T cells from atopic individuals produce IgE-inducing activity incompletely blocked by anti-interleukin-4 antibody
✍ Scribed by Xiaohong Zhang; Barbara Polla; Conrad Hauser; Rudolf H. Zubler
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 494 KB
- Volume
- 22
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
Genkve T cells from atopic individuals produce IgE-inducing activity incompletely blocked by anti-interleukin-4 antibody*
We investigated peripheral blood B and T lymphocyte functions in atopic individuals. B cells were co-cultured with mutant EL4 thymoma cells in the presence of a standard T cell supernatant (T-SN) with or without exogenous interleukin (1L)-4. IgE secretion in this assay was found to be IL-4 dependent, but not significantly different for atopic patients (n=25) vs. normal controls (n=25). Phytohemagglutinin plus phorbol 12-myristate 13-acetate (PHA+PMA)induced T-SN from patients or controls was tested on normal B cells in the same assay system (in the absence of exogenous IL-4). Compared to the controls, the IgE-inducing activity was significantly increased for patients with asthma or allergic rhinitis (n=12; p<0.005) but not for patients with atopic dermatitis (n=13). The difference between the asthma or allergic rhinitis vs. the atopic dermatitis groups was significant (p>0.05). Since the assay was not inhibited by interferon (1FN)-y, this difference can not be attributed to IFN-y concentrations. Other T cell activities may be different between the patient groups or atopic T cells from the respiratory mucosa may recirculate more than those from the skin. In any case, theT cells rather than the B cells were found to be abnormal in atopic individuals. If atopicT cells were stimulated with PHA+PMA not as immediately but after a resting period of 48 h in culture medium alone, the IgE-inducing activity, but not the total Ig-inducing activity or the IL-2 secretion, disappeared. In addition, a mean of 37 % O of the IgE-inducing activity (range of 13 9' 0 to 79 % for five very active T-SN) was not inhibited by an anti-IL-4 antibody which neutralized exogenous IL-4, indicating a participation of factors capable of bypassing the requirement for IL-4 for the IgE response.