Hand‐foot‐and‐mouth‐disease‐induced Koebner phenomenon in psoriasis

Wu, Chen‐Yu; Lin, Feng-Ling

doi:10.1111/ddg.13824

Cited by 7 publications

(9 citation statements)

References 10 publications

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“…The presence of psoriatic lesions in those body areas, which are not usually affected by psoriasis suggest the key role of Koebner phenomenon in spreading psoriasis [13,14,31]. There is wide variety of triggers/agents that may induce Koebernization such as irradiations [44], Mantoux test [46,47], surgical incision [19,48], needle puncture [49], prosthesis [50], secondary syphilis [51], cupping therapy [52,53], ECG [55], itching [56], and viral infections [57]. Regarding role of injury in initiating Koebernization, the deep tissue injury is more critical and superficial injury alone is not sufficient to induce the development of new psoriatic lesions [58][59][60].…”

Section: Summarized Discussionmentioning

confidence: 99%

“…However, a large number of studies have shown the development of new psoriatic lesions after tattooing skin as a Koebner reaction [18,[39][40][41][42][43]. The other factors/agents that are reported to exacerbate psoriasis as Koebner reaction include megavoltage irradiations [44], radiotherapy for carcinoma of breast [45], exposure to purified protein derivative (PPD)/Mantoux test [46,47], surgical incision during breast reconstruction [19,48], needle acupuncture [49], prosthesis after amputation of the leg [50], secondary syphilis [51], cupping therapy, a traditional Chinese medicine [52,53], striae distensae and striae gravidarum [17,54], ECG [55], itching (one of the core features of psoriasis)-induced skin injury [56], and viral infection-induced hand-foot-and-mouth disease [57].…”

Section: Agents That May Trigger New Psoriatic Lesions In Uninvolved mentioning

confidence: 99%

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Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Liu

2019

Bioscience Reports

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Koebner phenomenon refers to the emergence of new psoriatic lesions in the healthy skin regions following an injury/trauma to psoriatic patients. The occurrence of psoriatic lesions at unusual areas of the body regions such as on penis, around eyes and on keloids suggest that the Koebner phenomenon may be responsible for these lesions. A number of agents/triggers have been reported to induce the development of new psoriatic lesions in healthy skin areas and these include, tattooing skin, radiations, skin incision, viral infections and striae etc. The different mechanisms that contribute in inducing the development of new psoriatic lesions as Koebernization include the involvement of mast cell-derived inflammatory mediators such as tryptase, IL-6, IL-8, IL-17, and IL-36γ. Moreover, an increased expression of nerve growth factor (NGF) and vascular endothelial growth factor (VEGF) also contribute in Koebernization. Apart from these, there is a critical role of α 2 β1 integrins, S100A7 (psoriasin) and S100A15 (koebnerisin), change in the ratio of CD4+/CD8+ T cells, down-regulation of mechanosensitive polycystin 1 protein, decrease in inflammation controlling atypical chemokine receptor 2 (ACKR2), reduced expression of N-methyl-d-aspartate (NMDA) receptors (NMDARs) on the keratinocytes and increase in levels of chemokines (CXCL8 and CCL20) in inducing formation of new psoriatic lesions. The present review discusses the role of Koebner phenomenon in the development of new psoriatic lesions. Moreover, it also describes the mechanisms involved in Koebernization in the form of discussion of different key targets that may be potentially modulated pharmacologically to attenuate/halt the development of new psoriatic lesions.

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Section: Summarized Discussionmentioning

confidence: 99%

Section: Agents That May Trigger New Psoriatic Lesions In Uninvolved mentioning

confidence: 99%

Koebner phenomenon leading to the formation of new psoriatic lesions: evidences and mechanisms

Liu

2019

Bioscience Reports

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“…Infections with streptococci, medications such as lithium, antimalarials, or ß-blockers, or physical or chemical stress may trigger the disease. Minimal trauma can induce rapid immigration and activation of immune cells including T-cells and neutrophils (132), the so-called Köbner phenomenon (133, 134). Feedback loops between adaptive immune cells (T cells), innate immune cells (neutrophilic granulocytes, macrophages, dendritic cells), and resident skin cells (keratinocytes, endothelial cells) result in an amplification and chronification of the inflammatory response.…”

Section: Contribution Of Resident Skin Cells To Immunological Processmentioning

confidence: 99%

Adaptive and Innate Immunity in Psoriasis and Other Inflammatory Disorders

2019

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Over the past three decades, a considerable body of evidence has highlighted T cells as pivotal culprits in the pathogenesis of psoriasis. This includes the association of psoriasis with certain MHC (HLA) alleles, oligoclonal expansion of T cells in some cases, therapeutic response to T cell-directed immunomodulation, the onset of psoriasis following bone marrow transplantation, or induction of psoriasis-like inflammation by T cells in experimental animals. There is accumulating clinical and experimental evidence suggesting that both autoimmune and autoinflammatory mechanisms lie at the core of the disease. Indeed, some studies suggested antigenic functions of structural proteins, and complexes of self-DNA with cathelicidin (LL37) or melanocytic ADAMTSL5 have been proposed more recently as actual auto-antigens in some cases of psoriasis. These findings are accompanied by various immunoregulatory mechanisms, which we increasingly understand and which connect innate and adaptive immunity. Specific adaptive autoimmune responses, together with our current view of psoriasis as a systemic inflammatory disorder, raise the question of whether psoriasis may have connections to autoimmune or autoinflammatory disorders elsewhere in the body. While such associations have been suspected for many years, compelling mechanistic evidence in support of this notion is still scant. This review sets into context the current knowledge about innate and adaptive immunological processes in psoriasis and other autoimmune or autoinflammatory diseases.

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“…This pathogenesis has been reported in the literature; a patient developed psoriasis papules on the sites of previous HFMD blisters. 7 However, it is unlikely, because our patient presented with psoriasiform change on the extensor surfaces—a common location for psoriasis, not HFMD. No psoriasiform rash was observed on her hands.…”

Section: Discussionmentioning

confidence: 90%