Abstract
The immune mechanisms involved in glomerulonephritis can be considered at a number of different levels. First, there are mechanisms which involve specific recognition, that is binding of particular antigens or fragments of antigens by the recognition molecules of B cells (antibodies) or T cells (the T cell receptor). Second, there are a variety of non-specific mediator systems, often recruited by these specific elements, which are involved in the mediation of tissue damage. These include both cellular (e.g. neutrophils, monocytes) and non-cellular (e.g. complement) systems. Finally, a variety of mechanisms such as chemo-attractant cytokines (chemokines) and adhesion molecules on endothelium are involved in recruiting cellular members of both the specific and non-specific systems into the site of inflammation in the glomerulus. As exemplified by this last level there is considerable overlap between these divisions. Thus deposition of immune complexes, although clearly involving specific antibody/antigen systems, can in some circumstances be non-specific in the sense that the resulting damage does not depend on the particular specificity of the antibody. Similarly, the damage caused by cytotoxic T cells is presumably mediated at the molecular level by non-specific molecules such as perforin, but this is so closely bound up with specific recognition that it is of little help to attempt to separate the two. However, these distinctions do have some force, both conceptually and with respect to the degree of therapeutic specificity which could ultimately be achieved by the blockade of the various mechanisms. The rest of this chapter will consider examples from both animal models and, where possible, human disease which will help illustrate these mechanisms.
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Oliveira, D.B.G. (1999). Immune mechanisms in glomerulonephritis. In: Pusey, C.D. (eds) The Treatment of Glomerulonephritis. Developments in Nephrology, vol 40. Springer, Dordrecht. https://doi.org/10.1007/978-0-585-37972-2_1
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DOI: https://doi.org/10.1007/978-0-585-37972-2_1
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