Transmembrane activator and calcium-modulating cyclophilin ligand interactor mutations in common variable immunodeficiency: Clinical and immunologic outcomes in heterozygotes
Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance. Because most subjects with CVI...
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| Published in | Journal of allergy and clinical immunology Vol. 120; no. 5; pp. 1178 - 1185 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York, NY
Mosby, Inc
01.11.2007
Elsevier Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0091-6749 1097-6825 1085-8725 1097-6825 |
| DOI | 10.1016/j.jaci.2007.10.001 |
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| Abstract | Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance.
Because most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear.
TACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations.
Heterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased (
P = .012;
P = .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation.
Mutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency.
Additional causes of this common immune deficiency syndrome remain to be determined. |
|---|---|
| AbstractList | Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance.
Because most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear.
TACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations.
Heterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased (
P = .012;
P = .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation.
Mutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency.
Additional causes of this common immune deficiency syndrome remain to be determined. Background Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance. Objective Because most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear. Methods TACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations. Results Heterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased (P= .012;P= .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation. Conclusion Mutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency. Clinical implications Additional causes of this common immune deficiency syndrome remain to be determined. Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance. Because most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear. TACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations. Heterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased (P = .012; P = .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation. Mutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency. Additional causes of this common immune deficiency syndrome remain to be determined. Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance.BACKGROUNDMutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance.Because most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear.OBJECTIVEBecause most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear.TACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations.METHODSTACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations.Heterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased (P = .012; P = .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation.RESULTSHeterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased (P = .012; P = .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation.Mutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency.CONCLUSIONMutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency.Additional causes of this common immune deficiency syndrome remain to be determined.CLINICAL IMPLICATIONSAdditional causes of this common immune deficiency syndrome remain to be determined. Background Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable immunodeficiency (CVID). Mutations coincided with immunodeficiency in families, suggesting dominant inheritance. Objective Because most subjects with CVID have no immunodeficient family members and heterozygous mutations predominate, the role of TACI mutations in sporadic CVID is unclear. Methods TACI was sequenced from the genomic DNA of 176 subjects with CVID and family members. B cells of subjects with or without mutations were examined for binding to the ligand, a proliferation inducing ligand (APRIL), and for proliferation and immunoglobulin production after ligand stimulation. Data analysis was performed to assess the clinical relevance of TACI mutations. Results Heterozygous TACI mutations were found in 13 subjects (7.3%). Six with mutations (46%) had episodes of autoimmune thrombocytopenia, in contrast with 12% of 163 subjects without mutations; splenomegaly and splenectomy were significantly increased ( P = .012; P = .001.) B cells of some had impaired binding of APRIL and on culture with this ligand were defective in proliferation and immunoglobulin production; however, this was not different from B cells of subjects without mutations. Eight first-degree relatives from 5 families had the same mutations but were not immune-deficient, and their B cells produced normal amounts of IgG and IgA after APRIL stimulation. Conclusion Mutations in TACI significantly predispose to autoimmunity and lymphoid hyperplasia in CVID, but additional genetic or environmental factors are required to induce immune deficiency. Clinical implications Additional causes of this common immune deficiency syndrome remain to be determined. |
| Author | Grimbacher, Bodo Diaz, George Behrens, Timothy W. Cunningham-Rundles, Charlotte Zhang, Li Bussel, James Radigan, Lin Salzer, Ulrich |
