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Infection and Immunity, February 2002, p. 724-731, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.724-731.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Primary Role for CD4+ T Lymphocytes in Recovery from Oropharyngeal Candidiasis

C. S. Farah,1* S. Elahi,2 K. Drysdale,1 G. Pang,2 T. Gotjamanos,3 G. J. Seymour,1 R. L. Clancy,2 and R. B. Ashman1

Oral Biology and Pathology, School of Dentistry, University of Queensland, Brisbane, Queensland 4072,1 Discipline of ImmunologyMicrobiology, University of Newcastle, Newcastle, New South Wales 2300,,2 Department of Pathology, QEII Medical Centre, University of Western Australia, Nedlands, Western Australia 6907, Australia3

Received 23 July 2001/ Returned for modification 9 August 2001/ Accepted 8 November 2001

Oropharyngeal candidiasis is associated with defects in cell-mediated immunity and is commonly seen in human immunodeficiency virus positive individuals and AIDS patients. A model for oral candidiasis in T-cell-deficient BALB/c and CBA/CaH nu/nu mice was established. After inoculation with 108 Candida albicans yeasts, these mice displayed increased levels of oral colonization compared to euthymic control mice and developed a chronic oropharyngeal infection. Histopathological examination of nu/nu oral tissues revealed extensive hyphae penetrating the epithelium, with polymorphonuclear leukocyte microabscess formation. Adoptive transfer of either naive or immune lymphocytes into immunodeficient mice resulted in the recovery of these animals from the oral infection. Reconstitution of immunodeficient mice with naive CD4+ but not CD8+ T cells significantly decreased oral colonization compared to controls. Interleukin-12 and gamma interferon were detected in the draining lymph nodes of immunodeficient mice following reconstitution with naive lymphocytes. This study demonstrates the direct requirement for T lymphocytes in recovery from oral candidiasis and suggests that this is associated with the production of cytokines by CD4+ T helper cells.

* Corresponding author. Mailing address: Oral Biology and Pathology, The University of Queensland, Brisbane, QLD 4072, Australia. Phone: 61 7 3365 8840. Fax: 61 7 3365 1109. E-mail: c.farah{at}uq.edu.au.

Editor: T. R. Kozel

Infection and Immunity, February 2002, p. 724-731, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 70.2.724-731.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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