Anshu Agrawal

TL;DR: It is demonstrated that distinct Toll-like receptor (TLR) ligands instruct human DCs to induce distinct Th cell responses by differentially modulating mitogen-activated protein kinase signaling.

TL;DR: iMGLs were used to examine the effects of Aβ fibrils and brain-derived tau oligomers on AD-related gene expression and to interrogate mechanisms involved in synaptic pruning, and whole-transcriptome analysis demonstrates that they are highly similar to cultured adult and fetal human microglia.

TL;DR: It is demonstrated that different Toll-like receptor (TLR) ligands induce distinct dendritic cell activation and immune responses in vivo, and differentially bias Th responses in vitro and in vivo.

TL;DR: Results from real-time PCR and protein expression by flow cytometry demonstrated an increased expression of phosphatase and tensin homolog, a negative regulator of the PI3K-signaling pathway, in DCs from the aging, and may be responsible for the defect in AKT phosphorylation and, therefore, the altered innate immune response ofDCs from elderly humans.

TL;DR: It is demonstrated that LT severely impairs the function of dendritic cells and host immune responses by disrupting the mitogen-activated protein (MAP) kinase intracellular signalling network, and suggest a role for LT in suppressing host immunity during B. anthracis infections.