Tlr7, a Toll-like receptor, is a crucial pattern recognition receptor in the innate immune system. It recognizes pathogen-derived single-stranded RNA (ssRNA), triggering the release of pro-inflammatory cytokines or type-I interferons, which is essential for immunoregulation [2,5]. TLR7 signaling is associated with pathways like MyD88-dependent signaling, and is important for the recognition of RNA viruses and initiation of antiviral immunity [2,4].

In systemic lupus erythematosus (SLE), TLR7 signaling in B cells is a major driver of autoimmunity. TLR7, along with cytokines like IFNγ, IL-21, BAFF and type 1 IFNs, promotes autoreactive germinal centers formation, autoantibody production, and the development of certain B cell subsets [1]. In TLR9-deficient MRL/lpr mice with accelerated SLE, B cell-specific TLR7 deficiency greatly improved disease, highlighting the role of B cell-intrinsic TLR7 expression in driving severe lupus [6].

In rosacea, TLR7 promotes skin inflammation via activating the NFκB-mTORC1 axis, as overexpressing TLR7 in keratinocytes stimulates the mTORC1 pathway through NFκB signaling, leading to cytokine and chemokine production and CD4+ T cell migration [3].

In pustular psoriasis, the TLR7-MyD88-DC-CXCL16 axis promotes neutrophil migration to skin lesions and stimulates the inflammatory response, as TLR7 induces DC secretion of CXCL16, which activates neutrophils [7].

In conclusion, Tlr7 plays a vital role in the innate immune response, especially in recognizing ssRNA and initiating antiviral immunity. Its dysregulation is implicated in multiple diseases such as SLE, rosacea, and pustular psoriasis. Studies using gene-knockout mouse models, like B cell-specific TLR7-deficient mice in SLE, have been crucial in revealing its role in disease-associated biological processes, providing insights into potential therapeutic strategies for these diseases.