Hypersensitivity Pneumonitis: An Immunopathology Review (Report) - Archives of Pathology & Laboratory Medicine

Hypersensitivity Pneumonitis: An Immunopathology Review (Report)

By Archives of Pathology & Laboratory Medicine

  • Release Date - Published: 2008-02-01
  • Book Genre: Health & Fitness
  • Author: Archives of Pathology & Laboratory Medicine
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Hypersensitivity Pneumonitis: An Immunopathology Review (Report) Archives of Pathology & Laboratory Medicine read online review & book description:

Hypersensitivity pneumonitis (HSP) is an immunologically mediated alveolar and interstitial lung disease caused by repeated inhalation of organic dusts and occupational antigens. (1,2) Although there are numerous inciting agents that may elicit HSP, the pathogenesis and the disease that ensues are similar. There are a number of unexplained features of HSP including (1) why do so few of the exposed individuals develop clinical HSP, (2) what triggers the acute episode after prolonged periods of previous sensitization, and (3) what leads to disease progression. It is known that, following exposure to inhaled environmental antigens, most individuals develop precipitating antibodies. However, only a few individuals will become symptomatic. (3) The reason for this is not clear. It is likely that genetic susceptibility is important in determining the susceptibility of some individuals for the development of HSP. It has been shown, for example, that polymorphisms in the major histocompatibility complex, tumor necrosis factor (TNF) [alpha], and tissue inhibitor of metalloproteinase 3 are associated with the development of or resistance to HSP. (4,5) The application of genome-wide association studies to HSP6 should allow us to further understand the genetic risk factors associated with this disease. As the disease may present acutely after antigenic challenge, it has been hypothesized that the inhaled antigen, when it enters the alveolar space, crosses the alveolar endothelium and binds to circulating antibody leading to immune complex deposition within the lung eliciting an inflammatory response. Although this is an attractive hypothesis, there are little clinical data that support it. (7,8) The acute phase, which is mediated by neutrophils, is followed by a chronic phase mediated by lymphocytes and macrophages, which is thought to represent a delayed-type hypersensitivity response. This may eventually result in the formation of granuloma and in time progress to pulmonary fibrosis. (1,2) Some experimental studies have shown that animals whose immune response is skewed toward a [T.sub.H]1 response over a [T.sub.H]2 response are more likely to develop HSP. (9-11) Most current information about the pathogenesis of HSP has been obtained by studying the cells and inflammatory mediators present in bronchoalveolar lavage (BAL) fluid and by studying lung biopsies. Bronchoalveolar lavage fluid is thought to provide a fairly accurate representation of intrapulmonary events and be representative of the immunologic and inflammatory mechanisms that lead to the pulmonary manifestations of HSP. (12,13)

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