Plasmacytoid dendritic cells are absent in skin lesions of polymorphic light eruption

Wackernagel, Alexandra; Massone, Cesare; Höefler, Gerald; Steinbauer, Elisabeth; Kerl, Helmut; Wolf, Peter

doi:10.1111/j.1600-0781.2007.00267.x

Cited by 35 publications

(25 citation statements)

References 38 publications

(43 reference statements)

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“…3,5,7 We now show the presence of PDCs in skin lesions of DM as well. This raises the possibility of a role for these cells in DM, as has recently been suggested by Wenzel et al 11 PDCs are capable of secreting IFN-a, and patients with systemic LE typically have increased levels of IFN-a in their skin.…”

Section: Discussionsupporting

confidence: 56%

“…In a recent review of polymorphous light eruption (PMLE), immunostaining with CD123 showed no PDCs in biopsies from 27 patients, while they were identified in biopsies of LE and psoriasis in that study. 3 This refutes a common pathogenic pathway for LE and PMLE, although it does not exclude a role for UV exposure in the recruitment of PDCs in connective tissue disorders. In addition, in that study and in ours, PDCs are an infrequent finding in normal skin, present only as single cells in some biopsies.…”

Section: Discussionmentioning

confidence: 88%

“…2 PDCs resemble plasma cells histologically, yet can be accurately identified in routine formalin-fixed paraffin-embedded sections using antibodies to CD123, which labels interleukin-3 receptor a chain protein expressed at high levels on the surface of these cells. [3][4][5][6][7] Although PDCs were originally identified in secondary lymphoid tissue and in the circulation, they have recently been observed in large numbers in skin lesions of LE as well as other inflammatory conditions including psoriasis and atopic dermatitis. 5,7,8 A malignant counterpart of PDCs has now been identified as the CD41/CD561 hematodermic malignancy, further stimulating interest in this unique dendritic cell.…”

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confidence: 99%

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Plasmacytoid dendritic cells are present in cutaneous dermatomyositis lesions in a pattern distinct from lupus erythematosus

2008

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Background: Plasmacytoid dendritic cells (PDCs) are CD123‐positive dendritic cells (DCs) capable of producing interferon‐α (IFN). They are thought to play a role in anti‐viral immunity and the pathogenesis of lupus erythematosus (LE). Given the histologic similarities between LE and dermatomyositis (DM), we evaluated the presence and distribution of PDCs in lesional skin of both diseases.Methods: Twenty‐eight biopsies of DM and 27 biopsies of LE were labeled with antibodies to CD123 to identify PDCs. The presence and relative distribution of CD123+ cells was recorded.Results: PDCs are present in LE and DM, albeit in greater numbers in LE lesions. Interestingly, PDCs are preferentially located in the epidermis of DM, and are primarily located in the dermis of LE.Conclusions: Skin lesions of DM contain PDCs. Because PDCs are thought to participate in the pathogenesis of LE, this finding suggests that they may play a role in DM as well. The preferential epidermal localization of PDCs in DM suggests that their contribution to disease pathogenesis or maintenance in DM may be distinct from LE. Finally, although not pathognomonic, the different patterns of PDC localization in LE and DM may prove a helpful criterion for distinguishing between these two entities histologically.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

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Plasmacytoid dendritic cells are present in cutaneous dermatomyositis lesions in a pattern distinct from lupus erythematosus

2008

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“…15,18,19 However, in skin lesions of autoimmune diseases such as lupus erythematosus and dermatomyositis, its expression is increased. 20 …”

Section: Discussionmentioning

confidence: 99%

Oral chronic graft-versus-host disease: analysis of dendritic cells subpopulations

Botari

Nunes

Souza

et al. 2014

An. Bras. Dermatol.

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The graft-versus-host disease is the major cause of morbidity and mortality in patients who have undergone hematopoietic stem cell transplantation. Aiming at contributing to the understanding of the role of myeloid and plasmacytoid dendritic cells, and natural killer cells in chronic graft-versus-host disease, we examined biopsies of jugal mucosa of 26 patients with acute myeloid leukemia who had undergone allogenic hematopoietic stem cell transplantation. Half of these patients developed oral chronic graft-versus-host disease. Microscopic sections were immunohistochemically stained for anti-CD1a, anti-CD123 and anti-CD56. We calculated the number of immunostained cells in the corium per square millimeter and applied the Mann-Whitney test. Results showed a statistically significant increase of myeloid dendritic cells (CD1a+; p=0,02) and natural killer cells (CD56; p=0,04) in patients with oral chronic graft-versus-host disease. CD123 immunostaining showed no statistical difference between groups. It was concluded that myeloid dendritic cells and natural killer cells participate in the development of oral chronic graft-versus-host disease.

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“…Additionally, a lack of skin infiltration by plasmacytoid dendritic cells may contribute to the pathogenesis of PLE (36). Photohardening works in PLE by restoring the normal UV immune suppressive pathways (10), allowing for the effective prevention of a Th1-driven immune reaction to potential UV-induced cutaneous photoantigens (37).…”

Section: Or Induction Of Regulatory T Cells (Tregs) (22) Interestingmentioning

confidence: 99%

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

Wolf

Gruber‐Wackernagel

Bambach

et al. 2014

Experimental Dermatology

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The pathogenesis of polymorphic light eruption (PLE) has been linked to a lack of UV-induced immune suppression. To determine the role of Langerhans cells (LC), mast cells and regulatory T cells, biopsies from PLE patients were taken from exposed sites in spring before and after photohardening with 311 nm or PUVA as well as again in summer. Skin sections were assessed for the presence of Langerin/CD1a+ LC and CD3+, CD4+, CD25+ or FoxP3+ T cells and mast cells. Photohardening transiently decreased the density of epidermal LC and significantly increased a low baseline mast cell density in the papillary dermis of PLE patients. Baseline T cell numbers in the skin were low, and there was no difference in PLE patients among any time point. This suggests that LC suppression together with recruitment of mast cells into photohardened skin may be a key cellular event underlying the mechanism by which phototherapy protects from PLE.

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Plasmacytoid dendritic cells are absent in skin lesions of polymorphic light eruption

Abstract: The results confirm the potential significance of PDCs in LE and psoriasis, however the absence of PDCs in PLE contradicts the hypothesis that these cells might play a role in the latter disease.

Cited by 35 publications

References 38 publications

Plasmacytoid dendritic cells are present in cutaneous dermatomyositis lesions in a pattern distinct from lupus erythematosus

Plasmacytoid dendritic cells are present in cutaneous dermatomyositis lesions in a pattern distinct from lupus erythematosus

Oral chronic graft-versus-host disease: analysis of dendritic cells subpopulations

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

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