This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kobrynski, L. J.
Right arrow Articles by Douglas, S. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kobrynski, L. J.
Right arrow Articles by Douglas, S. D.

 Previous Article  |  Next Article 

Clinical and Diagnostic Laboratory Immunology, 11 1996, 740-745, Vol 3, No. 6
Copyright © 1996 by the American Society for Microbiology. All rights reserved.

Production of T-helper cell subsets and cytokines by lymphocytes from patients with chronic mucocutaneous candidiasis

LJ Kobrynski, L Tanimune, L Kilpatrick, DE Campbell and SD Douglas
Division of Allergy, Immunology, and Infectious Diseases, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine 19104, USA.

Chronic mucocutaneous candidiasis (CMC) is a heterogeneous group of disorders 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 studied in CMC patients. We studied T-helper cell subsets by flow cytometry and cytokine production by stimulated lymphocytes in six CMC patients, two healthy pediatric controls, and five healthy adult controls. Peripheral blood lymphocytes were stimulated in vitro with phytohemagglutinin or Candida albicans extract, and the production of interleukin-2R (IL-2R), IL-4, IL-10, and gamma interferon in the supernatants was measured by enzyme-linked immunosorbent assay. CMC patients had a decrease in the CD29+/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 significant. There was no difference in the production of IL-10 or gamma interferon by the patient lymphocytes. CMC patients produced more IL-4 than the controls (P < 0.001), whereas the controls tended to produce more IL-2R than the patients (P = 0.19). These findings support the concept that a decrease in CD4+/CD29+ T-helper inducer cells along with T-helper cell dysregulation may lead to defective memory responses to antigens in CMC patients and a decrease in cell-mediated immunity due to inhibition of TH1 cells by increased levels of IL-4.


This article has been cited by other articles:

  • Romani, L. (2000). Innate and adaptive immunity in Candida albicans infections and saprophytism. J. Leukoc. Biol. 68: 175-179 [Abstract] [Full Text]  
  • Vazquez-Torres, A., Jones-Carson, J., Wagner, R. D., Warner, T., Balish, E. (1999). Early Resistance of Interleukin-10 Knockout Mice to Acute Systemic Candidiasis. Infect. Immun. 67: 670-674 [Abstract] [Full Text]  
  • Katial, R. K., Sachanandani, D., Pinney, C., Lieberman, M. M. (1998). Cytokine Production in Cell Culture by Peripheral Blood Mononuclear Cells from Immunocompetent Hosts. CVI 5: 78-81 [Abstract] [Full Text]