Tlr7, a Toll-like receptor, is a key pattern recognition receptor in the innate immune system. It recognizes pathogen-derived single-stranded RNA (ssRNA), which is crucial for the innate immune response to viral infection. TLR7 can also recognize self-derived ssRNA. It signals through the MyD88 pathway, triggering the release of pro-inflammatory cytokines or type-I interferons, playing a vital role in immunoregulation [3,5].

In systemic lupus erythematosus (SLE), TLR7 signaling in B cells, along with disease-associated cytokines like IFNγ, IL-21, BAFF, and type 1 IFNs, drives autoimmunity, promoting autoreactive germinal centers and autoantibody production [1]. In TLR9-deficient MRL/lpr mice with accelerated SLE, B cell-specific TLR7 deficiency greatly improves disease, highlighting the cis-regulatory interaction between TLR9 and TLR7 within the B cell compartment and suggesting potential therapeutic strategies [6]. In rosacea, TLR7 promotes skin inflammation by activating the NFκB-mTORC1 axis, and in pustular psoriasis, the TLR7-MyD88-DC-CXCL16 axis activates neutrophils to elicit an inflammatory response [4,7]. Also, hyperactive TLR7 signaling is a driver of autoimmune disease in mouse models, and disrupted degradative sorting of TLR7 is associated with human lupus [2].

In conclusion, Tlr7 is essential for the innate immune response to RNA viruses and for immunoregulation. Its dysregulation is implicated in various immune-related diseases such as SLE, rosacea, and pustular psoriasis. Studies using gene-knockout (KO) or conditional-knockout (CKO) mouse models have been crucial in understanding its role in these disease conditions, providing insights for potential therapeutic approaches.