PRODUCTION OF T-HELPER CELL SUBSETS AND CYTOKINES BY LYMPHOCYTES FROMPATIENTS WITH CHRONIC MUCOCUTANEOUS CANDIDIASIS

Citation
Lj. Kobrynski et al., PRODUCTION OF T-HELPER CELL SUBSETS AND CYTOKINES BY LYMPHOCYTES FROMPATIENTS WITH CHRONIC MUCOCUTANEOUS CANDIDIASIS, Clinical and diagnostic laboratory immunology, 3(6), 1996, pp. 740-745
Citations number
33
Categorie Soggetti
Immunology,"Infectious Diseases","Medical Laboratory Technology",Microbiology
ISSN journal
1071412X
Volume
3
Issue
6
Year of publication
1996
Pages
740 - 745
Database
ISI
SICI code
1071-412X(1996)3:6<740:POTCSA>2.0.ZU;2-B
Abstract
Chronic mucocutaneous candidiasis (CMC) is a heterogeneous group of di sorders characterized by recurrent and persistent superficial candidal infections. Cytokine-induced dysregulation of T-helper cell function has been described in other immune-deficient states but has not been s tudied in CMC patients. We studied T-helper cell subsets by flow cytom etry and cytokine production by stimulated lymphocytes in six CMC pati ents, two healthy pediatric controls, and five healthy adult controls. Peripheral blood lymphocytes were stimulated in vitro with phytohemag glutinin or Candida albicans extract, and the production of interleuki n-2R (IL-2R), IL-4, IL-10, and gamma interferon in the supernatants wa s measured by enzyme-linked immunosorbent assay. CMC patients had a de crease in the CD4(+)/CD29(+) cell population compared with the numbers in controls (P < 0.02). The percentage of CD4(+)/CD45RA(+) cells was greater in patients than in controls, but the difference was not signi ficant. There was no difference in the production of IL-10 or gamma in terferon by the patient lymphocytes. CMC patients produced more IL-4 t han the controls (P < 0.001), whereas the controls tended to produce m ore IL-2R than the patients (P = 0.19). These findings support the con cept that a decrease in CD4(+)/CD29(+) T-helper inducer cells along wi th T-helper cell dysregulation may lead to defective memory responses to antigens in CMC patients and a decrease in cell-mediated immunity d ue to inhibition of T(H)1 cells by increased levels of IL-4.