# |
PMID |
Sentence |
1 |
24806599
|
Here we show that the coupling of ITAM-Syk-CARD9 signalling to interleukin-1 (IL-1) secretion in DCs is crucial for allergic sensitization to haptens.
|
2 |
24806599
|
Both MyD88 and Caspase recruitment domain-containing protein 9 (CARD9) signalling are required for contact hypersensitivity (CHS).
|
3 |
24806599
|
Naïve T cells require signals received through IL-1R1-MyD88 for effector differentiation, whereas DCs require CARD9 and spleen tyrosine kinase (Syk) signalling for hapten-induced IL-1α/β secretion and their ability to prime T cells.
|
4 |
24806599
|
DC-specific deletion of CARD9, DAP12, Syk or NLRP3, but not MyD88, is sufficient to abolish CHS.
|
5 |
24806599
|
All tested haptens, but not irritants, can induce Syk activation, leading to both the CARD9/BCL10-dependent pro-IL-1 synthesis (signal1) and reactive oxygen species-mediated NLRP3 inflammasome activation (signal2), required for IL-1 secretion.
|
6 |
26021803
|
Evidence for TLR4 and FcRγ-CARD9 activation by cholera toxin B subunit and its direct bindings to TREM2 and LMIR5 receptors.
|
7 |
26021803
|
Indeed, CTX-induced IL-6 production was substantially reduced in MyD88(-/-) or TLR4(-/-) macrophages.
|
8 |
26021803
|
CTB targeted not only GM1 and TLR4 but also TREM2 and LMIR5/CD300b.
|
9 |
26021803
|
CTB-TREM2 interaction initiated signal transduction through adaptor protein DAP12.
|
10 |
26021803
|
In summary, CTB targets TLR4, FcRγ-CARD9, TREM2, and LMIR5.
|