Soluble cytokine receptor CD30 in atopic disorders: a case-control study

Citation
U. Latza et al., Soluble cytokine receptor CD30 in atopic disorders: a case-control study, CLIN EXP AL, 29(1), 1999, pp. 97-104
Citations number
36
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
09547894 → ACNP
Volume
29
Issue
1
Year of publication
1999
Pages
97 - 104
Database
ISI
SICI code
0954-7894(199901)29:1<97:SCRCIA>2.0.ZU;2-Q
Abstract
Background The cytokine receptor CD30 is an activation marker of T cells wh ich preferentially associates with the production of the TH2 cytokine IL-4. Therefore, it may potentially be a candidate marker for atopic disorders a nd a target molecule for new therapeutic approaches. Objective To test the hypothesis that elevated levels of soluble CD30 (sCD3 0) are significantly associated with atopic disorders after adjustment for other predictors of atopy. Methods The presence of elevated sCD30 (greater than or equal to 20 U/mL) i n atopic disorders was evaluated in a nested case-control study. Cases (n = 60) were blood donors with specific IEE antibodies, total serum levels of IgE greater than or equal to 100 kU/L and presence or history of allergic s ymptoms. Controls (n = 59) were blood donors without presence or history of allergic symptoms and serum levels of IgE < 50 kU/L. sCD30 was determined from serum samples by an enzyme-linked immunosorbent assay. Odds ratios (OR ) and confidence intervals (CI) were calculated from logistic regression co efficients. Results Mean sCD30 levels for cases were 75 U/mL (SD 110 U/mL) as compared with 35 U/mL (SD 59 U/mL) for controls. Serum levels of sCD30 were elevated in 65% of cases and 32% of controls (OR 3.9, 95% CI 1.8-8.4). The odds rat io for elevated sCD30 as a predictor of atopic disorders slightly decreased to 3.7 after controlling for smoking, age and gender. Blood eosinophilia w hich was a strong predictor of atopy (OR 11.7) was a weak confounder of the association between sCD30 levels and atopic disorders. Family history of a llergy, another strong predictor of atopy (OR 8.6), did not confound the as sociation. Conclusions The results are consistent with the hypothesis that CD30 is inv olved in the pathogenesis of atopic disorders independent of eosinophilia a nd family history of allergy.