ArticleFrontiers in immunology2023
In-depth blood immune profiling of Good syndrome patients.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Oligoclonal expansion of atypical Vδ2Nature communications · 2026Article
- When Central Tolerance Fails: Thymic Malignancies at the Intersection of Cancer Immunity and Autoimmunity.Cancers · 2026Review
- Good's Syndrome Mirrors a Combined Immunodeficiency with Anti-Cytokine Antibodies in the Total Absence of B Cells.Journal of clinical immunology · 2026Article
- Autoimmunity in thymic epithelial tumors: a not yet clarified pathologic paradigm associated with several unmet clinical needs.Frontiers in immunology · 2024Review
- B-cell immune dysregulation with low soluble CD22 levels in refractory seronegative myasthenia gravis.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
20 authors at 11 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Good syndrome (GS) is a rare adult-onset immunodeficiency first described in 1954. It is characterized by the coexistence of a thymoma and hypogammaglobulinemia, associated with an increased susceptibility to infections and autoimmunity. The classification and management of GS has been long hampered by the lack of data about the underlying immune alterations, a controversy existing on whether it is a unique diagnostic entity Methods: Here, we used high-sensitive flow cytometry to investigate the distribution of up to 70 different immune cell populations in blood of GS patients (n=9) compared to age-matched CVID patients (n=55) and healthy donors (n=61). Results: All 9 GS patients displayed reduced B-cell counts -down to undetectable levels (<0.1 cells/μL) in 8/9 cases-, together with decreased numbers of total CD4 Discussion: Our findings provide a more accurate definition of the immune cell defects of GS patients and contribute to a better discrimination among GS patients between those with a pure B-cell defect
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