Introduction
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect any organ (Livingston et al., 2011) including skin, joints, kidneys, lungs and nervous system (Ginzler&Tayar., 2013). The overall incidence of SLE ranges from 7.4 to 159.4 cases per 100,000 people. (Ortega et al., 2010). The disease is more prevalent in women, with a female: male ratio of about 10:1 in most studies. (Pons -Estel et al., 2010).
Lupus nephritis (LN) is one of the most serious complications of systemic lupus erythematosus (SLE). (De Zubiria Salgado and Herrera-Diaz., 2012). The true prevalence of clinical lupus nephritis in persons with SLE is probably around 50%, being higher in certain ethnic groups and in children. (Dooley et al., 2007).
Autoimmunity plays a major role in the pathogenesis of lupus nephritis. The immunologic mechanisms include production of autoantibodies directed against nuclear elements. (Yung and Chan., 2008). These autoantibodies form pathogenic immune complexes intravascularly, which are deposited in glomeruli. Alternatively, autoantibodies may bind to antigens already located in the glomerular basement membrane, forming immune complexes in situ. Immune complexes promote an inflammatory response by activating complement and attracting inflammatory cells, including lymphocytes, macrophages, and neutrophils. (D'Agati et al., 2007).
The current classification system divides lupus nephritis into six classes based on proliferative or membranous changes (although tubulointerstitial nephritis, thrombotic micro angiopathy or vascular disease may be significant contributors to disease in some patients. ( Micha., 2012).
The prognosis of the lesion is predicted by the class, activity and chronicity of the glomerular pathology. Biopsies could comprehensively review a well-recognized relationship between the histological features on biopsy and the clinical course of lupus nephritis. (Mittal et al., 2005).
The principal goal of therapy in lupus nephritis is to normalize renal function or, at least, to prevent the progressive loss of renal function. Therapy differs depending on the pathologic lesion. )Dooley., 2007), (Houssiau and Ginzler., 2008).
T cells are important mediators in both mouse models and human patients in the progression of lupus nephritis. Mechanisms by which T cells contribute to tissue injury include activating and providing help to nephritogenic antibody-producing B cells, recruiting macrophages and dendritic cells (DCs), and producing cytokines. (Nowling & Gilkeson., 2011).
It is hypothesized that intrarenal B cells form part of a local system with pivotal involvement in the pathogenesis of lupusnephritis. It enhances immunological responses and exaggerate the local immune response to persisting autoimmune damage in the tubulointerstitium. (shen et al., 2012).
The majority of B cells in lupus nephritis patients displayed a mature non-antibody producing phenotype with antigen presenting ability. (Steinmetz et al., 2008). So, it is important to analyse the intra renal B cell infilterate to reveal its relationship with clinical outcome. (shen et al., 2012).
CD20 is a human B lymphocyte specific marker, which is a cell surface molecule. It is also expressed in B-cell differentiation subsets, including mature B cells and all subgroups of pre-B cells. (Sarwal et al., 2003).
CD3 is a highly specific T lymphocyte marker. It is found bound to membranes of all mature T cells. The presence of CD3 at all stages of T-cell development, makes it a useful immunohistochemical marker for T-cells in tissue sections. (leong et al., 2003), (Kuby et al., 2007).
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