{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T18:38:21Z","timestamp":1791398301158,"version":"4.3.3"},"reference-count":32,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2012,10,5]],"date-time":"2012-10-05T00:00:00Z","timestamp":1349395200000},"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":[[2012,10,5]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>Common variable immunodeficiency disorders (CVID) are a group of heterogeneous conditions that have in common primary failure of B cell function, although numerous T cell abnormalities have been described, including reduced proliferative response and reduced regulatory T cells. This study compared the T cell phenotype of CVID patients subdivided into clinical phenotypes as well as patients with partial antibody deficiencies [immunoglobulin (Ig)G subclass deficiency and selective IgA deficiency], X-linked agammaglobulinaemia (XLA) and healthy and disease controls. Absolute numbers of T cell subpopulations were measured by four-colour flow cytometry: naive T cells, central and effector memory and terminally differentiated (TEM) T cells, using CD45RA and CCR7 expression. Early, intermediate and late differentiation status of T cells was measured by CD27\/CD28 expression. Putative follicular T cells, recent thymic emigrants and regulatory T cells were also assessed. Significant reduction in naive CD4 T cells, with reduced total CD4 and recent thymic emigrant numbers, was observed in CVID patients, most pronounced in those with autoimmune cytopenias or polyclonal lymphoproliferation. These findings suggest a lack of replenishment by new thymically derived cells. CD8 naive T cells were reduced in CVID patients, most significantly in the autoimmune cytopenia subgroup. There was a reduction in early differentiated CD4 and CD8 T cells and increased CD8 TEM in the CVID patients, particularly autoimmune cytopenia and polyclonal lymphoproliferation subgroups, suggesting a more activated T cell phenotype, due perhaps to an antigen-driven process. XLA patients had significantly reduced putative follicular T cells, which may depend on B cells for survival, while no significant alterations were observed in the T cells of those with IgG subclass deficiency or selective IgA deficiency.<\/jats:p>","DOI":"10.1111\/j.1365-2249.2012.04643.x","type":"journal-article","created":{"date-parts":[[2012,7,13]],"date-time":"2012-07-13T12:18:46Z","timestamp":1342181926000},"page":"202-211","source":"Crossref","is-referenced-by-count":132,"title":["T cell phenotypes in patients with common variable immunodeficiency disorders: associations with clinical phenotypes in comparison with other groups with recurrent infections"],"prefix":"10.1093","volume":"170","author":[{"given":"E A L","family":"Bateman","sequence":"first","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L","family":"Ayers","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R","family":"Sadler","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Lucas","sequence":"additional","affiliation":[{"name":"Clinical Immunology, John Radcliffe Hospital, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C","family":"Roberts","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Woods","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K","family":"Packwood","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Burden","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"Harrison","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N","family":"Kaenzig","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of California at Los Angeles, Los Angeles, CA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H M","family":"Chapel","sequence":"additional","affiliation":[{"name":"Clinical Immunology, John Radcliffe Hospital, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B L","family":"Ferry","sequence":"additional","affiliation":[{"name":"Department of Clinical Laboratory Immunology, Churchill Hospital"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,10,5]]},"reference":[{"key":"2021122708262008500_b1","doi-asserted-by":"crossref","first-page":"190","DOI":"10.1006\/clim.1999.4799","article-title":"Diagnostic criteria for primary immunodeficiencies. 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