C-type lectin receptor Dectin3 deficiency balances the accumulation and function of FoxO1-mediated LOX-1⁺ M-MDSCs in relieving lupus-like symptoms.

ABSTRACT: Recent studies indicate that Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) can function as the signal of pattern recognition receptors, which play a pivotal role in the pathogenesis of the autoimmune disease. Systemic lupus erythematosus (SLE) is a classic autoimmune disease. Previous reports mainly focused on the potential role of TLRs in regulating the development of SLE, but little is known about the role of CLRs in the progression of SLE. Our previous studies showed that the inflammation-mediated accumulation of myeloid-derived suppressor cells (MDSCs) including granulocytic (G-MDSCs) and monocytic (M-MDSCs) participated in the pathogenesis of lupus. Mice deficient in Card9 (the downstream molecule of CLRs) were more susceptible to colitis-associated cancer via promotin

SUBMITTER: Li D 

PROVIDER: S-EPMC8417277 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature