{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,2]],"date-time":"2025-11-02T15:46:38Z","timestamp":1762098398318},"reference-count":58,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2010,11,9]],"date-time":"2010-11-09T00:00:00Z","timestamp":1289260800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,12,1]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The considerable clinical heterogeneity of patients with common variable immunodeficiency disorders (CVID) shares some similarity with bone-marrow failure disorders such as Diamond\u2013Blackfan anaemia (DBA) and Shwachman\u2013Diamond syndrome (SDS), now recognized as defects in ribosome biogenesis or ribosomopathies. The recognition of a patient with DBA who subsequently developed CVID lends support to our previous finding of a heterozygous mutation in the SBDS gene of SBDS in another CVID patient, suggesting that ribosome biogenesis defects are responsible for a subset of CVID. Genetic defects in the ribosomal translational machinery responsible for various bone marrow failure syndromes are recognized readily when they manifest in children, but diagnosing these in adults presenting with complex phenotypes and hypogammaglobulinaemia can be a challenge. In this perspective paper, we discuss our clinical experience in CVID patients with ribosomopathies, and review the immunological abnormalities in other conditions associated with ribosomal dysfunction. With genetic testing available for various bone marrow failure syndromes, our hypothesis that ribosomal abnormalities may be present in patients with CVID could be proved in future studies by testing for mutations in specific ribosomal genes. New knowledge might then be translated into novel therapeutic strategies for patients in this group of immunodeficiency disorders.<\/jats:p>","DOI":"10.1111\/j.1365-2249.2010.04280.x","type":"journal-article","created":{"date-parts":[[2010,11,9]],"date-time":"2010-11-09T14:11:25Z","timestamp":1289311885000},"page":"96-103","source":"Crossref","is-referenced-by-count":26,"title":["Do ribosomopathies explain some cases of common variable immunodeficiency?"],"prefix":"10.1093","volume":"163","author":[{"given":"S","family":"Khan","sequence":"first","affiliation":[{"name":"Department of Immunology, Frimley Park Hospital, Frimley, Surrey"},{"name":"Centre for Immunoglobulin Therapy, Scunthorpe General Hospital, Scunthorpe"}]},{"given":"J","family":"Pereira","sequence":"additional","affiliation":[{"name":"Centro Hospitalar de Coimbra, Unidade de Hematologia Molecular, Coimbra, Portugal"}]},{"given":"P J","family":"Darbyshire","sequence":"additional","affiliation":[{"name":"Paediatric Oncology and Haematology, Birmingham Children's Hospital"}]},{"given":"S","family":"Holding","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hull Royal Infirmary, Hull, UK"}]},{"given":"P C","family":"Dor\u00e9","sequence":"additional","affiliation":[{"name":"Department of Immunology, Hull Royal Infirmary, Hull, UK"}]},{"given":"W A C","family":"Sewell","sequence":"additional","affiliation":[{"name":"Centre for Immunoglobulin Therapy, Scunthorpe General Hospital, Scunthorpe"}]},{"given":"A","family":"Huissoon","sequence":"additional","affiliation":[{"name":"Department of Immunology, Birmingham Heartlands Hospital, Birmingham"}]}],"member":"286","published-online":{"date-parts":[[2010,11,9]]},"reference":[{"key":"2021122708481888400_b1","doi-asserted-by":"crossref","first-page":"489","DOI":"10.1016\/S0140-6736(08)61199-X","article-title":"Common variable immunodeficiency: a new look at an old 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