| First Author | Zhu LL | Year | 2013 |
| Journal | Immunity | Volume | 39 |
| Issue | 2 | Pages | 324-34 |
| PubMed ID | 23911656 | Mgi Jnum | J:208235 |
| Mgi Id | MGI:5562511 | Doi | 10.1016/j.immuni.2013.05.017 |
| Citation | Zhu LL, et al. (2013) C-type lectin receptors Dectin-3 and Dectin-2 form a heterodimeric pattern-recognition receptor for host defense against fungal infection. Immunity 39(2):324-34 |
| abstractText | 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-kappaB 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. |
