown to cause congenital B cell lymphocytosis. The mutation was associated with a dramatically greater lymphocytosis than in previously described cases, disproportionate to the level of constitutive NF-κB activation. However, comparative review of the patient’s clinical history, combined with additional genomic and functional analyses, underscore other important variables that may affect pathophysiology or regulate mutant CARD11 function in B cell proliferation and disease. We now refer to these patients as having BENTA disease (B cell Expansion with NF-κB and T cell Anergy).
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      headline:Germline CARD11 Mutation in a Patient with Severe Congenital B Cell Lymphocytosis
      description:Activating germline mutations in CARD11 have recently been linked to a rare genetic disorder associated with congenital B cell lymphocytosis. We describe a patient with a similar clinical phenotype who had a de novo germline G123D CARD11 mutation. Whole exome sequencing was performed on DNA from the patient and his biological parents. Laboratory studies examined characteristics of the patient’s B and T lymphocytes. A CARD11 cDNA containing the mutation was transfected into a lymphocyte cell line to gain an understanding of its function. RNA sequencing was performed on samples from the patient and from patients with alternate germline CARD11 mutations and differential gene expression analysis was performed. The patient had a decade-long history of severe polyclonal B lymphocytosis in the 20,000–90,000 lymphocytes/mm3 range, which was markedly exacerbated by EBV infection and splenectomy at different times. He had a heterozygous germline CARD11 mutation causing a G123D amino acid substitution, which was demonstrated to induce NF-κB activation in unstimulated lymphocytes. In contrast to previous patients with CARD11 mutations, this patient’s B cells exhibited higher expression of several cell cycle progression genes, as well as enhanced proliferation and improved survival following B cell receptor stimulation. This is the third reported germline and first de novo CARD11 mutation shown to cause congenital B cell lymphocytosis. The mutation was associated with a dramatically greater lymphocytosis than in previously described cases, disproportionate to the level of constitutive NF-κB activation. However, comparative review of the patient’s clinical history, combined with additional genomic and functional analyses, underscore other important variables that may affect pathophysiology or regulate mutant CARD11 function in B cell proliferation and disease. We now refer to these patients as having BENTA disease (B cell Expansion with NF-κB and T cell Anergy).
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      name:Sivasish Sindiri
      affiliation:
            name:National Cancer Institute, National Institutes of Health
            address:
               name:Oncogenomics Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Wei Wang
      affiliation:
            name:National Institute of Allergy and Infectious Diseases, NIH
            address:
               name:Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Lela Kardava
      affiliation:
            name:National Institute of Allergy and Infectious Diseases, NIH
            address:
               name:Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Susan Moir
      affiliation:
            name:National Institute of Allergy and Infectious Diseases, NIH
            address:
               name:Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Clifton L. Dalgard
      affiliation:
            name:Uniformed Services University of the Health Sciences
            address:
               name:Department of Anatomy, Physiology & Genetics, Uniformed Services University of the Health Sciences, Bethesda, USA
               type:PostalAddress
            type:Organization
      name:Jeffrey A. Moscow
      affiliation:
            name:University of Kentucky
            address:
               name:Department of Pediatrics and Markey Cancer Center, College of Medicine, University of Kentucky, Lexington, USA
               type:PostalAddress
            type:Organization
      name:Javed Khan
      affiliation:
            name:National Cancer Institute, National Institutes of Health
            address:
               name:Oncogenomics Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Andrew L. Snow
      affiliation:
            name:Uniformed Services University of the Health Sciences
            address:
               name:Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Oncogenomics Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, USA
      name:Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, USA
      name:Laboratory of Host Defenses, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, USA
      name:Department of Pediatrics and Markey Cancer Center, College of Medicine, University of Kentucky, Lexington, USA
      name:Department of Pathology, College of Medicine, University of Kentucky, Lexington, USA
      name:Department of Anatomy, Physiology & Genetics, Uniformed Services University of the Health Sciences, Bethesda, USA
      name:Oncogenomics Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, USA
      name:Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, USA
      name:Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, USA
      name:Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, USA
      name:Department of Anatomy, Physiology & Genetics, Uniformed Services University of the Health Sciences, Bethesda, USA
      name:Department of Pediatrics and Markey Cancer Center, College of Medicine, University of Kentucky, Lexington, USA
      name:Oncogenomics Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, USA
      name:Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, USA
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