Systemic lupus erythematosus (SLE), formerly named ‘disseminated lupus erythematosus’, is an organ-non-specific autoimmune disease that has a largely unknown aetiology. Multiple susceptibility genes as well as environmental factors are found to be involved in the lupus pathogenesis (multi-factorial) [1, 2]. Also known as the prototype of autoimmune diseases, lupus is very intriguing both clinically and immunologically for its systemic nature and complexity in pathogenesis. The disease is characterized by multi-organ involvement and presence of autoantibodies to a variety of self antigens, particularly of the nuclear components [3]. Deposition of the immune complexes may trigger complement activation causing tissue damages. The broad auto-reactivities and hyperactivity of B cells are known to be predominately T cell-dependent [4], but the cellular and molecular mechanisms underlying such a systemic loss of B and T cell tolerance are yet to be fully understood. In contrast to B cell hyperactivity [5], reduced Interleukin 2 (IL-2) production and aberrant responsiveness of T cells are characteristic of SLE [6, 7]. Moreover, impaired cellular immunity, complement deficiency, defects in the clearance of dying cells by macrophages [8-10], roles of DC and the disrupted mechanisms of tolerance induction [11-14] are among many immunological characteristics of, or potential mechanisms proposed for, the disease.