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Characterization of lymphocyte subsets in patients with common variable immunodeficiency reveals subsets of naive

Marcela Vlková1, Eva Fronková, Veronika Kanderová

  • 1Department of Clinical Immunology and Allergology, St. Anne's University Hospital and Faculty of Medicine, Masaryk University, Brno, Czech Republic. marcela.vlkova@fnusa.cz

Journal of Immunology (Baltimore, Md. : 1950)
|November 3, 2010
PubMed

Insights

Common variable immunodeficiency (CVID) involves increased naive B cells, with specific subsets showing abnormal proliferation and developmental pathways. These findings suggest a refined understanding of B cell development in CVID patients.

Area of Science:

  • Immunology
  • Cell Biology
  • Human Genetics

Background:

  • Common variable immunodeficiency (CVID) is characterized by impaired B cell immunity.
  • Elevated frequencies of naive B cell subsets, specifically CD27(neg)CD21(neg)CD38(neg) B cells, are observed in CVID patients.
  • Understanding the phenotype, frequency, and proliferation history of these B cell subsets is crucial for CVID pathogenesis.

Purpose of the Study:

  • To investigate the phenotype, frequency, and proliferation history of naive B cell subsets in CVID patients.
  • To define distinct subpopulations within the CD27(neg)CD21(neg)CD38(neg) B cell subset and analyze their proliferative capacity.
  • To explore the relationship between naive B cell subsets and proposed developmental pathways in CVID.

Main Methods:

  • Analysis of B cell subsets from 48 CVID patients and 49 healthy controls using polychromatic flow cytometry.
  • Assessment of B cell replication history via PCR-based detection of kappa deletion excision circles (κ-TRECs).
  • Stratification of CVID patients into groups with normal (CVID-21norm) or increased (CVID-21lo) CD27(neg)CD21(neg)CD38(neg) B cell proportions.

Main Results:

  • Two distinct subpopulations of CD27(neg)CD21(neg)CD38(neg) B cells were identified based on CD24 expression.
  • The CD27(neg)CD21(neg)CD38(neg) B cell subset exhibited markedly increased proliferation in CVID-21lo patients, suggesting developmental arrest.
  • A significant underrepresentation of the follicular (FO) I subset was observed in CVID-21lo patients, while FO II cells were increased.
  • Replication history analysis implied a refined naive B cell developmental scheme where transitional B cells develop into FO II and FO I cells.

Conclusions:

  • The CD27(neg)CD21(neg)CD38(neg) B cells increased in CVID patients may originate from FO subsets following CD21 loss.
  • Increased proliferation in specific CVID B cell subsets points towards developmental arrest rather than increased bone marrow output.
  • These findings contribute to a refined model of human naive B cell development and offer insights into CVID pathophysiology.

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