Scarring skin lesions of discoid lupus erythematosus are characterized by high numbers of skin-homing cytotoxic lymphocytes associated with strong expression of the type I interferon-induced protein MxA

Wenzel, Joerg; Uerlich, Manfred; Wörrenkämper, E; Freutel, S; Bieber, Thomas; Tüting, Thomas

doi:10.1111/j.1365-2133.2005.06784.x

Cited by 123 publications

(88 citation statements)

References 27 publications

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“…It was detected that the number of CD8 + cells were appreciably higher than CD4 + cells in the DLE lesions. This was appreciably different from other authors (11,12), but a similar result was also obtained by Wenzel et al (13). The CD4/CD8 ratio, which ranged approximately from 0.7 to 1.7 (mean 1.0), was a slight decrease compared to that in normal skin (1.1), but there was no statistical significance between them.…”

Section: Discussioncontrasting

confidence: 55%

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie

Jinnin

Zhang

et al. 2011

BST

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Section: Discussioncontrasting

confidence: 55%

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie

Jinnin

Zhang

et al. 2011

BST

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“…Additionally, increased activity of CTLs appears to be more associated with the destructive and scarring types of CLE, such as DLE. Given their presence in CLE lesions and production of pro-apoptotic molecules, CTLs appear to play a role in CLE, though the level of their significance is not certain [63,64].…”

Section: Cytotoxic Cd8+ T Cellsmentioning

confidence: 99%

Pathophysiology of Cutaneous Lupus Erythematosus

Lin

Dutz

Sontheimer

et al. 2007

Clinic Rev Allerg Immunol

101

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The pathophysiology of cutaneous lupus erythematosus (CLE) encompasses the complex interactions between genetics, the environment, and cells and their products. Recent data have provided enhanced understanding of these interactions and the mechanism by which they cause disease. A number of candidate genes have been identified which increase the risk of developing CLE. Ultraviolet radiation, the predominant environmental exposure associated with CLE, appears to initiate CLE lesion formation by inducing apoptosis, precipitating autoantigen presentation, and promoting cellular production of specific cytokines. Autoantibodies are a well-known entity in CLE, but their exact role remains unclear. Finally, cells ranging from native skin cells to innate and adaptive immune cells produce cytokines and other molecules and play specific roles in lesion formation and perpetuation. Native skin cells implicated in CLE include keratinocytes and endothelial cells. Innate immune cells crucial to CLE pathophysiology include dendritic cells and neutrophils. The primary adaptive immune cells thought to be involved include Th1 cells, Th17 cells, cytotoxic T cells, and invariant natural killer T cells. Though the pathophysiology of CLE has yet to be fully characterized, current research provides direction for future research and therapies.

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“…Lesional skin from LE patients has shown a high number of plasmacytoid dendritic cells (pDCs) which are the primary cellular source of IFN-α in LE skin lesions [20]. Interferon-inducible protein-10 (IP-10 or CXCL10), a monokine induced by gamma interferon (MIG or CXCL9) and interferon-a/p-inducible Mx 78 kDa protein (MxA), is downstream surrogate marker for IFN-α expression [21]. IP-10 and MIG recruit CXCR-3 expressing T cells into skin and are abundantly expressed in patients with LE [19].…”

Section: Pathophysiology Of Malar Rash Photosensitivity and Discoidmentioning

confidence: 99%

Cutaneous manifestations of systemic lupus erythematosus

2018

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Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease of unknown etiology with many clinical manifestations. The skin is one of the target organs most variably affected by the disease. The American College of Rheumatology (ACR) established 11 criteria as a classificatory instrument to operationalise the definition of SLE in clinical trials. They were not intended to be used to diagnose individuals and do not do well in that capacity. Cutaneous lesions account for four of these 11 revised criteria of SLE. Skin lesions in patients with lupus may be specific or nonspecific. This paper covers the SLE-specific cutaneous changes: malar rash, discoid rash, photosensitivity, and oral mucosal lesions as well as SLE nonspecific skin manifestations, their pathophysiology, and management. A deeper thorough understanding of the cutaneous manifestations of SLE is essential for diagnosis, prognosis, and efficient management. Thus, dermatologists should cooperate with other specialties to provide optimal care of SLE patient.

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Scarring skin lesions of discoid lupus erythematosus are characterized by high numbers of skin-homing cytotoxic lymphocytes associated with strong expression of the type I interferon-induced protein MxA

Abstract: Our results provide evidence that type I IFNs and potentially autoreactive cytotoxic lymphocytes targeting adnexal structures are highly associated with scarring lupus erythematosus lesions and might be responsible for their scarring character.

Cited by 123 publications

References 27 publications

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Pathophysiology of Cutaneous Lupus Erythematosus

Cutaneous manifestations of systemic lupus erythematosus

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