Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie, Yong; Jinnin, Masatoshi; Zhang, Xiaoyong; Wakasugi, Shoji; Makino, Takamitsu; Inoue, Yoshio; Fukushima, Satoshi; Masuguchi, Shinichi; Sakai, Keisuke; Ihn, Hironobu

doi:10.5582/bst.2011.v5.2.83

Cited by 18 publications

(23 citation statements)

References 18 publications

(19 reference statements)

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“…Various studies have demonstrated that the predominant cells in DLE are T cells [6, 7] consisting of both CD4 + helper T cells and CD8 + cytotoxic T cells [5, 7–9]. In addition, DLE lesional skin exhibits significant amounts of protein products of CD8 + T cells including the T-cell restricted intracellular antigen 1 (TIA-1) and granzyme B [5, 6].…”

Section: Introductionmentioning

confidence: 99%

“…However, the literature has not been as consistent on the expression of B cells in DLE lesional skin [7, 17]. Investigators have observed a marked influx of B cells at the DEJ and in the perivascular area [6, 7, 18] and reported B cells to account for up to greater than 25% of the infiltrate in DLE lesional skin [19].…”

Section: Introductionmentioning

confidence: 99%

“…Investigators have observed a marked influx of B cells at the DEJ and in the perivascular area [6, 7, 18] and reported B cells to account for up to greater than 25% of the infiltrate in DLE lesional skin [19]. However, Tebbe et al [20] and Lee et al [21] noted that B cells were either rare or absent in the dermis of DLE lesional skin.…”

Section: Introductionmentioning

confidence: 99%

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Site-Specific Analysis of Inflammatory Markers in Discoid Lupus Erythematosus Skin

Thorpe

Gray

Kumar

et al. 2014

The Scientific World Journal

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Prior studies identified T cells, B cells, and macrophages in the inflammatory infiltrate and up-regulation of their protein products in discoid lupus erythematosus (DLE) skin; however, they lacked rigorous analyses to define their specific locations in skin. Thus, we compared expressions of selected T cell, B cell, and macrophage markers in five areas of DLE, psoriasis, and normal skin. Immunostainings for CD3, CD4, CD8, CD20, CD68, CXCR3, CXCL10, and TIA-1 were performed in biopsies of 23 DLE lesional skin, 11 psoriasis lesional skin, and 5 normal skin. Three independent observers used a graded scale to rate each marker's presence in the epidermis, dermatoepidermal junction (DEJ), perivascular area, periadnexal area, and deep dermis. DLE lesional skin contained an increased abundance of CD3+, CD8+, and CD68+ cells at the DEJ, and CD20+ and CD68+ cells in the periadnexal area versus psoriasis and normal skin. CXCR3, CXCL10, and TIA-1 were elevated in periadnexal sites of DLE lesional skin versus psoriasis lesional skin. The aggregation of T cells, B cells, macrophages, and their protein products (CXCR3, CXCL10, and TIA-1) in the DEJ and periadnexal area of DLE lesional skin may contribute to the pathology of DLE through a coordinated, sophisticated process.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Site-Specific Analysis of Inflammatory Markers in Discoid Lupus Erythematosus Skin

Thorpe

Gray

Kumar

et al. 2014

The Scientific World Journal

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“…B cells act not only as antigen-presenting cells but also produce autoantibodies and secrete cytokines in autoimmune diseases such as CLE [ 49 ]. In DLE, specifically, it has been demonstrated that there is a higher density of B lymphocytes circulating peripherally and in lesional skin [ 50 – 52 ]. Interestingly, however, B cell-depleting therapies seem to lack efficacy in chronic cutaneous lupus erythematosus, such as DLE, while showing some effect in ACLE and SCLE [ 49 ].…”

Section: Cells and Their Productsmentioning

confidence: 99%

“…As to why B cell-depleting therapy may provoke flaring of cutaneous disease, it may be that B cell-produced IL-10, an anti-inflammatory cytokine, is decreased after rituximab or that B-cell lysis may be pro-inflammatory [ 53 ]. Exactly how B cells participate in the pathophysiology of CLE has yet to be elucidated, but possible mechanisms include enhancement of autoimmune helper T cells and local secretion of autoantibodies, opsonization, and subsequent activation of the complement system [ 52 , 54 ].…”

Section: Cells and Their Productsmentioning

confidence: 99%

Pathophysiology of cutaneous lupus erythematosus

Achtman¹,

Werth²

2015

Arthritis Res Ther

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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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Assessment of Response to B-Cell Depletion Using Rituximab in Cutaneous Lupus Erythematosus

et al. 2018

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Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Cited by 18 publications

References 18 publications

Site-Specific Analysis of Inflammatory Markers in Discoid Lupus Erythematosus Skin

Site-Specific Analysis of Inflammatory Markers in Discoid Lupus Erythematosus Skin

Pathophysiology of cutaneous lupus erythematosus

Assessment of Response to B-Cell Depletion Using Rituximab in Cutaneous Lupus Erythematosus

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