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• W2044897954 abstract "Yesterday I evaluated a new patient with sarcoidosis who asked whether the disease was caused by her work as a short-order cook. The week previously, a patient wondered whether his work in a textile mill caused his sarcoidosis, while another was convinced that her sarcoidosis resulted from furniture polish fumes. In the past, I would have given my standard answer to such queries: although we do not know what causes sarcoidosis, there is no evidence suggesting an excessive number of cases in short-order cooks, textile workers, and those exposed to furniture polish. In short, these patients’ exposures had been unlikely culprits in the development of their disease. This is no longer my answer to my patients’ questions, and the provocative article by Reich in this issue of CHEST (see page 367) explains the reason for abandoning it. There is mounting evidence suggesting that the “cause” of sarcoidosis does not relate to a specific exposure but rather to an abnormal host immunologic response to one of several exposures. A necessary interplay between specific combinations of exposures and host responses in the pathogenesis of sarcoidosis would explain why so many studies have come to conflicting conclusions regarding the etiology of the disease. For example, two studies1Fidler HM Rook GA Johnson NM et al.Mycobacterium tuberculosis DNA in tissue affected by sarcoidosis.BMJ. 1993; 306: 546-549Crossref PubMed Scopus (113) Google Scholar2Saboor SA Johnson NMcl McFadden J et al.Detection of mycobacterial DNA in sarcoidosis and tuberculosis with polymerase chain reaction.Lancet. 1992; 339: 1012-1015Abstract PubMed Scopus (225) Google Scholar using polymerase chain reaction techniques have detected mycobacterial DNA in the lung tissue of 44% and 50%, respectively, of sarcoidosis patients, while other studies3Bocart D Lecossier D DeLassence A et al.A search for mycobacterial DNA in granulomatous tissues from patients with sarcoidosis using the polymerase chain reaction.Am Rev Respir Dis. 1992; 145: 1142-1148Crossref PubMed Scopus (121) Google Scholar4Ghossein RA Ross DG Salomon N et al.A search for mycobacterial DNA in sarcoidosis using the polymerase chain reaction.Am J Clin Pathol. 1994; 101: 733-737Crossref PubMed Scopus (83) Google Scholar5Popper HH Winter E Hofler G DNA of Mycobacterium tuberculosis in formalin-fixed, paraffin-embedded tissue in tuberculosis and sarcoidosis detected by polymerase chain reaction.Am J Clin Pathol. 1994; 101: 738-741Crossref PubMed Scopus (128) Google Scholar6Thakker B Black M Foulis AK Mycobacterial nucleic acids in sarcoid lesions [letter].Lancet. 1992; 339: 1537Abstract PubMed Scopus (21) Google Scholar have established that mycobacterial DNA was rare or absent in sarcoidosis. As stated by Reich, one study linked sarcoidosis to human-made mineral fibers,7Drent M Bomans PH Van Suylen RJ et al.Association of man-made mineral fibre exposure and sarcoid-like granulomas.Respir Med. 2000; 94: 815-820Abstract Full Text PDF PubMed Scopus (65) Google Scholar whereas another large study of human-made mineral fiber workers found no such association.8Hughes JM Jones RN Glindmeyer HW et al.Follow up study of workers exposed to man made mineral fibers.Br J Ind Med. 1993; 50: 658-667PubMed Google Scholar Although some studies have shown a higher prevalence of Propionibacterium acnes and Chlamydia species in the lungs of sarcoidosis patients than in control subjects,9Ishige I Usui Y Takemura T et al.Quantitative PCR of mycobacterial and propionibacterial DNA in lymph nodes of Japanese patients with sarcoidosis.Lancet. 1999; 354: 120-123Abstract Full Text Full Text PDF PubMed Scopus (265) Google Scholar10Gaede KI Wilke G Brade L et al.Anti-chlamydophila immunoglobulin prevalence in sarcoidosis and usual interstitial pneumoniae.Eur Respir J. 2002; 19: 267-274Crossref Scopus (13) Google Scholar these findings have not been universal.11Blasi F Rizzato G Gambacorta M et al.Failure to detect the presence of Chlamydia pneumoniae in sarcoid pathology specimens.Eur Respir J. 1997; 10: 2609-2611Crossref Scopus (17) Google Scholar12Eishi Y Suga M Ishige I et al.Quantitative analysis of mycobacterial and propionibacterial DNA in lymph nodes of Japanese and European patients with sarcoidosis.J Clin Microbiol. 