Recurrent sarcoid granulomas in a transplanted lung derive from recipient immune cells: Fig. 1—

Milman, Nils; Andersen, Claus B; Burton, Christopher M.; Iversen, Martin

doi:10.1183/09031936.05.00127404

Cited by 33 publications

(14 citation statements)

References 15 publications

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“…Epidemiologic data, including reports of case-clustering, increased susceptibility with certain occupations, and transmissibility via transplant, all support this theory (21,22). Infectious agents have long been suspected as possible causes of sarcoidosis, but early studies failed to yield convincing support for various organisms.…”

Section: Etiology and Pathogenesismentioning

confidence: 82%

A Concise Review of Pulmonary Sarcoidosis

Baughman

Culver²,

Judson

2011

Am J Respir Crit Care Med

438

330

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This is an update on sarcoidosis, focusing on etiology, diagnosis, and treatment. In the area of etiopathogenesis, we now have a better understanding of the immune response that leads to the disease as well as genetic factors that modify both the risk for the disease and its clinical outcome. Several groups have also identified possible agents as a cause for sarcoidosis. Although none of these potential causes has been definitely confirmed, there is increasing evidence to support that one or more infectious agents may cause sarcoidosis, although this organism may no longer be viable in the patient. The diagnosis of sarcoidosis has been significantly aided by new technology. This includes the endobronchial ultrasound, which has been shown to increase the yield of needle aspiration of mediastinal and hilar lymph nodes. The positive emission tomography scan has proven useful for selecting possible biopsy sites by identifying organ involvement not appreciated by routine methodology. It has also helped in assessing cardiac involvement. The biologic agents, such as the anti-tumor necrosis factor antibodies, have changed the approach to refractory sarcoidosis. There is increasing evidence that the clinician can identify which patient is most likely to benefit from such therapy. As new and more potent antiinflammatory agents have been developed, it is clear that there are other factors that burden the patient with sarcoidosis, including fatigue and sarcoidosis-associated pulmonary hypertension. There have been several recent studies demonstrating treatment options for these problems.

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Section: Etiology and Pathogenesismentioning

confidence: 82%

A Concise Review of Pulmonary Sarcoidosis

Baughman

Culver²,

Judson

2011

Am J Respir Crit Care Med

438

330

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“…It is suggested that apoptosis (programmed cell death) may be associated with the course of granulomatous inflammation in pulmonary sarcoidosis (25). These processes depend on various, mostly unknown, genetic and environmental factors simultaneously (26,27). The influence of ethnic and genetic factors determines the heterogeneous clinical course of sarcoidosis (17).…”

Section: Discussionmentioning

confidence: 99%

BAL fluid cells in newly diagnosed pulmonary sarcoidosis with different clinical activity

Danila¹,

Jurgauskienė²,

Norkūnienė³

et al. 2009

Upsala Journal of Medical Sciences

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BackgroundSarcoidosis is associated with an increase in the number of alveolar T cells (CD3+ cells) and an increase of the CD3+CD4+ lymphocyte subset. However, the number of lymphocytes and the CD4/CD8 ratio in bronchoalveolar lavage (BAL) fluid are highly variable in sarcoidosis. Comparative studies have demonstrated that geographic and ethnic factors are linked to the specific characteristics of patients with sarcoidosis.Aim of the studyTo investigate peculiarities of BAL fluid (BALF) cell patterns in different clinical activity of pulmonary sarcoidosis at the time of diagnosis.Material and methodsA total of 308 non-treated patients (138 asymptomatic and 170 with sarcoidosis-related symptoms) and 40 previously empirically steroid-treated patients with newly diagnosed sarcoidosis have been prospectively examined.ResultsSignificant BAL fluid lymphocytosis and increased CD4/CD8 ratio were characteristic for all three sarcoidosis patient groups. A total of 12% of asymptomatic patients, 3% of patients with sarcoidosis-related symptoms, and 5% of previously treated symptomatic patients had normal BALF cell counts. Non-treated patients with sarcoidosis-related symptoms had significantly higher lymphocytosis (45±19% versus 39±17%, P<0.01), CD4/CD8 ratio (9.3±5.0 versus 5.7±4.5, P<0.001), and total BALF cell count (411±322 106/mL versus 334±273 106/mL, P<0.05), compared with asymptomatic patients. However, previously treated symptomatic patients had lower lymphocytosis (39±15% versus 45±19%, P=0.058), and total BALF cell count (292±166 106/mL versus 411±322 106/mL, P<0.05) compared with non-treated symptomatic patients. The same trend was noticed for CD4/CD8 ratio (8.3±4.8), although a statistically significant difference was not achieved.ConclusionsIndependently of clinical symptoms at the time of diagnosis sarcoid patients have significantly different BAL fluid cell patterns compared to healthy persons. BAL fluid cell changes are more prominent in corticosteroid non-treated patients with clinically active sarcoidosis. Treatment with systemic corticosteroids may modify typical BALF cellular patterns of sarcoidosis.

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“…Most commonly, sarcoidosis is discovered in donor solid organ allografts in recipients with a history of sarcoidosis [73][74][75][76][77][78][79][80], presumably inducing a granulomatous response by the recipient's immune system [81]. One report of sarcoidosis presenting following bone marrow transplantation suggests that this susceptibility may depend on donor MHC haplotypes [82].…”

Section: Models Of Sarcoidosis Pathobiologymentioning

confidence: 99%

Etiologies of Sarcoidosis

Chen

Möller

2015

Clinic Rev Allerg Immunol

125

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Since sarcoidosis was first described more than a century ago, the etiologic determinants causing this disease remain uncertain. Studies suggest that genetic, host immunologic, and environmental factors interact together to cause sarcoidosis. Immunologic characteristics of sarcoidosis include non-caseating granulomas, enhanced local expression of T helper-1 (and often Th17) cytokines and chemokines, dysfunctional regulatory T-cell responses, dysregulated Toll-like receptor signaling, and oligoclonal expansion of CD4+ T cells consistent with chronic antigenic stimulation. Multiple environmental agents have been suggested to cause sarcoidosis. Studies from several groups implicate mycobacterial or propionibacterial organisms in the etiology of sarcoidosis based on tissue analyses and immunologic responses in sarcoidosis patients. Despite these studies, there is no consensus on the nature of a microbial pathogenesis of sarcoidosis. Some groups postulate sarcoidosis is caused by an active viable replicating infection while other groups contend there is no clinical, pathologic, or microbiologic evidence for such a pathogenic mechanism. The authors posit a novel hypothesis that proposes that sarcoidosis is triggered by a hyperimmune Th1 response to pathogenic microbial and tissue antigens associated with the aberrant aggregation of serum amyloid A within granulomas, which promotes progressive chronic granulomatous inflammation in the absence of ongoing infection.

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Recurrent sarcoid granulomas in a transplanted lung derive from recipient immune cells: Fig. 1—

Cited by 33 publications

References 15 publications

A Concise Review of Pulmonary Sarcoidosis

A Concise Review of Pulmonary Sarcoidosis

BAL fluid cells in newly diagnosed pulmonary sarcoidosis with different clinical activity

Etiologies of Sarcoidosis

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