UVB‐induced leucocyte trafficking in the epidermis of photosensitive lupus erythematosus patients: Normal depletion of Langerhans cells

Janssens, Artiena Soe; Lashley, Eileen; Out-Luiting, Coby; Willemze, Rein; Pavel, S.; Gruijl, Frank R. de

doi:10.1111/j.0906-6705.2005.00279.x

Cited by 18 publications

(18 citation statements)

References 20 publications

(25 reference statements)

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“…Previous investigations have shown an abnormal neutrophil and CD11a/CD68 cell infiltration into the skin of patients with PLE after UVB irradiation (30,32,46). Janssens et al.…”

Section: Discussionmentioning

confidence: 99%

“…To that end, Janssens et al. (31) showed that medical photohardening might work by normalizing the UV‐induced cell migratory response in patients with PLE, whereas in systemic lupus erythematosus, UV exposure generally leads to exacerbation of disease (32,33). In patients with PLE, UV‐induced LC depletion and neutrophil influx is impaired, whereas following phototherapy normal cell migratory responses were re‐established and were not statistically different from normal controls (31).…”

Section: Introductionmentioning

confidence: 99%

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Photohardening restores the impaired neutrophil responsiveness to chemoattractants leukotriene B4 and formyl-methionyl-leucyl-phenylalanin in patients with polymorphic light eruption

Gruber‐Wackernagel¹,

Heinemann²,

Kónya³

et al. 2011

Experimental Dermatology

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A failure to induce immune suppression after UV exposure has been implicated in the pathogenesis of polymorphic light eruption (PLE). This immunological resistance has been linked to an impaired neutrophil infiltration into the skin following UV exposure. Therapeutic photohardening can restore this abnormal neutrophil infiltration in PLE skin and is thought to be responsible for the prophylactic efficacy. The aim of this study was to elucidate the pathogenic mechanism of the described neutrophil deficiency in PLE. Peripheral blood neutrophil responses to the chemoattractants leukotriene B4 (LTB(4)) and formyl-methionyl-leucyl-phenylalanin (fMLP) were investigated in vitro. Samples from 10 patients with PLE before and after 6 weeks of photohardening therapy were assessed. Flow cytometry was used to measure the changes associated with neutrophil activation. We found a significantly reduced neutrophil responsiveness to LTB(4) and fMLP in PLE patients, which was restored to normal levels after phototherapy. Indeed, PLE neutrophil responsiveness to these two chemoattractants after (but not before) phototherapy was similar to that of age- and sex-matched healthy control subjects. This indicates that an abnormal chemotactic potential to neutrophils is a crucial factor in the pathogenesis of PLE. Normalization following photohardening may therefore account for the therapeutic efficacy by restoring UV-induced neutrophil skin infiltration. Our results reveal a completely novel pathogenic mechanism involved in PLE and offer unique targets for therapy.

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“…Previous investigations have shown an abnormal neutrophil and CD11a/CD68 cell infiltration into the skin of patients with PLE after UVB irradiation (30,32,46). Janssens et al.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Photohardening restores the impaired neutrophil responsiveness to chemoattractants leukotriene B4 and formyl-methionyl-leucyl-phenylalanin in patients with polymorphic light eruption

Gruber‐Wackernagel¹,

Heinemann²,

Kónya³

et al. 2011

Experimental Dermatology

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“…A gradual decrease in epidermal LCs during UV irradiation and reduced numbers of these cells were found in lesional epidermis of CLE patients [64]. A gradual decrease in epidermal LCs during UV irradiation and reduced numbers of these cells were found in lesional epidermis of CLE patients [64].…”

Section: Dendritic Cellsmentioning

confidence: 94%

Tissue Injury and the Skin

Kuhn¹,

Böhm²,

Luger³

2011

Systemic Lupus Erythematosus

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“…The above-mentioned immunogenetic background as described for SCLE may result in tortuous immunological reactions that result in the production of specific autoantibodies. However, dendritic cells [81][82][83], as well as T lymphocytes and natural killer (NK) cells appear to be involved at different stages and result in the different skin manifestations of LE [84][85][86][87]. In the further disease process, dermal tissue, including extracellular matrix substances, and subsequent inflammatory dermal and epidermal processes result in the clinical pictures presented above [88][89][90][91][92][93].…”

Section: Prognosis Of Cutaneous Lupus Erythematosusmentioning

confidence: 99%

Cutaneous lupus erythematosus: clinical features, prognosis and laboratory findings

Sticherling

2006

Expert Review of Dermatology

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The skin is one of the major organs involved in systemic lupus erythematosus (SLE) and may provide the first sign of the disease. Cutaneous manifestations comprise various specific and nonspecific symptoms that can be isolated or combined and are not amply reflected by currently available scoring systems. From the dermatological viewpoint, three distinct subsets of cutaneous lupus erythematosus can be defined that include chronic cutaneous lupus erythematosus (CCLE), subacute cutaneous lupus erythematosus (SCLE) and acute cutaneous lupus erythematosus. These, in turn, comprise different subsets and result in a heterogenous group of diseases. Based on case history, clinical and laboratory data, as well as organ imaging examinations, they need to be differentiated for prognostic and therapeutic reasons. Whereas CCLE rarely develops into SLE, SCLE and SLE are more closely related. Basic laboratory examinations should be performed on all patients at first diagnosis, whereas specific laboratory examinations will depend on individual data. Altogether, monitoring of lupus erythematosus (LE) patients for internal organ manifestations at any stage of their disease is mandatory. Even in seemingly isolated cutaneous LE, other LE entities should be excluded. Therapy should be initiated in an individually tailored way as either topical external or systemic treatment based on the extent and severity of organ involvement and should be regularly adapted. Thus, both dermatologists and rheumatologists should cooperate to provide optimal patient care.

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UVB‐induced leucocyte trafficking in the epidermis of photosensitive lupus erythematosus patients: Normal depletion of Langerhans cells

Abstract: Immunohistopathology of irradiated uninvolved skin of photosensitive LE patients did not reveal the same pathologic trafficking of LCs and neutrophils as described for PLE patients. We conclude that different mechanisms are operative in the pathogenesis of PLE and photosensitive LE.

Cited by 18 publications

References 20 publications

Photohardening restores the impaired neutrophil responsiveness to chemoattractants leukotriene B4 and formyl-methionyl-leucyl-phenylalanin in patients with polymorphic light eruption

Photohardening restores the impaired neutrophil responsiveness to chemoattractants leukotriene B4 and formyl-methionyl-leucyl-phenylalanin in patients with polymorphic light eruption

Tissue Injury and the Skin

Cutaneous lupus erythematosus: clinical features, prognosis and laboratory findings

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