[P1-2-28] Investigation of regulatory mechanism of oral candidiasis by Th17 cells
Keywords:微生物、獲得免疫、真菌
Oral candidiasis is an opportunistic infection caused by Candida albicans (C. albicans), an endemic fungus of the oral cavity, and occurs in susceptible hosts such as the elderly and immunocompromised patients whose defenses are significantly compromised. In Japan, where the super-aging society is becoming more serious, the number of patients with oral candidiasis has been increasing in recent years and is of great social concern. Although effective chemotherapy is desired for C. albicans infections, there are very few safe and effective antifungal drugs. Recent reports have revealed that Th17 cells, characterized by cytokine IL-17A production, play an important role in the host immune response against C. albicans. However, the mechanisms of Th17 cell differentiation, such as the antigens that induce differentiation into Th17 cells and the sites where the immune response is induced, remain largely unknown. We hypothesized that understanding and controlling the Th17 cell immune response specific to C. albicans could lead to the development of new preventive and therapeutic strategies against oral candidiasis. The aim of this study is to elucidate the host immune response mechanism by Th17 cells in oral candidiasis, focusing on antigens derived from C. albicans that are important for inducing Th17 cell differentiation and the sites where the immune response occurs. We have constructed a mouse model of oral candidiasis using C. albicans SC5314. Using the constructed mouse model of oral candidiasis, we report on the progress in narrowing down C. albicans-derived antigens that induce Th17 cells and the dynamics of Th17 cell responses in vivo.