The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
IL-1 family members and STAT activators induce cytokine production by Th2, Th17, and Th1 cells
Open accessAbstract
Expression of T1ST2, the IL-33R, by Th2 cells requires GATA3. Resting Th2 cells express little GATA3, which is increased by IL-33 and a STAT5 activator, in turn increasing T1ST2 from its low-level expression on resting Th2 cells. Th2 cells that have upregulated T1ST2 produce IL-13, but not IL-4, in response to IL-33 plus a STAT5 activator in an antigen-independent, NF-κB-dependent, cyclosporin A (CsA)-resistant manner. Similarly, Th17 cells produce IL-17A in response to IL-1β and a STAT3 activator and Th1 cells produce IFNγ in response to IL-18 and a STAT4 inducer. Thus, each effector Th cell produces cytokines without antigenic stimulation in response to an IL-1 family member and a specific STAT activator, implying an innate mechanism through which memory CD4 T cells are recruited by an induced cytokine environment.
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Cites
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Cited by
Differentiation of Effector CD4 T Cell Populations
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“TIR8 inhibits NF-kB and JNK activation following stimulation of IL-1R family members or TLRs (IL-1RI, IL-18R, ST2, TLR1, TLR2, TLR3, TLR4, TLR7, and TLR9) (Bulek et al., 2009; Garlanda et al., 2004; Lech et al., 2008; Wald et al., 2003), by interfering with the recruitment of TIR-containing adaptor molecules (Wald et…”
InfluentialCompartmentalized Control of Skin Immunity by Resident Commensals
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Metadata
- Authors
- Guo, L., Wei, G., Zhu, J., Liao, W., Leonard, W. J., Zhao, K., & Paul, W.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2009-08-11
- Volume
- 106
- Issue
- 32
- Pages
- 13463-13468
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2158300165
- Cited by
- 417
- References
- 36
- FWCI
- 11.20
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Guo, L., Wei, G., Zhu, J., Liao, W., Leonard, W. J., Zhao, K., & Paul, W. (2009). IL-1 family members and STAT activators induce cytokine production by Th2, Th17, and Th1 cells. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0906988106
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