In TREML4 -/- mice macrophages that are hyporesponsive to TLR7 agonists, macrophages fail to produce type I interferons due to impaired phosphorylation of the transcription factor STAT1 by the mitogen-activated protein kinase p38 and decreased recruitment of the adaptor MYD88 to TLR7. TREML4 deficiency reduced the production of inflammatory cytokines and autoantibodies in MRL/lpr mice, suggesting that TLR7 is a vital component of antiviral immunity and a predecessor factor in the pathogenesis of rheumatic diseases such as systemic lupus erythematosus (SLE).
In TREML4 -/- mice macrophages that are unresponsive to TLR7 stimuli, macrophages fail to produce type I interferons due to impaired activation of the transcription factor STAT1 by p38 MAPK and decreased recruitment of MYD88. This deficiency in TREML4 resulted in reduced production of inflammatory cytokines and autoantibodies in MRL/lpr mice, highlighting TLR7's importance in antiviral immunity and its role as a precursor to rheumatic diseases such as SLE.