Reversible relapse of pemphigus foliaceus triggered by topical imiquimod suggests that Toll-like receptor 7 inhibitors may be useful treatments for pemphigus

Sebaratnam, Deshan F; Martin, Linda K.; Rubin, Adam I.; Tran, Kim; Pas, Hendrikus; Marr, Penelope; Edmonds, John; Murrell, Dédée F.

doi:10.1111/j.1365-2230.2010.03918.x

Cited by 16 publications

(22 citation statements)

References 9 publications

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“…first described pemphigus at locations that were local and distant from a topical contact site (contact pemphigus). Some chemicals can induce pemphigus, but little is known about pemphigus induced by imiquimod . The present report describes the third known instance of PF induced by imiquimod.…”

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confidence: 68%

Pemphigus foliaceus induced by topical imiquimod treatment

Shiraishi

Sayama

2018

Int J Dermatology

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mentioning

confidence: 68%

Pemphigus foliaceus induced by topical imiquimod treatment

Shiraishi

Sayama

2018

Int J Dermatology

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“…Alternatively, or additionally, pemphigus autoimmunity may be triggered via the pathway involving activation of toll-like receptors (TLRs). This mechanism has been suggested by a recent demonstration of reversible relapse of PF triggered by the TLR7 agonist imiquimod [163]. In this scenario, B-cell tolerance is broken due to ligation of B-cell receptor and TLR by self-antigen/TLR ligand, leading to breakage of T-cell tolerance and activation of autoreactive B and T cells [164].…”

Section: Regulation Of Pemphigus Autoimmunitymentioning

confidence: 99%

Pemphigus autoimmunity: Hypotheses and realities

2011

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The goal of contemporary research in pemphigus vulgaris and pemphigus foliaceus is to achieve and maintain clinical remission without corticosteroids. Recent advances of knowledge on pemphigus autoimmunity scrutinize old dogmas, resolve controversies, and open novel perspectives for treatment. Elucidation of intimate mechanisms of keratinocyte detachment and death in pemphigus has challenged the monopathogenic explanation of disease immunopathology. Over 50 organ-specific and non-organ-specific antigens can be targeted by pemphigus autoimmunity, including desmosomal cadherins and other adhesion molecules, PERP cholinergic and other cell membrane (CM) receptors, and mitochondrial proteins. The initial insult is sustained by the autoantibodies to the cell membrane receptor antigens triggering the intracellular signaling by Src, epidermal growth factor receptor kinase, protein kinases A and C, phospholipase C, mTOR, p38 MAPK, JNK, other tyrosine kinases, and calmodulin that cause basal cell shrinkage and ripping desmosomes off the CM. Autoantibodies synergize with effectors of apoptotic and oncotic pathways, serine proteases, and inflammatory cytokines to overcome the natural resistance and activate the cell death program in keratinocytes. The process of keratinocyte shrinkage/detachment and death via apoptosis/oncosis has been termed apoptolysis to emphasize that it is triggered by the same signal effectors and mediated by the same cell death enzymes. The natural course of pemphigus has improved due to a substantial progress in developing of the steroid-sparing therapies combining the immunosuppressive and direct anti-acantholytic effects. Further elucidation of the molecular mechanisms mediating immune dysregulation and apoptolysis in pemphigus should improve our understanding of disease pathogenesis and facilitate development of steroid-free treatment of patients.

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“…TLR7 inhibitors have been proposed for pemphigus foliaceus since topical imiquimod, a TL7 agonist, is a trigger factor. Pemphigus-like lesions have been observed in sites of topical imiquimod treatment [61].…”

Section: Pemphigusmentioning

confidence: 99%

Therapeutic targeting of Toll-like receptors in cutaneous disorders

Matin

Tabatabaie

Mohammadinejad

et al. 2015

Expert Opinion on Therapeutic Targets

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Although non-specific therapeutic strategies seem to reduce the symptoms in majority of patients, a considerable proportion remain untreated or have to deal with inevitable adverse effects of such therapies. Since TLRs regulate many patholophysiological processes, they could be good candidates for more specific therapeutic approaches. TLR targeting as the first recipient of invading pathogens is a growing concept in this field.

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Reversible relapse of pemphigus foliaceus triggered by topical imiquimod suggests that Toll-like receptor 7 inhibitors may be useful treatments for pemphigus

Cited by 16 publications

References 9 publications

Pemphigus foliaceus induced by topical imiquimod treatment

Pemphigus foliaceus induced by topical imiquimod treatment

Pemphigus autoimmunity: Hypotheses and realities

Therapeutic targeting of Toll-like receptors in cutaneous disorders

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