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• W1972202295 abstract "Hypersensitivity pneumonitis is an immunologic inflammatory pulmonary disease caused by the inhalation of and sensitization to any of a wide variety of environmental organic dust antigens. Susceptible individuals are sensitized by inhalation of the antigen, and with repeat exposure they develop acute respiratory symptoms of cough and shortness of breath along with systemic symptoms of chills, fever, malaise, anorexia, and weight loss. Restrictive and diffusion defects along with nodular pulmonary infiltrates representing granulomatous and lymphocytic involvement are characteristic features. The immune nature of the disease is certain because of the demonstration of cellular and humoral responses to the antigen as well as reproduction of the acute episode with purposeful inhalation challenge with antigen and a return to normal respiratory function after avoidance of exposure.1Yamasaki H Kinoshita T Ohmura M Ando K Soda T Sakata T et al.Lowered responsiveness of bronchoalveolar lavage T lymphocytes in hypersensitivity pneumonitis.Am J Respir Cell Mol Biol. 1991; 4: 417Google Scholar Evaluation of the pulmonary environment by bronchoalveolar lavage demonstrates characteristic immune activity. After inhalation of antigen, acute neutrophilia occurs, followed by lymphocytosis. Alveolar macrophages are activated, as detected by activation markers, and proinflammatory molecules such as interleukin-1, interleukin-8, monocyte chemotactic protein-1, and tumor necrosis factor can be found in the alveolar fluid. The lymphocytosis is largely the result of the influx or expansion of CD8+ cells representing immune suppressor/ cytotoxic cells. Evidence suggests that a failure to suppress the activated immune response occurs, and the interstitial lymphocytic and granulomatous infiltration occurs unchecked as a result of uncontrolled TH1 activity.2Dakhama A Israel-Assayag E Lormier Y. Altered immunosuppressive activity of alveolar macrophages in farmer's lung disease.Eur Resp J. 1996; 9: 1456-1462Google Scholar Interestingly, in individuals who are similarly exposed to antigen but are not ill, pulmonary lymphocytosis composed largely of CD8+ cells also occurs, but the cells appear to function normally in regulating the inflammatory response, and no disease occurs.3Salvaggio JE. Inhaled particles and respiratory disease.J Allergy Clin Immunol. 1994; 94: 304Google Scholar Thus, aside from host susceptibility, the nature of the antigen and the resulting immune response are key in the development of the disease. Evidence points to the alveolar macrophage as the orchestrator in the development of hypersensitivity pneumonitis. Patients with the disease have lung macrophages that express increased activation markers such as CD254Israel-Assayag E Dakhama A Lavigne S Laviolette M Lormier Y. Expression of costimulatory molecules on alveolar macrophages in hypersensitivity pneumonitis.Am J Respir Crit Care Med. 1999; 159: 1830-1834Google Scholar; secrete increased levels of tumor necrosis factor, interleukin-1, macrophage inflammatory protein-1-α, and interleukin-8; have enhanced antigen-presenting capacity; and attract inflammatory cells to the area.5Grammar LC. Occupational allergic alveolitis.Am J Allergy Asthma Immunol. 1999; 83: 602-606Google Scholar The increase in activated macrophages is accompanied by neutrophilia with increased levels of respiratory burst.6Vogelmeier C Krombach F Munzing S. Activation of blood neutrophils in acute episodes of farmers lung.Am Dev Respir Dis. 1993; 148: 396-400Google Scholar Thus the inflammatory milieu is established. Lymphocytes are also activated in this disease as the cell surface marker CD25—the interluekin-2 receptor—and costimulatory molecules such as CD28 and CTLA4 can be detected on cells or in alveolar fluid.4Israel-Assayag E Dakhama A Lavigne S Laviolette M Lormier Y. Expression of costimulatory molecules on alveolar macrophages in hypersensitivity pneumonitis.Am J Respir Crit Care Med. 1999; 159: 1830-1834Google Scholar The up-regulation of macrophage cell surface markers such as CD80 and CD86, which play a role in the control of lymphocyte proliferation, suggests an immuno-regulatory defect in the disease, resulting in a lymphocytic alveolitis. In the current issue, Schuyler, Gott, and Cherne use an established murine model to provide further evidence that hypersensitivity pneumonitis is a T cell disease with the generation of TH1 cytokines and chemokines via interaction with macrophage-derived factors.7Schuyler M Gott K Cherne A. Mediators of hypersensitivity pneumonitis.J Lab Clin Med. 2000; 136: 29-38Google Scholar In previous studies they have shown that the lesions of murine hypersensitivity pneumonitis can be transferred with T cells and specifically with TH1 but not with TH2 cells.8Schuyler M Gott K Cherne A Edwards B. TH1 CD4+ cells adoptively transfer experimental hypersensitivity pneumonitis.Cell Immunol. 1997; 177: 169-175Google Scholar In the present study they demonstrate in a murine model of farmer's lung with the offending antigen that chemokines and cytokines of the TH1 phenotype can be demonstrated in the bronchoalveolar lavage fluids of sensitized mice. Further, they show the secretion of macrophage factors including interleukin-1, interleukin-6, and tumor necrosis factor, which enhance lymphocyte expansion and promote TH1 differentiation. Interleukin-12, another macrophage product that is a potent TH1 differentiation factor, was also detected. The murine model establishes the alveolar macrophage and the differentiation to TH1 cells as prime in the pulmonary inflammation, resulting in hypersensitivity pneumonitis. Schuyler's model, however, does not distinguish between sick individuals and the 50% of individuals similarly exposed who remain asymptomatic in spite of having lymphocytic alveolitis. Careful evaluation of the immunoregulatory factors and cytokine and chemokine assays in such individuals should provide additional key information in the orchestration of this disease by immune effector cells." @default.
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• W1972202295 date "2000-07-01" @default.
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• W1972202295 title "Immunologic orchestration of hypersensitivity pneumonitis" @default.
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• W1972202295 doi "https://doi.org/10.1016/s0022-2143(00)70044-8" @default.
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