Rethinking T cell immunity in oropharyngeal candidiasis

Abstract

The disproportionate increase in oropharyngeal candidiasis (OPC) compared with systemic and vaginal candidiasis in female patients with AIDS has been a paradox for almost three decades. New data now show that severe OPC develops in Th17-deficient mice, but not Th1-deficient mice, implicating Th17-induced effector molecules in resistance to oral disease. These findings clarify and extend our current thinking about how CD4 T cell deficiency influences susceptibility to OPC.

Figure 1.

Schematic representation of the states of infection with C. albicans in humans and mice. (A) In humans, infection with C. albicans occurs during the perinatal period and likely reflects a small fungal inoculum. A period of colonization is followed by a state of commensalism. Neither colonization nor commensalism result in sufficient host damage to affect homeostasis such that it translates into disease (above dotted line), although impaired immunity or changes in microflora can lead to a change in this balance, leading to disease. Host damage can be caused directly by the fungus and/or by the resulting inflammatory response (B) In mice, infection is induced experimentally with a large fungal inoculum. The inoculum used by Conti et al. did not cause disease in normal mice, but induced host damage and disease in mice lacking IL-12p35 (impaired Th1 response) and more severe damage/disease in mice lacking IL-17p19 (impaired Th17 response).