Novel mechanism balancing tolerance versus immune regulation

Santhakumar Manicassamy, PhD
Santhakumar Manicassamy, PhD
Santhakumar Manicassamy, PhD
Santhakumar Manicassamy, PhD
As published in The Journal of Immunology, Santhakumar Manicassamy, PhD, and colleagues including Cancer Center members Drs. Mellor and Munn, have discovered how the immune system’s dendritic cells suppress autoimmune inflammation. Furthermore, they found that in the absence of a molecule called beta-catenin, this suppression is by-passed, inducing a pro-inflammatory state. They have thereby identified an underlying mechanism responsible for balancing tolerance versus immune regulation, governed within a single cell type. In dendritic cells, activation of the Dectin-1 receptor induces inflammatory responses through the production of pro-inflammatory cytokines IL-6, -12, and -23, whereas activation of the TLR2 receptor suppresses inflammation via the PI3K/AKT/beta-catenin pathway, which produces the anti-inflammatory cytokine IL-10 and the enzyme retinaldehyde dehydrogenase 2. The research suggests the therapeutic importance of TLR2 signaling as a novel strategy against autoimmune disease, chronic infection, and cancer, where tolerance dominates. [The Journal of Immunology. 2014 193:4203-4213.]
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Written by Allison Brown

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