The Four Types of Immune Sensitivity Reactions & Renal Examples for Each

Basic Clinical Immunology:  there are four types of hypersensitivity reactions.  Below is a listing of all four types and, since this is a Nephrology Blog, renal examples for each one.

Type I Immune Reaction (anaphylactic):  Type I hypersensitivity reactions are IgE-mediated responses which occur relatively rapidly following exposure to a previously-encountered antigen.  A classic example of this in nephrology is the "Type A" dialyzer reaction which can manifest as acute hypotension within minutes of beginning dialysis.  Classically, this has been due to treatment of dialyzer cartridges with ethylene oxide, and fortunately this type of reaction is much less common today than previously.  

Type II Immune Reaction (antibody-mediated):  Type II immune reactions are caused by antibodies which react with self-antigens, and the direct toxicity which results in this interaction.  Two good renal examples are Goodpasture's Syndrome (in which an antibody against an epitope in the glomerular basement membrane results in rapidly progressive glomerulonephritis) and membranous nephropathy (see my recent post on the exciting discovery of an antibody against phospholipase A2 receptor, a podocyte antigen, thereby causing proteinuria).

Type III Immune Reaction (immune complex-mediated):  Type III immune reactions are also antibody-mediated, but they involve the deposition of pre-formed immune complexes and resultant complement activation.  Immune complexes GN's such as lupus nephritis and post-strep glomerulonephritis are the classic examples here. 

Type IV Reaction (delayed hypersensitivity):  Type IV immune reactions are mediated predominantly by T-cells, which explains why the lag time from exposure to immune response is somewhat delayed compared to the other immune reaction types.  A good illustrative example from the field of transplant nephrology is the acute cellular rejection response that occurs within a few days of a renal transplant.  Such reactions are best managed by agents which diminish T-cell function (e.g., calcineurin inhibitors, thymoglobulin, etc).