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A defect in the early phase of T-cell receptor-mediated T-cell activation
in patients with common variable immunodeficiency
MB Fischer, I Hauber, H Eggenbauer, V Thon, E Vogel, E Schaffer, J Lokaj, J Litzman, HM Wolf and JW Mannhalter
Institute of Immunology, University of Vienna, Austria.
Common variable immunodeficiency (CVID) is characterized by an impairment
of specific antibody production and a decrease in all or selected Ig
isotypes. Abnormalities at the level of the B cells, T cells, and
antigen-presenting cells have been described. In the present study, we have
focused our attention on T-cell activation in CVID. T cells from 15 of 24
patients failed to respond to recall antigens (eg, tetanus toxoid,
Escherichia coli). Of these 15 patients, 11 were studied in detail and
showed significantly decreased T-cell proliferative responses and/or
decreased interleukin-2 and interferon- gamma production on T-cell
receptor-mediated stimulation with recall antigens and superantigens
(staphylococcal enterotoxins [SE]); however, T-cell response to mitogens
(anti-CD3 monoclonal antibody, phytohemagglutinin) was normal. The defect
in interleukin-2 and interferon-gamma release on tetanus toxoid stimulation
could also be documented in purified CD4 T cells of the patients and was
present in patients with high and normal CD8 counts alike. Furthermore,
patients' T cells failed to mount a significant elevation in free
intracellular calcium (Ca++ flux) in response to superantigen, whereas the
response to phorbol myristate acetate and ionomycin, bypassing
receptor-mediated signaling, was unimpaired. These results indicate a
defect in the early phase of T-cell activation after triggering of the
T-cell receptor in a significant subgroup of CVID patients.
Volume 84,
Issue 12,
pp. 4234-4241,
12/15/1994
Copyright © 1994 by The American Society of Hematology
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