Role of basophils in the pathogenesis of minimal change nephrotic syndrome: A literature review

Abstract

A number of studies have verified that minimal change nephrotic syndrome (MCNS) may result from the dysfunction of T cells and B cells, although the precise mechanisms are yet to be elucidated. It is widely recognized that MCNS is a T helper (Th)2-dominant glomerular disease caused by an imbalanced Th1/Th2 immune response. Increased levels of the Th2 cytokines, interleukin (IL)-4 and IL-13, have been demonstrated to be closely associated with disease activity. In addition, basophils can affect the Th1/Th2 balance by enhancing the Th2 response and impairing the Th1 response, which are then involved in the development of numerous diseases. However, whether basophils are vital in the pathogenesis of MCNS remains unknown. Frequent positivity of the human basophil degranulation test in patients with MCNS has been observed. Thus, basophils should be analyzed in order to determine their role in the pathogenesis of MCNS.

Level Of 25(OH)D Serum, Expression of Interleukin 4 And Glucocorticoid Receptor of Mononuclear Cell In Steroid Resistance Nephrotic Syndrome Children

“…Pan et al and [18] consistently agree with Hafez [4] about imbalance of Th1/Th2 and domination of Th2 response in NS [4,18,27]. In MCNS, there was an increased of IL-4, IL-8 and GRO-Ɣ (growth regulated protein) production.…”

Urinary Interleukin-8 as a Biomarker for Steroid Resistance in Childhood Onset Nephrotic Syndrome

“…CXCL8/IL8 was shown to induce changes in the permeability of the GBM via decreasing the synthesis of heparan sulfate proteoglycans, which provoke proteinuria in rats [17] . In human GN, the expression of CXCL8/IL8 has mainly been detected in association with glomerular cell proliferation and confined either to the expanded mesangial areas and crescents [9,18,19] or spread over the whole glomeruli [19]. Podocytes express chemokines receptors and usually has the potential to respond to various soluble products of the immune system [20].…”

Urinary excretion of IL-1β, IL-6 and IL-8 cytokines during relapse and remission of idiopathic nephrotic syndrome

“…IL-8 (also named CXCL-8) was shown to induce changes in the permeability of the GBM via decreasing the synthesis of heparan sulfate proteoglycans, which eventually induced proteinuria in rats. 7 Podocytes express CXCR chemokine receptors and usually has the potential to respond to various soluble products of the immune system. 27 …”

“…Initially, imbalance between Th1 and Th2 helper cells with the increase in Th2 cytokines was postulated to be the key abnormality in INS. 7 – 9 Nevertheless, recently, a decrease in the number and/or function of T-regulatory cells (Tregs), which are important modulators of the functions of the effector T-cells, was reported to be a prerequisite for the development of INS. 1 , 3 , 10 – 12 …”