2002; 40: 198-204Crossref PubMed Scopus (349) Google Scholar Our current understanding is that the development of sarcoidosis requires at least the three following major events: exposure to an antigen; acquired cellular immunity directed against the antigen mediated through antigen-presenting cells and antigen-specific T-lymphocytes; and the appearance of immune effector cells that promote a nonspecific inflammatory response.13Newman LS Rose CS Maier LA Sarcoidosis.N Engl J Med. 1997; 336: 1224-1234Crossref PubMed Scopus (1386) Google Scholar More specifically, alveolar macrophages from patients with pulmonary sarcoidosis show enhanced antigen-presenting capacity by the enhanced expression of human leukocyte antigen (HLA; major histocompatibility complex)-class II molecules, which is probably induced by an interaction with the sarcoidosis antigen and possibly interferon (INF)-γ.14Costabel U Sarcoidosis: clinical update.Eur Respir J. 2001; 18: 56s-68sGoogle Scholar These macrophages recognize, process, and present the putative antigen to CD4+ T cells of the T helper (Th)-1 type.14Costabel U Sarcoidosis: clinical update.Eur Respir J. 2001; 18: 56s-68sGoogle Scholar These activated macrophages produce IL-12, which induces a lymphocyte shift toward a Th-1 profile and causes T lymphocytes to secrete INF-γ. These activated T cells release IL-2 and chemotactic factors that recruit monocytes and macrophages to the site of disease activity.14Costabel U Sarcoidosis: clinical update.Eur Respir J. 2001; 18: 56s-68sGoogle Scholar IL-2 is also activated and expands various T-cell clones.15Konishi K Moller D Saltini C et al.Spontaneous expression of the interleukin 2 receptor gene and presence of functional interleukin 2 receptors on T lymphocytes in the blood of individuals with active pulmonary sarcoidosis.J Clin Invest. 1988; 82: 775-781Crossref PubMed Scopus (65) Google Scholar INF-γ is able to further activate macrophages and to transform them into giant cells, which are important building blocks of the granuloma.14Costabel U Sarcoidosis: clinical update.Eur Respir J. 2001; 18: 56s-68sGoogle Scholar16Steffen M Petersen J Oldigs M et al.Increased secretion of tumor necrosis factor-alpha, interleukin-1-beta, and interleukin-6 by alveolar macrophages from patients with sarcoidosis.J Allergy Clin Immunol. 1993; 91: 939-949Abstract Full Text PDF PubMed Scopus (98) Google Scholar Therefore, the evidence suggests that the immunologic process that leads to sarcoidosis begins when an antigen is presented by a macrophage via HLA class II molecules to a T lymphocyte. This induces a Th-1 T-lymphocyte response whereby cytokines are released that result in granuloma formation. Scandinavian investigators17Grunewald J Janson CH Eklund A et al.Restricted Vα2.3 gene usage by CD4+ T lymphocytes in bronchoalveolar lavage fluid from sarcoidosis patients correlates with HLA-DR3.Eur J Immunol. 1992; 22: 129-135Crossref PubMed Scopus (136) Google Scholar have demonstrated a strong association of a specific class of lung T cells bearing Vα2.3 T-cell-antigen receptors in patients with clinically active acute sarcoidosis. These patients express HLA-DR3, DQ2. These results suggest that a single antigen paired with a single antigen-presenting molecule may trigger the immunologic response that results in this sarcoidosis phenotype.13Newman LS Rose CS Maier LA Sarcoidosis.N Engl J Med. 1997; 336: 1224-1234Crossref PubMed Scopus (1386) Google Scholar However, many other sarcoidosis patients have more than one T-cell clone or no increase in oligoclonal T cells.13Newman LS Rose CS Maier LA Sarcoidosis.N Engl J Med. 1997; 336: 1224-1234Crossref PubMed Scopus (1386) Google Scholar In addition, different sarcoidosis phenotypes are associated with different HLA class II molecules.18Martinetti M Luisetti M Cuccia M HLA and sarcoidosis: new pathogenetic insights.Sarcoidosis Vasc Diffuse Lung Dis. 2002; 19: 83-95PubMed Google Scholar These data support the concept that there are multiple sarcoidosis antigens or epitopes recognized by different T-cell clones that are paired with different HLA class II molecules.13Newman LS Rose CS Maier LA Sarcoidosis.N Engl J Med. 1997; 336: 1224-1234Crossref PubMed Scopus (1386) Google Scholar Reich further speculates that the granulomatous response of sarcoidosis represents an “immunologic fallback position” in persons who are unable to clear the immunologic agents in a more efficient manner. The data to support this conjecture are minimal. Reich’s foundation for this concept consists of one abstract19Munro CS Mitchell DN Poulter LW et al.Immunological processes active in developing Kveim responses differ in normal and sarcoidosis subjects [abstract].Am Rev Respir Dis. 1986; 133: A244Google Scholar that examined the intradermal injection of Kveim reagent. In that study, healthy subjects demonstrated features of delayed hypersensitivity, including infiltrates of Th and suppressor cells with markers of activation (eg, Tac+ and Leu9+) and dendritic Langerhans cells (eg, OKT6 and RFD+) with strong HLA-DR expression 11 and 18 days after intradermal injection. In contrast, Kveim-positive sarcoidosis patients failed to develop this response. These findings suggest that the granulomas of sarcoidosis may be the result of a sluggish delayed hypersensitivity response, which subserves the antigen, allowing it to remain undetected or to be inadequately cleared from tissue. Although a paucity of investigational data supports the model of ineffective clearance of putative sarcoid antigens by the sarcoid granuloma, Reich cites an abundance of clinical evidence. This concept would explain why corticosteroids might promote the relapse of sarcoidosis20Gottlieb JE Isreal HL Steiner RM et al.Outcome in sarcoidosis.Chest. 