Batf3-dependent CD103⁺ dendritic cell accumulation is dispensable for mucosal and systemic antifungal host defense

ABSTRACT

Dendritic cells (DCs) are critical for defense against a variety of pathogens and the formation of adaptive immune responses. The transcription factor Batf3 is critical for the development of CD103⁺CD11b⁻ DCs, which promote IL-12–dependent protective immunity during viral and parasitic infections, dampen Th2 immunity during helminthic infection, and exert detrimental effects during bacterial infection. Whether CD103⁺ DCs modulate immunity during systemic or mucosal fungal disease remains unknown. Herein, we report that Batf3 is critical for accumulation of CD103⁺ DCs in the kidney and tongue at steady state, for their expansion during systemic and oropharyngeal candidiasis, and for tissue-specific production of IL-12 in kidney but not tongue during systemic and oropharyngeal candidiasis, respectively. Importantly, deficiency of CD103⁺ DCs does not impair survival or fungal clearance during systemic or oropharyngeal candidiasis, indicating that Batf3-dependent CD103⁺ DC accumulation mediates pathogen- and tissue-specific immune effects.

KEYWORDS:

• Batf3
• CD103
• dendritic cells
• fungal infection
• IL-12
• innate immunity
• oropharyngeal candidiasis
• systemic candidiasis

This article refers to:

Identifying host immune effectors critical for protection against Candida albicans infections

Abbreviations

CFUs	=	colony-forming units
DCs	=	Dendritic cells
OPC	=	oropharyngeal candidiasis
PAS	=	Periodic acid-Schiff
p.i.	=	post-infection

Disclosure of potential conflicts of interest

No potential conflicts of interest were disclosed.

Funding

This work was supported in part by the Intramural Research Program of the NIH, NIAID. JKL was supported by NIH grant 1R01AI108715.