TANK-binding kinase 1 (TBK1) is a key signaling kinase involved in innate immune and inflammatory responses. TBK1 drives immune cells to participate in the inflammatory response by activating the NF-κB and interferon regulatory factor signaling pathways in immune cells, promoting the expression of pro-inflammatory genes, and regulating immune cell function. Thus, it plays a crucial role in initiating a signaling cascade that establishes an inflammatory environment. In inflammation-related diseases, TBK1 acts as a bridge linking inflammation to immunity, metabolism, or tumorigenesis, playing an important role in the pathogenesis of immune-mediated inflammatory diseases, metabolic, inflammatory syndromes, and inflammation-associated cancers by regulating the activation of inflammatory pathways and the production of inflammatory cytokines in cells. In this review, we focused on the mechanisms of TBK1 in immune cells and inflammatory-related diseases, providing new insights for further studies targeting TBK1 as a potential treatment for inflammation-related diseases. Thus, optimizing and investigating highly selective cell-specific TBK1 inhibitors is important for their application in these diseases.

Introduction: CXCL13 regulates the homing of lymphocytes. It is highly expressed in kidney and serum of SLE patients, and correlates with disease activity, but its value in LN is unclear. This study was to investigate the expression and diagnostic value of CXCL13 and its regulated CXCR5⁺ T cells in LN.Methods: In mice, the association of serum CXCL13 levels with renal function was analyzed. And CXCR5⁺ T cell was detected by H&E staining and immunofluorescence in kidney, and by flow cytometry in spleen. In clinical studies, the association of CXCL13 and CXCR5⁺ T cells with disease activity was verified, and their diagnostic efficacy was assessed by ROC curves.Results: CXCL13 was elevated in both mouse and patients, and was positively correlated with disease severity. Serum CXCL13 had an AUC of 0.9287 in the diagnosis of SLE and 0.6244 in differential diagnosis of LN. And in MRL/lpr mice, CXCL13 was involved in the development of nephritis by promoting the recruitment of CXCR5⁺ T cells to the kidney. In the peripheral blood of LN patients, CXCR5⁺ T cells were significantly reduced. Combined detection of CXCR5⁺ T cell subsets resulted in an AUC of 0.9672 for the diagnosis of SLE and 0.7867 for the differential diagnosis of LN.Discussion: Serum CXCL13 has high accuracy in the diagnosis of SLE, and circulating CXCR5⁺ T cells may serve as a novel biomarker for the diagnosis of SLE and LN, which might complement the poor performance of serum CXCL13 in the diagnostic efficacy of LN.