| AuthorAffiliation | c Immunology, Genentech, South San Francisco b Division of Rheumatology and Clinical Immunology, Medical School, University of Freiberg a Department of Medicine, Pediatrics and the Immunobiology Center, Mount Sinai Medical School, New York e Department of Pediatrics, Mount Sinai Medical Center, New York f Department of Pediatrics, Weil Medical School of Cornell University, New York d Department of Immunology and Molecular Pathology, Royal Free Hospital, University College London |
| AuthorAffiliation_xml | – name: c Immunology, Genentech, South San Francisco – name: e Department of Pediatrics, Mount Sinai Medical Center, New York – name: a Department of Medicine, Pediatrics and the Immunobiology Center, Mount Sinai Medical School, New York – name: d Department of Immunology and Molecular Pathology, Royal Free Hospital, University College London – name: f Department of Pediatrics, Weil Medical School of Cornell University, New York – name: b Division of Rheumatology and Clinical Immunology, Medical School, University of Freiberg |
| Author_xml | – sequence: 1 givenname: Li surname: Zhang fullname: Zhang, Li organization: Department of Medicine, Pediatrics and the Immunobiology Center, Mount Sinai Medical School, New York, NY – sequence: 2 givenname: Lin surname: Radigan fullname: Radigan, Lin organization: Department of Medicine, Pediatrics and the Immunobiology Center, Mount Sinai Medical School, New York, NY – sequence: 3 givenname: Ulrich surname: Salzer fullname: Salzer, Ulrich organization: Division of Rheumatology and Clinical Immunology, Medical School, University of Freiberg, Freiberg, Germany – sequence: 4 givenname: Timothy W. surname: Behrens fullname: Behrens, Timothy W. organization: Immunology, Genentech, South San Francisco, Calif – sequence: 5 givenname: Bodo surname: Grimbacher fullname: Grimbacher, Bodo organization: Division of Rheumatology and Clinical Immunology, Medical School, University of Freiberg, Freiberg, Germany – sequence: 6 givenname: George surname: Diaz fullname: Diaz, George organization: Department of Pediatrics, Mount Sinai Medical Center, New York, NY – sequence: 7 givenname: James surname: Bussel fullname: Bussel, James organization: Department of Pediatrics, Weil Medical School of Cornell University, New York, NY – sequence: 8 givenname: Charlotte surname: Cunningham-Rundles fullname: Cunningham-Rundles, Charlotte email: Charlotte.Cunningham-Rundles@MSSM.edu organization: Department of Medicine, Pediatrics and the Immunobiology Center, Mount Sinai Medical School, New York, NY |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19691155$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/17983875$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2007 American Academy of Allergy, Asthma & Immunology American Academy of Allergy, Asthma & Immunology 2008 INIST-CNRS Copyright Elsevier Limited Nov 2007 |
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| Keywords | BAFF IgA ITP IgG immune thrombocytopenia purpura CFSE Common variable immune deficiency B cell CVID TACI splenectomy AIHA APRIL Transmembrane activator and calcium-modulating cyclophilin ligand interactor Common variable immunodeficiency B cell–activating factor A proliferation inducing ligand Carboxyfluorescein succinimidyl ester Autoimmune hemolytic anemia Prognosis Calcium Ligand Hemopathy Inorganic element Splenectomy Isomerases Immunology Activator Surgery Evolution Genetics cis-trans-Isomerases Immunopathology Immunoglobulins Peptidylprolyl isomerase Enzyme B-Lymphocyte Heterozygosity Platelet Treatment Mutation Immune thrombocytopenic purpura Transmembrane activator and CAML interactor |
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| Snippet | Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable... Background Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common... Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common variable... Background Mutations in the gene coding for transmembrane activator and calcium-modulating cyclophilin ligand interactor (TACI) have been identified in common... |
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| SubjectTerms | Adolescent Adult Aged Aged, 80 and over Allergy and Immunology Arthritis Autoimmunity - genetics B cell B-Lymphocytes - immunology Biological and medical sciences Calcium Cell growth Common variable immune deficiency Common Variable Immunodeficiency - diagnosis Common Variable Immunodeficiency - genetics Defects Deoxyribonucleic acid DNA DNA Mutational Analysis Ear diseases Female Fundamental and applied biological sciences. Psychology Fundamental immunology Genetic testing Genotype & phenotype Heterozygote Humans Hyperplasia - genetics IgA IgG Immune system immune thrombocytopenia purpura Immunopathology Inflammatory bowel disease Ligands Lymphocyte Activation Male Medical sciences Middle Aged Mutation Pedigree Pneumonia Prognosis Purpura, Thrombocytopenic, Idiopathic - genetics Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis splenectomy TACI Transmembrane Activator and CAML Interactor Protein - genetics Transmembrane Activator and CAML Interactor Protein - metabolism Tumor Necrosis Factor Ligand Superfamily Member 13 - metabolism |
| Title | Transmembrane activator and calcium-modulating cyclophilin ligand interactor mutations in common variable immunodeficiency: Clinical and immunologic outcomes in heterozygotes |
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