期刊
IMMUNITY
卷 39, 期 2, 页码 324-334出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.05.017
关键词
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类别
资金
- Shanghai Basic Research Program [12JC1408401]
- National Basic Research Program of China (Program 973) [2013CB531602]
- NIH [AI050848, GM065899]
- Tongji University
C-type lectin receptors (CLRs) play critical roles as pattern-recognition receptors (PRRs) for sensing Candida albicans infection, which can be life-threatening for immunocompromised individuals. Here we have shown that Dectin-3 (also called CLECSF8, MCL, or Clec4d), a previously uncharacterized CLR, recognized alpha-mannans on the surfaces of C. albicans hyphae and induced NF-kappa B activation. Mice with either blockade or genetically deleted Dectin-3 were highly susceptible to C. albicans infection. Dectin-3 constantly formed heterodimers with Dectin-2, a well-characterized CLR, for recognizing C. albicans hyphae. Compared to their respective homodimers, Dectin-3 and Dectin-2 heterodimers bound alpha-mannans more effectively, leading to potent inflammatory responses against fungal infections. Together, our study demonstrates that Dectin-3 forms a heterodimeric PRR with Dectin-2 for sensing fungal infection and suggests that different CLRs may form different hetero- and homodimers, which provide different sensitivity and diversity for host cells to detect various microbial infections.
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