The Diagnostic Utility of T Immunoglobulin G and T Immunoglobulin M Biomarkers in Patients With Systemic Lupus Erythematosus Disease : Associations With Disease Activity and Damage

The SLE is heterogeneous multisystem autoimmune disease with complex pathogenesis involves multiple cellular components of the innate and adaptive immune systems, presence of autoantibodies and immune complexes, engagement of the complement system, dysregulation of several cytokines including type I interferons, and disruption of the clearance of nucleic acids after cell death(1,2,3).

Among the putative mechanisms leading to the pathogenic breakdown of immune tolerance in SLE is the development of auto reactive T Cells, which contribute to pathologic activation of B cells, dysfunction of regulatory T Cells and aberrant production of pro-inflammatory cytokines (4,5) Autoantibodies targeting the T Cell Receptor (TCR)/CD3 have been demonstrated to activate Ca2+/calmodulin-dependent kinase IV (CaMKIV), resulting in diminished IL-2 production and low serum IL-2 levels are commonly observed in SLE (6,7,8,9) T Cell autoantibodies have been shown to influence T Cell signalling, migration, and adhesion, contributing to organ-specific targeting in SLE. These findings suggest that T Cell autoantibodies are active participants in disease pathogenesis and , supporting their potential as biomarkers for diagnosis and disease activity (10) Delays in SLE diagnosis, often due to the limitations of current biomarkers, can lead to worsened outcomes (11). Improved diagnostic markers, such as the T Cell biomarkers described here, could help reduce these delays , improve patient care and improve the ability of clinicians to differentiate between SLE and patients with falsely positive ANA (12) To the best of our knowledge, only a limited number of studies have explored the role of T cell autoantibodies in diagnosing and monitoring disease activity in SLE (12), and none have examined their association with lupus nephritis and disease damage index .