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1.  CD8 T-cells and E-cadherin in host responses against oropharyngeal candidiasis 
Oral Diseases  2011;18(2):153-161.
Oropharyngeal candidiasis (OPC) is the most common oral infection in HIV+ persons. Previous studies suggest a role for CD8+ T-cells against OPC when CD4+ T-cells are lost, but enhanced susceptibility to infection occurs when CD8+ T-cell migration is inhibited by reduced tissue E-cadherin.
Conduct a longitudinal study of tissue CD8+ T-cells and E-cadherin expression before, during, and after episodes of OPC.
Oral fungal burden was monitored and tissue was evaluated for CD8+ T-cells and E-cadherin over a one-year period in HIV+ persons with a history of, or an acute episode of OPC.
While longitudinal analyses precluded formal interpretations, point prevalence analyses of the dataset revealed that when patients experiencing OPC were successfully treated, tissue E-cadherin expression was similar to patients who had not experienced OPC, and higher numbers of CD8+ T-cells were distributed throughout OPC− tissue under normal expression of E-cadherin.
These results suggest that 1) reduction in tissue E-cadherin expression in OPC+ patients is not permanent, and 2) high numbers of CD8+ T-cells can be distributed throughout OPC− tissue under normal E-cadherin expression. Together these results extend our previous studies and continue to support a role for CD8+ T-cells in host defense against OPC.
PMCID: PMC3252461  PMID: 21958417
oropharyngeal candidiasis; HIV; CD8+ T-cells; E-cadherin
2.  Candida-Host Interactions in HIV Disease 
Advances in Dental Research  2011;23(1):45-49.
Oropharyngeal candidiasis (OPC), caused primarily by Candida albicans, is the most common oral infection in HIV+ persons. Although Th1-type CD4+ T cells are the predominant host defense mechanism against OPC, CD8+ T cells and epithelial cells become important when blood CD4+ T cells are reduced below a protective threshold during progression to AIDS. In an early cross-sectional study, OPC+ tissue biopsied from HIV+ persons had an accumulation of activated memory CD8+ T cells at the oral epithelial–lamina propria interface, with reduced expression of the adhesion molecule E-cadherin, suggesting a protective role for CD8+ T cells but a dysfunction in the mucosal migration of the cells. In a subsequent 1-year longitudinal study, OPC− patients with high oral Candida colonization (indicative of a preclinical OPC condition), had higher numbers of CD8+ T cells distributed throughout the tissue, with normal E-cadherin expression. In OPC+ patients, where lack of CD8+ T cell migration was associated with reduced E-cadherin, subsequent evaluations following successful treatment of infection revealed normal E-cadherin expression and cellular distribution. Regarding epithelial cell responses, intact oral epithelial cells exhibit fungistatic activity via an acid-labile protein moiety. A proteomic analysis revealed that annexin A1 is a strong candidate for the effector moiety. The current hypothesis is that under reduced CD4+ T cells, HIV+ persons protected from OPC have CD8+ T cells that migrate to the site of a preclinical infection under normal expression of E-cadherin, whereas those with OPC have a transient reduction in E-cadherin that prohibits CD8+ T cells from migrating for effector function. Oral epithelial cells concomitantly function through annexin A1 to keep Candida in a commensal state but can easily be overwhelmed, thereby contributing to susceptibility to OPC.
PMCID: PMC3144040  PMID: 21441480
AIDS; Candida albicans; epithelial cells; T cells; mucosal immunity; cytokines

Results 1-2 (2)