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Reversible dysfunction of T-lymphocytes in common variable immunodeficiency.

W H Marshall, P W Allderdice, H W Edstrom

Canadian Medical Association Journal

|June 4, 1977

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This study identifies a reversible T-lymphocyte defect in common variable immunodeficiency (CVID). Normal leukocytes restored the patient's impaired cell-mediated immunity, revealing a crucial missing factor.

Area of Science:

Immunology
Clinical Medicine

Background:

Common variable immunodeficiency (CVID) is a primary immunodeficiency characterized by hypogammaglobulinemia and increased susceptibility to infections.
Cell-mediated immunity can also be affected in CVID, though the underlying mechanisms are not fully understood.

Observation:

A 30-year-old male patient with fatal sinopulmonary infections presented with CVID, lymphopenia, and cutaneous anergy.
Despite impaired phytohemagglutinin (PHA) response in vitro, intradermal PHA injection elicited a strong cutaneous reaction, indicating residual cell-mediated immunity.

Findings:

The patient's T-lymphocyte response to PHA was restored to normal levels upon co-culture with normal leukocytes.
This restoration suggests a reversible, cellular defect in T-lymphocytes, rather than a serum factor, was responsible for the impaired PHA response.

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Low counts of macrophage precursor cells were noted but deemed insufficient to explain the PHA response defect.

Implications:

This research highlights a specific functional T-lymphocyte defect in CVID that can be corrected by external factors.
Understanding this cellular defect may lead to novel therapeutic strategies for CVID patients with compromised cell-mediated immunity.
The familial occurrence of lymphoma and CVID in relatives warrants further investigation into genetic predispositions.