T cell regulation, anti-idiotypic immunity, and the nephritogenic immune response

E. G. Neilson, B. Zakheim

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


It is generally agreed that most forms of nephritis probably have an immunologic basis. This belief is supported by a large number of studies focusing on the nephritogenic immune response as it occurs locally within the kidney. One outgrowth of these immunologic investigations is the now classical subdivision of renal histopathology into the effector pathways of antibody, immune deposit, and cell-mediated disease. The thorough study of these effector pathways has greatly enhanced our understanding of the inflammatory mechanisms directly involved in developing immunopathology. There is, however, another aspect to immune-mediated renal disease which is the rapidly growing area of immune regulation. Interest in this subject has emerged as one of several fascinating developments within the field of basic immunology and has been sustained because a variety of experimental observations now suggests that immune regulation has an important role in defining the natural history of an immune response. In the context of renal disease, immune regulation can be viewed as a complex network of antibody and cell-mediated circuits usually operating to produce feedback suppression and down-regulating leading to the eventual control of on-going renal injury. The interdigitation of such regulatory systems with more traditional areas of renal immunology has not been formally defined. As this integration occurs, however, the subject of immune regulation will more than likely find a permanent and, perhaps, prominent place withint the broader view of the nephritogenic immune response.

Original languageEnglish (US)
Pages (from-to)289-302
Number of pages14
JournalKidney international
Issue number3
StatePublished - 1983

ASJC Scopus subject areas

  • Nephrology


Dive into the research topics of 'T cell regulation, anti-idiotypic immunity, and the nephritogenic immune response'. Together they form a unique fingerprint.

Cite this