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Curtis B. Wilson

JAMA. 1992;268(20):2904-2909.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

SINCE the turn of the century, animal models have provided an understanding of the many possible ways in which the immune system can cause human renal injury. These models have refined and expanded our knowledge of how nephritogenic antigen and antibody interactions lead to phlogogenic immune deposit formation, immune mediator activation, and induction of damage to surrounding renal structures, which in turn produce histological and pathophysiological changes.^1,2

In addition, antibody reactions that are capable of inducing selective glomerular (or tubular) cell damage have been defined. Cellular immune reactions clearly are important in tubulointerstitial injury, and studies continue to define cellular immune contributions to glomerular injury. Knowledge of the humoral and cellular mediation pathways that magnify antibody-induced injury has expanded with the appreciation, at the molecular level, of proinflammatory cytokines, growth factors, adhesion molecules, and extracellular matrix interactions responsible for inflammation and subsequent sclerosis. The cells of the glomerulus (and . . . [Full Text PDF of this Article]

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