1997; 111: 623-631Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar21Reich JM Mortality of intrathoracic sarcoidosis in referral vs population-based settings: influence of stage, ethnicity, and corticosteroid therapy.Chest. 2002; 121: 32-39Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar22Rizzato G Montemurro L Colombo P The late follow-up of chronic sarcoidosis patients previously treated with corticosteroids.Sarcoidosis Vasc Diffuse Lung Dis. 1998; 15: 52-58PubMed Google Scholar by possibly further inhibiting the already sluggish granulomatous response. It would also explain why patients who have a brisk immunologic response, such as those with erythema nodosum, have a good prognosis. And, it would explain why individuals with combined variable immunodeficiency, many of whom have an associated deficiency in T lymphocytes, have a high rate of developing sarcoidosis.23Fasano MB Sullivan KE Sarpong SB et al.Sarcoidosis and common variable immunodeficiency: report of 8 cases and review of the literature.Medicine. 1996; 75: 251-261Crossref PubMed Scopus (200) Google Scholar However, the concept that sarcoidosis granulomas are inefficient at clearing antigens does not explain all the clinical aspects of the disease. For instance, it does not explain the sarcoidosis-like reaction that can occur when highly active antiretroviral therapy is given to HIV-infected patients.24Naccache J Antoine M Wislez M et al.Sarcoid-like pulmonary disorder in human immunodeficiency virus-infected patients receiving antiretroviral therapy.Am J Respir Crit Care Med. 1999; 159: 2009-2013Crossref PubMed Scopus (97) Google Scholar It is likely that the antigens that cause sarcoidosis are present in the HIV-infected individual who has a low CD4+ count. However, the CD4+ lymphocyte number and function is inadequate to mount a significant Th-1-induced granulomatous response until highly active antiretroviral therapy is administered.25Judson MA Highly active antiretroviral therapy for HIV with tuberculosis: pardon the granuloma [editorial].Chest. 2002; 122: 399-400Abstract Full Text Full Text PDF Scopus (10) Google Scholar Therefore, in this example, sarcoidosis develops in a better constituted immune system, not in a more defective one. Inefficient clearance by sarcoid granulomas also would not explain the development of sarcoidosis in allografts following transplantation,26Barbers RG Role of transplantation (lung, liver, and heart) in sarcoidosis.Clin Chest Med. 1997; 18: 865-874Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar as supposedly these transplanted organs would be free of the antigen in the excised tissues that caused the granulomatous response. Possibly, granulomas are formed in this instance by the immunologic response cross-reacting with allograft tissue instead of an antigen. Regardless of the answers to these concerns, it is sobering to consider Reich’s argument that there is not any one single agent and that there is not one discrete immunologic defect that causes sarcoidosis. For sarcoidosis to occur, patients may have to experience a specific interaction between one or several exposures and one or several abnormal immunologic responses. If this model is correct, it will be extremely difficult to prove. And perhaps the absence of proof for any etiology of sarcoidosis may be the most compelling argument supporting Reich’s hypothesis. We still have not figured out the cause of sarcoidosis perhaps because there is not just one cause. What Is Sarcoidosis?CHESTVol. 124Issue 1PreviewI recently consulted on a young woman who had acquired fever, profuse pulmonary shadowing, and liver function abnormalities following a 1997 visit from her residence in upstate New York to the Mississippi Valley. An open-lung biopsy at that time revealed noncaseating epithelioid granulomas (NCG) consistent with sarcoidosis; fungal elements were not evident. The treating physician initiated prednisone therapy, but after a week, a histoplasmosis complement fixation titer of 512, later supplemented by isolation of Histoplasma capsulatum organisms from the biopsy sample, led to its replacement with a short course of amphotericin B, followed by months of itraconazole therapy, with the expectation that her progressive disseminated histoplasmosis would resolve. Full-Text PDF" @default.
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• W2044897954 title "The Etiologic Agent of Sarcoidosis" @default.
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