Sarcoidosis-associated MHC Ags and the development of cutaneous and nodal granulomas following allogeneic hematopoietic cell transplant

Pukiat, Sulada; McCarthy, Philip L.; Hahn, Theresa; Morrison, Carl; Shanahan, Thomas; Qiu, Jingxin; Liu, H

doi:10.1038/bmt.2010.235

Cited by 6 publications

(5 citation statements)

References 7 publications

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“…However when similar samples are disinfected they do not cause granuloma formation, suggesting a cell-mediated or microbial origin ( Ikonomopoulos et al, 2000 , 2006 ). Similarly several case reports indicate that sarcoidosis might be transmittable via organ transplantations ( Burke et al, 1990 ; Heyll et al, 1994 ; Padilla et al, 2002 ; Pukiat et al, 2011 ; Das et al, 2012 ). Likewise, there are reports of both successful antibiotic and antifungal treatment of sarcoidosis perhaps related to the potential sarcoid antigens, Mycobacterium tuberculosis, Propionibacterium acnes, and more recently, fungi ( Terčelj et al, 2007 , 2011a ; Drake et al, 2013 ; Takemori et al, 2014 ).…”

Section: Etiologymentioning

confidence: 85%

Interleukin-12 family cytokines and sarcoidosis

2014

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Sarcoidosis is a systemic granulomatous disease predominantly affecting the lungs. It is believed to be caused by exposure to pathogenic antigens in genetically susceptible individuals but the causative antigen has not been identified. The formation of non-caseating granulomas at sites of ongoing inflammation is the key feature of the disease. Other aspects of the pathogenesis are peripheral T-cell anergy and disease progression to fibrosis. Many T-cell-associated cytokines have been implicated in the immunopathogenesis of sarcoidosis, but it is becoming apparent that IL-12 cytokine family members including IL-12, IL-23, IL-27, and IL-35 are also involved. Although the members of this unique cytokine family are heterodimers of similar subunits, their biological functions are very diverse. Whilst IL-23 and IL-12 are pro-inflammatory regulators of Th1 and Th17 responses, IL-27 is bidirectional for inflammation and the most recent family member IL-35 is inhibitory. This review will discuss the current understanding of etiology and immunopathogenesis of sarcoidosis with a specific focus on the bidirectional impact of IL-12 family cytokines on the pathogenesis of sarcoidosis.

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Section: Etiologymentioning

confidence: 85%

Interleukin-12 family cytokines and sarcoidosis

2014

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“… 1 Thorough literature review found 9 cases of sarcoidosis after allogeneic HSCT, all reported in nondermatologic literature ( Table I ). 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 Five of the 9 cases describe cutaneous findings, 4 of which had cutaneous biopsies showing noncaseating granulomas. An additional 5 cases of sarcoidosis have been reported after autologous HSCT.…”

Section: Discussionmentioning

confidence: 99%

More immune dysregulation: Sarcoidosis and chronic graft-versus-host disease after allogeneic stem cell transplant

2016

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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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Sarcoidosis-associated MHC Ags and the development of cutaneous and nodal granulomas following allogeneic hematopoietic cell transplant

Cited by 6 publications

References 7 publications

Interleukin-12 family cytokines and sarcoidosis

Interleukin-12 family cytokines and sarcoidosis

More immune dysregulation: Sarcoidosis and chronic graft-versus-host disease after allogeneic stem cell transplant

Etiologies of Sarcoidosis

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