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When antibodies bind to persistent antigens, they can create immune complexes. These antigen-antibody complexes can get lodged in small blood vessels and stimulate inappropriate inflammation of the surrounding tissue. Immune complex disorders are among the most common immune-mediated diseases. The location in the body where the immune complexes are deposited determines the signs and the course of the disease.
Glomerulonephritis Glomerular Disease Not every disease is caused by infection with bacteria, viruses, or other outside agents. There are a variety of noninfectious disorders that can impair the urinary system. All of these diseases... read more is inflammation of the glomeruli [the microscopic filtering units] in the kidneys. The inflammation develops when immune complexes become trapped in the glomeruli. This leads to activation of the body’s inflammatory defense system, which, in turn, damages the glomeruli. The immune complexes often form as a consequence of some other disease, especially infections with feline leukemia virus Congenital and Inherited Disorders Affecting Multiple Body Systems of Cats A variety of structural and functional defects have been described in animals. These defects are usually classified by the body system primarily affected, and many are discussed under the appropriate... read more [FELV], feline immunodeficiency virus Congenital and Inherited Disorders Affecting Multiple Body Systems of Cats A variety of structural and functional defects have been described in animals. These defects are usually classified by the body system primarily affected, and many are discussed under the appropriate... read more [FIV], or feline infectious peritonitis [FIP] Feline Infectious Peritonitis [FIP] Feline infectious peritonitis [often called FIP] is a severe, usually fatal disease caused by a feline coronavirus. Coronaviruses are a family of viruses that chiefly cause respiratory infections... read more virus. Inflammatory diseases or cancer may also be the cause. However, in many cats with glomerulonephritis, the triggering cause cannot be determined. Glomerulonephritis results in an excessive loss of protein in the urine [proteinuria]. The finding of protein in the urine during a urine test [urinalysis] may be the first indication that your cat has glomerulonephritis. Other signs include trouble breathing or the abnormal accumulation of fluid in the abdomen or under the skin. Treatment includes managing any underlying diseases, reducing the amount of protein lost in the urine, managing any existing kidney disease, and, possibly, giving immunosuppressive drugs to reduce the formation of the immune complexes. If it goes untreated, the disease can lead to chronic kidney failure.
Systemic lupus erythematosus [often simply called lupus] is an autoimmune disease that is rare in cats. Pets with lupus form immune complexes and have antibodies in their blood that are targeted against their own body tissues. Lupus causes widespread abnormalities of the skin, mouth, muscles, nervous system, blood vessels, lungs, kidneys, joints, nervous system, and blood [anemia and/or decreased platelet numbers]. Cats with lupus can develop life-threatening glomerulonephritis [see above]. Multiple organs are usually affected. The history, signs of disease, physical exam, and a blood test are used to diagnose lupus. Longterm treatment with corticosteroids and other drugs that suppress the immune system are prescribed to treat the disorder. Your veterinarian will determine the most appropriate treatment for your pet.
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| Immune complex |
| Immunology |
Type III hypersensitivity occurs when there is accumulation of immune complexes [antigen-antibody complexes] that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes. There are three steps that lead to this response.[1] The first step is immune complex formation, which involves the binding of antigens to antibodies to form mobile immune complexes. The second step is immune complex deposition, during which the complexes leave the plasma and are deposited into tissues. Finally, the third step is the inflammatory reaction, during which the classical pathway is activated and macrophages and neutrophils are recruited to the affected tissues. Such reactions may progress to immune complex diseases.
