Abstract
Hypersensitivity pneumonitis (HP) is an interstitial lung disease due to a combined type III and IV reaction with a granulomatous inflammation, caused by cytotoxic delayed hypersensitivity lymphocytes, in a Th1/Th17 milieu, chaperoned by a deficient suppressor function of T regulatory cells. Skewing toward a Th2 phenotype is reported for chronic HP. Phenotypic expression and severity depends on environmental and/or host genetic and immune co-factors. The wide spectrum of causative antigens is continuously up-dated with new sources of airborne organic particles and drug-induced HP. The diagnosis requires a detailed history, measurement of environmental exposure, pulmonary function tests, imaging, detection of serum specific antibodies, broncho-alveolar lavage, antigen-induced lymphocyte proliferation, environmental or laboratory-controlled inhalation challenge and lung biopsy. Complete antigen avoidance is the best therapeutic measure, although very difficult to achieve in some cases. Systemic steroids are of value for subacute and chronic forms of HP, but do not influence long term outcome. Manipulation of the immune response in HP holds future promise.
Highlights
Hypersensitivity pneumonitis (HP) is an interstitial lung disease (ILD) due to a combined type III and IV reaction with a granulomatous inflammation
The current view is that HP is caused by cytotoxic delayed hypersensitivity lymphocytes, in a Th1/Th17 milieu (Figure 1)
Many individuals are exposed to environmental antigens known to induce HP only approximately 5–15% will develop the disease [1]
Summary
Hypersensitivity pneumonitis (HP) is an interstitial lung disease (ILD) due to a combined type III and IV reaction with a granulomatous inflammation. The diagnosis requires a detailed and careful history that would include social, environmental, and occupational status, measurement of environmental exposure, pulmonary function tests, imaging, detection of serum specific antibodies, examination of BALF, antigen-induced lymphocyte proliferation, environmental or laboratory-controlled inhalation challenge with the suspected antigen and lung biopsy (Figure 2). In FDL specific antibodies against avian antigens were positive only in the acute form of the disease, while antigen-induced lymphocyte proliferation in peripheral blood or BALF cells was positive in all the patients [80]. Patients with low total lung capacity and DLCO, low lymphocyte levels in BALF and a UIP-like pattern at the time of diagnosis have increased risk for acute exacerbations of chronic HP [101].
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