Immunophenotypical alterations in a subset of patients with common variable immunodeficiency (CVID)

• Published in: Clinical and experimental immunology Vol. 90; no. 1; pp. 25 - 30
• Main Authors: BAUMERT, E., WOLFF‐VORBECK, G., SCHLESIER, M., PETER, H. H.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.10.1992; Blackwell
• Subjects: adhesion molecules; Adult; Aged; AIDS/HIV; Antigens, Surface - metabolism; B-Lymphocytes - immunology; Biological and medical sciences; CD4-CD8 Ratio; Cell Adhesion Molecules - metabolism; common variable immunodeficiency; Common Variable Immunodeficiency - immunology; Female; Humans; Immunodeficiencies; Immunodeficiencies. Immunoglobulinopathies; Immunopathology; Killer Cells, Natural - immunology; Leukocyte Count; Lymphocyte Subsets - immunology; lymphocyte surface molecules; Male; Medical sciences; Middle Aged; T cell subpopulations; T-Lymphocyte Subsets - immunology; Human; Immunopathology; Flow cytometry; HLA-System; Phenotype; Common variable immunodeficiency; Major histocompatibility system; T-Lymphocyte; Biological marker; Cell subpopulation
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.1992.tb05826.x

SUMMARY We investigated the expression of surface molecules on lymphocytes from 20 patients with CVID and 40 healthy subjects. Lymphocytes were analysed by dual colour flow cytometry. We identified a subset of patients (8 of 20) characterized by low CD4/CD8 ratio (< 11), expansion of T cells co‐expressing the activation marker HLA‐DR and significant increase in CD8+ T cells co‐expressing CD57. Expression of the adhesion molecules LFA‐3 (CD58) and ICAM‐1 (CD54) was significantly increased in this subgroup. In addition, within theCD4+ T cells the percentage of CD29+ (memory) cells was increased, while the CD45RA and LAM‐1 (Leu‐8) antigens were depressed. These results indicate that in a subgroup of CVID patients T cells are activated in vivo and the CD57+CD8+ lymphocyte subpopulation, supposed to comprise functional suppressor T cells, is expanded. We suggest a chronic viral infection in these patients, but it is not clear whether this is primary or secondary to the underlying defect.