The SLE is heterogeneous multisystem autoimmune disease with complex pathogenesisinvolves multiple cellular components of the innate and adaptive immune systems, presenceof autoantibodies and immune complexes, engagement of the complement system,dysregulation of several cytokines including type I interferons, and disruption of theclearance of nucleic acids after cell death(1,2,3).Among the putative mechanisms leading to the pathogenic breakdown of immune tolerance inSLE is the development of auto reactive T Cells, which contribute to pathologicactivation of B cells, dysfunction of regulatory T Cells and aberrant production ofpro-inflammatory cytokines (4,5) Autoantibodies targeting the T Cell Receptor (TCR)/CD3have been demonstrated to activate Ca2+/calmodulin-dependent kinase IV (CaMKIV),resulting in diminished IL-2 production and low serum IL-2 levels are commonly observedin 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 findingssuggest that T Cell autoantibodies are active participants in disease pathogenesis and ,supporting their potential as biomarkers for diagnosis and disease activity (10) Delaysin SLE diagnosis, often due to the limitations of current biomarkers, can lead toworsened outcomes (11). Improved diagnostic markers, such as the T Cell biomarkersdescribed here, could help reduce these delays , improve patient care and improve theability 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 therole 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 .