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Published ahead of print on April 19, 2006
Journal of the American Society of Nephrology
© 2006 American Society of Nephrology
doi: 10.1681/ASN.2005091013
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FRONTIERS IN NEPHROLOGY

T Cells in Crescentic Glomerulonephritis

Peter G. Tipping 1 and Stephen R. Holdsworth

Centre for Inflammatory Diseases, Department of Medicine, Monash Institute of Medical Research, Monash University, Clayton, Victoria, Australia


1 To whom correspondence should be addressed. E-mail: peter.tipping{at}med.monash.edu.au.


  Abstract

Crescent formation in glomerulonephritis (GN) is a manifestation of severe glomerular injury that usually results in a poor clinical outcome. In humans, crescentic GN is frequently associated with evidence of either systemic or organ-specific autoimmunity. T cells play a major role in initiation of adaptive immune responses that lead to crescentic injury. In experimental models of crescentic GN, Th1 predominant immune responses have been shown to promote crescent formation. Perturbation of regulatory T cell function may contribute to development of autoimmune crescentic GN. The presence of T cells and macrophages in crescentic glomeruli, frequently in the absence of humoral mediators of immunity, suggest a dominant effector role for T cells in crescentic GN. The association of cellular immune mediators with local fibrin deposition implicates cell-mediated "delayed-type hypersensitivity-like" mechanisms in crescent formation. Intrinsic renal cells also contribute to T cell-driven effector mechanisms in crescentic GN, via expression of MHC II and co-stimulatory molecules and by production of chemokines and cytokines that amplify leukocyte recruitment and injury.


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