Targeting CD11b as Treatment for Lupus Save
Researchers from Rush University Medical Center have reported in the March 6 issue of the Journal of Clinical Investigation that engagement of the integrin CD11b with a novel compound, may improved outcomes in patients iwth systemic lupus erythematosus (SLE). (Citation source http://buff.ly/2mmqMVH)
Research has shown that lupus risk may be linked to mutations ITGAM (expressed as CD11b), with nearly 15 to 20 percent of lupus patients having ITGAM mutations. They analyzed blood samples from 171 lupus patients and found those with ITGAM mutations had higher levels of type I interferon (IFN I). ITGAM monitors toll-like receptors (TLR), which when activated leads to expression of type I interferon (IFN I).
If ITGAM is mutated, CD11b is defective, and is thus unable to suppress TLR activity. IFN 1 production ensues without regulation.
Using a rodent model of lupus, researchers have identified a new compound that binds to CD11b, activates it, leading to suppression of TLR activity.
The authors postulate that specifically modulating CD11b activity may lead to effective targeted treatment lupus patients.
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