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Invasive candidiasis (IC) is one of the leading causes of death among immunocompromised patients. Because of limited effective therapy treatment options, prevention of IC through vaccine is an appealing strategy. However, how to induce the generation of direct candidacidal antibodies in host remains unclear.  Gpi7  mutant  C. albicans  is an avirulent strain that exposes cell wall β-(1,3)-glucans. Here, we found that vaccination with the  gpi7  mutant strain could protect mice against invasive candidiasis caused by  C. albicans  and non- albicans Candida  spp. The protective effects induced by  gpi7  mutant relied on long-lived plasma cells (LLPCs) secreting protective antibodies against  C. albicans . Clinically, we verified a similar profile of IgG antibodies in the serum samples from patients recovering from IC to those from  gpi7  mutant-vaccinated mice. Mechanistically, we found cell wall β-(1,3)-glucan of  gpi7  mutant facilitated Dectin-1 receptor dependent nuclear translocation of non-canonical NF-κB subunit RelB in macrophages and subsequent IL-18 secretion, which primed protective antibodies generation  in vivo . Together, our study demonstrate that Dectin-1 engagement could trigger RelB activation to prime IL-18 expression and established a new paradigm for consideration of the link between Dectin-1 mediated innate immune response and adaptive humoral immunity, suggesting a previously unknown active vaccination strategy against  Candida  spp. infection.

Dectin-1 Facilitates IL-18 Production for the Generation of Protective Antibodies Against Candida albicans