Publications by authors named "Tiffanny N Newman"
Immunol Cell Biol
November 2014
Article Synopsis
- The UBASH3/STS/TULA family includes two proteins that act as important regulators of T-cell responses and inflammation by dephosphorylating specific targets.
- Mice lacking both family members (double knockout) show increased T-cell activation and inflammation, especially in a model of inflammatory bowel disease, compared to normal mice.
- The study suggests that these proteins influence T-cell signaling by affecting the phosphorylation of Zap-70, which is critical for T-cell receptor signaling.
Article Synopsis
- Amyloids, including β-amyloid and bacterial curli, play a key role in inflammation linked to diseases like Alzheimer's and infections.
- The study focused on how CD14 enhances immune system recognition of these amyloids by interacting with the TLR2/TLR1 complex.
- Findings show that both membrane-bound and soluble CD14 boost TLR2/TLR1 responses to curli, leading to higher production of inflammatory markers like IL-6 and nitric oxide, highlighting new avenues for dealing with amyloid-related conditions.
Infect Immun
February 2013
Article Synopsis
- Curli fibrils, a type of bacterial amyloid found in enterobacterial biofilms, are recognized by the TLR2/TLR1 receptor complex, which is crucial for the immune response in the gut.
- Infection with a curli-negative Salmonella enterica mutant led to greater intestinal barrier leakage and more bacterial spread compared to a curli-expressing strain, indicating curli's protective role.
- Blocking the signaling pathway involving TLR2 and PI3K eliminated these differences, highlighting the importance of this pathway in maintaining gut barrier integrity during bacterial infections.
Infect Immun
December 2012
Article Synopsis
- * A study using a mouse model showed that a mutant strain of Salmonella that couldn't produce curli amyloid fibrils resulted in lower levels of inflammatory cytokines IL-17A and IL-22, indicating the role of curli in immune response.
- * TLR2 is essential for producing IL-17A during Salmonella infections, as TLR2-deficient mice showed reduced cytokine expression, highlighting TLR2's role in regulating immune responses to bacterial entry in the gut.
Article Synopsis
- T-cell ubiquitin ligand-2 (TULA-2) is a newly identified phosphatase that plays a role in platelet signaling through glycoprotein VI (GPVI).
- The study found that TULA-2 interacts with and dephosphorylates Syk, a key signaling molecule in platelets, and its absence leads to increased Syk phosphorylation and heightened platelet activity.
- Mice lacking TULA-2 exhibited shorter bleeding times and a prothrombotic (increased clotting) phenotype, suggesting that TULA-2 is a crucial negative regulator of GPVI signaling in platelets.
