Literature DB >> 28782633

Plasma cell deficiency in human subjects with heterozygous mutations in Sec61 translocon alpha 1 subunit (SEC61A1).

Desirée Schubert1, Marie-Christine Klein2, Sarah Hassdenteufel2, Andrés Caballero-Oteyza3, Linlin Yang3, Michele Proietti3, Alla Bulashevska3, Janine Kemming3, Johannes Kühn3, Sandra Winzer3, Stephan Rusch3, Manfred Fliegauf3, Alejandro A Schäffer4, Stefan Pfeffer5, Roger Geiger6, Adolfo Cavalié7, Hongzhi Cao8, Fang Yang8, Yong Li9, Marta Rizzi10, Hermann Eibel3, Robin Kobbe11, Amy L Marks12, Brian P Peppers13, Robert W Hostoffer14, Jennifer M Puck15, Richard Zimmermann16, Bodo Grimbacher17.   

Abstract

BACKGROUND: Primary antibody deficiencies (PADs) are the most frequent primary immunodeficiencies in human subjects. The genetic causes of PADs are largely unknown. Sec61 translocon alpha 1 subunit (SEC61A1) is the major subunit of the Sec61 complex, which is the main polypeptide-conducting channel in the endoplasmic reticulum membrane. SEC61A1 is a target gene of spliced X-box binding protein 1 and strongly induced during plasma cell (PC) differentiation.
OBJECTIVE: We identified a novel genetic defect and studied its pathologic mechanism in 11 patients from 2 unrelated families with PADs.
METHODS: Whole-exome and targeted sequencing were conducted to identify novel genetic mutations. Functional studies were carried out ex vivo in primary cells of patients and in vitro in different cell lines to assess the effect of SEC61A1 mutations on B-cell differentiation and survival.
RESULTS: We investigated 2 families with patients with hypogammaglobulinemia, severe recurrent respiratory tract infections, and normal peripheral B- and T-cell subpopulations. On in vitro stimulation, B cells showed an intrinsic deficiency to develop into PCs. Genetic analysis and targeted sequencing identified novel heterozygous missense (c.254T>A, p.V85D) and nonsense (c.1325G>T, p.E381*) mutations in SEC61A1, segregating with the disease phenotype. SEC61A1-V85D was deficient in cotranslational protein translocation, and it disturbed the cellular calcium homeostasis in HeLa cells. Moreover, SEC61A1-V85D triggered the terminal unfolded protein response in multiple myeloma cell lines.
CONCLUSION: We describe a monogenic defect leading to a specific PC deficiency in human subjects, expanding our knowledge about the pathogenesis of antibody deficiencies.
Copyright © 2017 American Academy of Allergy, Asthma & Immunology. All rights reserved.

Entities:  

Keywords:  SEC61A1; antibody deficiency; calcium homeostasis; endoplasmic reticulum stress; multiple myeloma; plasma cell; protein translocation; translocon

Mesh:

Substances:

Year:  2017        PMID: 28782633      PMCID: PMC5797495          DOI: 10.1016/j.jaci.2017.06.042

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  42 in total

1.  Plasma cell differentiation requires the transcription factor XBP-1.

Authors:  A M Reimold; N N Iwakoshi; J Manis; P Vallabhajosyula; E Szomolanyi-Tsuda; E M Gravallese; D Friend; M J Grusby; F Alt; L H Glimcher
Journal:  Nature       Date:  2001-07-19       Impact factor: 49.962

2.  Distinct domains within yeast Sec61p involved in post-translational translocation and protein dislocation.

Authors:  B M Wilkinson; J R Tyson; P J Reid; C J Stirling
Journal:  J Biol Chem       Date:  2000-01-07       Impact factor: 5.157

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Authors:  H G Enoch; P J Fleming; P Strittmatter
Journal:  J Biol Chem       Date:  1979-07-25       Impact factor: 5.157

4.  Transcriptional profiling of mouse B cell terminal differentiation defines a signature for antibody-secreting plasma cells.

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6.  XBP-1 regulates a subset of endoplasmic reticulum resident chaperone genes in the unfolded protein response.

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10.  Membrane biogenesis during B cell differentiation: most endoplasmic reticulum proteins are expressed coordinately.

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2.  Hypomorphic caspase activation and recruitment domain 11 (CARD11) mutations associated with diverse immunologic phenotypes with or without atopic disease.

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Review 3.  B- and T-Cell Subset Abnormalities in Monogenic Common Variable Immunodeficiency.

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Review 6.  Complexity and Specificity of Sec61-Channelopathies: Human Diseases Affecting Gating of the Sec61 Complex.

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Review 8.  An Update on Sec61 Channel Functions, Mechanisms, and Related Diseases.

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Review 9.  Beyond monogenetic rare variants: tackling the low rate of genetic diagnoses in predominantly antibody deficiency.

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