LILRA2 is an activating innate immune receptor primarily expressed on myeloid cells that recognizes pathologically altered immunoglobulins and endogenous ligands to regulate inflammatory responses 1. LILRA2 specifically detects N-terminally truncated immunoglobulins generated by proteases from pathogenic bacteria (L. pneumophila, S. pneumoniae, M. hyorhinis, S. aureus) and fungi (C. albicans), binding cleaved IgM, IgG3, and IgG4 but not cleaved IgA1 1. Recently, solid-phase fibrinogen was identified as an endogenous LILRA2 ligand that induces inflammatory responses 2. Ligand engagement activates neutrophils and monocytes, triggering release of pro-inflammatory cytokines (CSF2, IL-6, CXCL8, CCL3) and chemokines 13. Importantly, LILRA2 activation on monocytes selectively modulates TLR4-mediated responses by downregulating TLR4 expression, thereby suppressing LPS-induced cytokine production 3. LILRA2 also inhibits dendritic cell differentiation and antigen presentation, suppressing adaptive immune responses 4. Dysregulated LILRA2 expression associates with poor prognosis in ovarian carcinoma 5, while LILRA2 polymorphisms contribute to susceptibility to systemic lupus erythematosus and microscopic polyangiitis 6. These findings establish LILRA2 as a novel therapeutic target for inflammatory and autoimmune diseases.