IRCTX muscle injury results in muscle fibrosis through macrophage-derived TGF-β1.
FAPs respond to TGF-β1 by differentiating into fibroblasts.
Conditional knockout and systemic inhibition of TGF-β1 attenuates IRCTX fibrosis.
NOD1 restricts replication of RNA viruses.
The cumulative effects between NOD1 and MDA5 normal form are conserved.
NOD1 degradation by the truncated form of MDA5 is specific to fish.
Zhx2 in macrophages accelerates sepsis.
Zhx2 promotes glycolysis in macrophages via Pfkfb3.
Type I IFN–mediated JAK–STAT signaling is impaired in Perforin-2–deficient cells.
Perforin-2 independently associates with IFNAR1 and IFNAR2 in resting cells.
Perforin-2 is critical for the activation of Jak1 and Tyk2 upon IFN-β stimulation.
pDCs express LIFR.
LIF inhibits pDC production of type I IFN.
LIF biases DC development towards cDCs at the expense of pDCs.
Dimerization of the BCAP Toll/IL1 domain is required for function.
BCAP TIR modulates the oligomerization state of TLR signaling adaptor MAL.
TIG domains are a promiscuous dimerization module in gene expression and signaling.
Spontaneous colitis in Itch-deficient mice is associated with altered gut microbiota.
Alterations in gut microbiota are independent of elevated IL-17 in Itch-deficient mice.
Bacteroides vulgatus induces colonic inflammation in Itch–/– mice.
CEACAM1 is an essential contributor in the NET–tumor cell interaction.
CEACAM1 is a potential target for preventing liver metastasis of colon cancer.
Expression of csMHCII is a determinant of the composition of the TME.
csMHCII is a factor determining the response to anti–PD-1 therapy.
Cas9 RNP electroporation deletes genes in naive CD8+ T cells transferred in vivo.
High efficiency gene deletion occurs even in the absence of T cell activation.
Multiple gene KO and HDR edited cells can be generated using this method.
