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Solar urticaria is a rare, immunologically mediated photodermatosis in which activation of cutaneous mast cells is triggered by specific wavelengths of solar electromagnetic radiation. This manifests clinically as the rapid development of cutaneous itch, erythema and wheal formation after several minutes of sun exposure. Disease mechanisms in solar urticaria remain incompletely elucidated and there have been few recent investigations of its pathobiology. Historic passive transfer experiments performed during the twentieth century provide support for a 'photoallergy' model of disease pathogenesis, wherein molecular alteration of a putative chromophore by solar electromagnetic radiation produces mast cell activation via an IgE‐dependent mechanism. However, this model does not account for several observations made during passive transfer experiments nor does it explain a range of subsequent clinical and photobiological observations made in solar urticaria patients. Furthermore, increased understanding of the molecular dynamics underpinning cutaneous mast cell responses highlights the need to reformulate our understanding of solar urticaria pathogenesis in the context of this contemporary scientific landscape. In this review, we discuss the current understanding of solar urticaria pathogenesis and, by incorporating recent scientific and clinical observations, develop new hypotheses to drive future investigation into this intriguing disorder. [ABSTRACT FROM AUTHOR]

During COVID‐19 infection, reduced function of natural killer (NK) cells can lead to both compromised viral clearance and dysregulation of the immune response. Such dysregulation leads to overproduction of cytokines, a raised neutrophil/lymphocyte ratio and monocytosis. This in turn increases IL‐6 expression, which promotes scar and thrombus formation. Excess IL‐6 also leads to a further reduction in NK function through downregulation of perforin expression, therefore forming a pathogenic auto‐inflammatory feedback loop. The perforin/granzyme system of cytotoxicity is the main mechanism through which NK cells and cytotoxic T lymphocytes eliminate virally infected host cells, as well as being central to their role in regulating immune responses to microbial infection. Here, we present epidemiological evidence suggesting an association between perforin expression and resistance to COVID‐19. In addition, we outline the manner in which a pathogenic auto‐inflammatory feedback loop could operate and the relationship of this loop to genes associated with severe COVID‐19. Such an auto‐inflammatory loop may be amenable to synergistic multimodal therapy. [ABSTRACT FROM AUTHOR]

Since first described by Kossard in 1994, frontal fibrosing alopecia ( FFA) has been something of an enigma. The clinical heterogeneity of FFA, its apparent rarity and investigators' suboptimal access to phenotypically consistent patient cohorts may all have had a negative impact on delineating disease pathogenesis. Moreover, there is a relative paucity of epidemiological, interventional and basic research studies, and there have been no advances in translational therapeutics, unlike for other inflammatory dermatoses, such as alopecia areata ( AA). Dermatologists anecdotally describe an increasing incidence in FFA over the last decade, which has led to the notion that the disorder may be induced by unknown environmental triggers. On the other hand, segregation of FFA in some families lends support to an unexplored genetic element implicated in disease pathogenesis. We herein review what is known about the pathobiology of FFA and formulate working hypotheses to advance insight into this intriguing hair disorder. [ABSTRACT FROM AUTHOR]

Nevertheless, major insights into key genetic determinants of contact allergy might be gained by examining those who demonstrate increased risk of contact allergy, irrespective of allergen structure or class. Bryld et al4 also examined nickel contact allergy among 630 Danish female twin pairs, demonstrating a slightly increased odds of nickel contact allergy (adjusted odds ratio 1.28, 95% confidence interval 0.33-5.00) in monozygotic compared with dizygotic twin pairs. Contact allergy occurs due to cutaneous interaction with environmental allergens that result in T-cell-mediated inflammation.1 Exposures to allergens could, therefore, be presumed to be the sole determinant of contact allergy. [Extracted from the article]

Keywords: benzyl salicylate; contact allergy; frontal fibrosing alopecia; patch test EN benzyl salicylate contact allergy frontal fibrosing alopecia patch test 483 484 2 09/21/21 20211001 NES 211001 Pastor-Nieto et al1 report a case series of 36 patients with frontal fibrosing alopecia (FFA) who have undergone patch testing. Subsequently, Pastor-Nieto et al1 propose several hypotheses to account for their observed association between benzyl salicylate sensitivity and FFA, notably suggesting that benzyl salicylate could be a sole or significant factor in FFA pathogenesis. [Extracted from the article]