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Review
. 2010:2010:457146.
doi: 10.1155/2010/457146. Epub 2010 Jun 29.

Cytokine overproduction, T-cell activation, and defective T-regulatory functions promote nephritis in systemic lupus erythematosus

Marco Tucci  1 , Stefania Stucci, Sabino Strippoli, Francesco Silvestris
Affiliations
Review

Cytokine overproduction, T-cell activation, and defective T-regulatory functions promote nephritis in systemic lupus erythematosus

Marco Tucci et al. J Biomed Biotechnol. 2010.

Abstract

Lupus nephritis (LN) occurs in more than one-third of patients with systemic lupus erythematosus. Its pathogenesis is mostly attributable to the glomerular deposition of immune complexes and overproduction of T helper- (Th-) 1 cytokines. In this context, the high glomerular expression of IL-12 and IL-18 exerts a major pathogenetic role. These cytokines are locally produced by both macrophages and dendritic cells (DCs) which attract other inflammatory cells leading to maintenance of the kidney inflammation. However, other populations including T-cells and B-cells are integral for the development and worsening of renal damage. T-cells include many pathogenetic subsets, and the activation of Th-17 in keeping with defective T-regulatory (Treg) cell function regards as further event contributing to the glomerular damage. These populations also activate B-cells to produce nephritogenic auto-antibodies. Thus, LN includes a complex pathogenetic mechanism that involves different players and the evaluation of their activity may provide an effective tool for monitoring the onset of the disease.

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Figures

Figure 1
Figure 1
Representation of pathogenetic mechanisms of lupus nephritis. LN is a disease that includes several mediators of glomerular inflammation. In this context, T-cell subsets, through the production of nephritogenic cytokines or by cooperating with B-cells, macrophages, and dendritic cells promote the activation of the glomerular immune response.
Figure 2
Figure 2
Th1/Th2 cytokine profile in SLE. (a) Patients with LN (n = 69) produced large amounts of both IL-12 and IL-18, both in sera (black column) and urine (gray column). By contrast, those with different organ damages (n = 181) excluding LN, showed the highest production of IL-6 and IL-10. (b) IL-6 was overproduced in patients with high levels of anti-dsDNA antibodies independently from the presence of LN. Other cytokines were poorly associated with nephritogenic antibody production.
See this image and copyright information in PMC

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