Types[edit]
Some clinical examples:
| Nuclear antigens |
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| Antibody complexes: specifically IgM to IgG |
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| Streptococcal cell wall antigens |
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| Hepatitis B virus surface antigen |
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| Several bacterial antigens |
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| Various |
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| Various |
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| Inhaled antigens [often mould or hay dust] |
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| Unknown, likely respiratory pathogen |
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| Unless else specified in boxes, then ref is:[2] |
Other examples are:
- Subacute bacterial endocarditis[3]
- Symptoms of malaria[4]
Signs and symptoms[edit]
Type III hypersensitivity occurs when there is an excess of antigen, leading to small immune complexes being formed that fix complement and are not cleared from the circulation. It involves soluble antigens that are not bound to cell surfaces [as opposed to those in type II hypersensitivity]. When these antigens bind antibodies, immune complexes of different sizes form.[5] Large complexes can be cleared by macrophages but macrophages have difficulty in the disposal of small immune complexes. These immune complexes insert themselves into small blood vessels, joints, and glomeruli, causing symptoms. Unlike the free variant, a small immune complex bound to sites of deposition [like blood vessel walls] are far more capable of interacting with complement; these medium-sized complexes, formed in the slight excess of antigen, are viewed as being highly pathogenic.[6]
Such depositions in tissues often induce an inflammatory response,[7] and can cause damage wherever they precipitate. The cause of damage is as a result of the action of cleaved complement anaphylotoxins C3a and C5a, which, respectively, mediate the induction of granule release from mast cells [from which histamine can cause urticaria], and recruitment of inflammatory cells into the tissue [mainly those with lysosomal action, leading to tissue damage through frustrated phagocytosis by PMNs and macrophages].[8]
Immune Complex Glomerulonephritis, as seen in Henoch-Schönlein purpura; this is an example of IgA involvement in a nephropathy
The reaction can take hours, days, or even weeks to develop, depending on whether or not there is immunological memory of the precipitating antigen. Typically, clinical features emerge a week following initial antigen challenge, when the deposited immune complexes can precipitate an inflammatory response. Because of the nature of the antibody aggregation, tissues that are associated with blood filtration at considerable osmotic and hydrostatic gradient [e.g. sites of urinary and synovial fluid formation, kidney glomeruli and joint tissues respectively] bear the brunt of the damage. Hence, vasculitis, glomerulonephritis and arthritis are commonly associated conditions as a result of type III hypersensitivity responses.[9]
As observed under methods of histopathology, acute necrotizing vasculitis within the affected tissues is observed concomitant to neutrophilic infiltration, along with notable eosinophilic deposition [fibrinoid necrosis]. Often, immunofluorescence microscopy can be used to visualize the immune complexes.[9] Skin response to hypersensitivity of this type is referred to as an Arthus reaction and is characterized by local erythema and some induration. Platelet aggregation, especially in microvasculature, can cause localized clot formation, leading to blotchy hemorrhages. This typifies the response to injection of foreign antigen sufficient to lead to the condition of serum sickness.[8]
See also[edit]
- Type I hypersensitivity
- Type II hypersensitivity
- Type IV hypersensitivity
- Type V hypersensitivity
References[edit]
- ^ Usman, Norina; Annamaraju, Pavan [2021], "Type III Hypersensitivity Reaction", StatPearls, Treasure Island [FL]: StatPearls Publishing, PMID 32644548, retrieved 2021-11-26
- ^ Table 5-3 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson [2007]. Robbins Basic Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-7. 8th edition.
- ^ Ibrahim AM, Siddique MS. "Subacute Bacterial Endocarditis Prophylaxis". National Center for Biotechnology Information, U.S. National Library of Medicine. Retrieved 22 July 2021.
- ^ "Type III Hypersensitivity Reaction". The Lecturio Medical Concept Library. Retrieved 22 July 2021.
- ^ "Hypersensitivity reactions". Retrieved 2008-09-26.
- ^ Parham, Peter [2009]. "12". The Immune System [3rd ed.]. New York, NY: Garland Science. p. 390.
- ^ "Chapter 19". Archived from the original on 2008-12-02. Retrieved 2009-01-08.
- ^ a b Parham, Peter [2009]. "12". The Immune System [3rd ed.]. New York, NY: Garland Science. p. 389.
- ^ a b Kumar, Vinay [2010]. "6". Robbins and Cotran Pathologic Mechanisms of Disease [8th ed.]. Philadelphia: Elsevier. pp. 204–205.