Immune aberrations in atopic dermatitis (AD) are multiple and interrelated. We investigated immunoregulatory cell markers and functional interactions of purified T- and B-enriched cells in a pokeweed mitogen (PWM)-stimulated IgG production assay in patients with AD. Atopic mononuclear leukocytes and autologous recombinations of purified atopic T and B cells were hyporesponsive to PWM stimulation of IgG synthesis. When atopic B cells were cultured with normal T cells, they were still less responsive than normal B cells. Atopic T cells generated normal levels of suppression in three responder systems. Radioresistant T-cell help was also in the normal range whereas nonirradiated AD T cells produced slightly less help than normal T cells. We noted reduced levels of T lymphocytes with FcIgG receptors (Tγ) and found that Tγ reduction correlated inversely with log serum IgE. In the light of normal T suppression, we critically examined AD cell adherence and contamination at various steps in the Tγ assay to rule out technical causes of Tγ reduction in AD. Lowered Tγ cells in AD were not associated with circulating IgG immune complexes and subsequent blockade of the FcIgG receptors. Thus, we have identified defects in the numbers of an immunoregulatory T cell, and in the generation of PWM-responsive B cells. A model is proposed in which the alterations in atopic cyclic nucleotide metabolism of T-cell helpers could result in abnormalities of immunoregulatory T cells and PWM-recruitable B cells.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Investigative Dermatology|
|State||Published - 1983|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology