Open questions in hidradenitis suppurativa research: a hair biologist's perspective
Identifieur interne : 007B86 ( Main/Exploration ); précédent : 007B85; suivant : 007B87Open questions in hidradenitis suppurativa research: a hair biologist's perspective
Auteurs : Ralf Paus [Allemagne]Source :
- Experimental Dermatology [ 0906-6705 ] ; 2006-06.
Abstract
To clarify the obscure cause(s) of hidradenitis suppurativa (HS), plausible, comprehensive, and testable hypothetical pathogenesis scenarios urgently need to be developed. HS is a chronic inflammatory disorder of the pilosebaceous unit, which occurs in intertriginous, ‘apocrine’ skin after puberty, and in more women than men. The clinical picture is dominated by late events resulting from follicular occlusion and its tissue‐destructive, inflammatory sequelae, aggravated by bacterial superinfection. Likely, HS originates from events in the hair follicle epithelium outer root sheath (ORS) rather than the apocrine gland and/or its duct. Genetic and endocrine factors influence HS incidence and course, at least in defined subpopulations. If follicular hyperkeratosis, leading to the retention of follicular material, represents the earliest histological abnormality, while inflammation and apocrine involvement are secondary ones, then the cause of hyperkeratosis and hyperproliferation of ORS keratinocytes must be identified. In normal skin epithelium, this typically results from inflammatory stimuli. Because the skin epithelium is a crucial element in the control of innate immunity, one may speculate that the primary defect in HS is an insufficiently controlled and/or abnormal release of pro‐inflammatory ‘danger’ signals from the follicle ORS (e.g. chemokines, defensins, TLR ligands). This may only lead to HS, if additional predisposing factors (e.g. genetically lowered threshold for activation, or defective suppression of, innate immune response loops; constitutive overexpression of TLRs or underexpression of immunoinhibitory signals) are present and once pro‐inflammatory stimuli are further up‐regulated, e.g. by microtrauma, (neuro‐) endocrine and/or local microbial signals. In this scenario, hyperkeratosis/hyperproliferation of ORS keratinocytes only represents the first visible sign of a primary imbalance of the intrafollicular controls of epithelial innate immune mechanisms. This chiefly calls for systematic exploration of the hair follicle innate immune system in as yet uninvolved intertriginous skin of HS patients versus normal controls as a key to unravelling the elusive pathogenesis of HS.
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DOI: 10.1111/j.0906-6705.2006.0436b.x
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HS is a chronic inflammatory disorder of the pilosebaceous unit, which occurs in intertriginous, ‘apocrine’ skin after puberty, and in more women than men. The clinical picture is dominated by late events resulting from follicular occlusion and its tissue‐destructive, inflammatory sequelae, aggravated by bacterial superinfection. Likely, HS originates from events in the hair follicle epithelium outer root sheath (ORS) rather than the apocrine gland and/or its duct. Genetic and endocrine factors influence HS incidence and course, at least in defined subpopulations. If follicular hyperkeratosis, leading to the retention of follicular material, represents the earliest histological abnormality, while inflammation and apocrine involvement are secondary ones, then the cause of hyperkeratosis and hyperproliferation of ORS keratinocytes must be identified. In normal skin epithelium, this typically results from inflammatory stimuli. Because the skin epithelium is a crucial element in the control of innate immunity, one may speculate that the primary defect in HS is an insufficiently controlled and/or abnormal release of pro‐inflammatory ‘danger’ signals from the follicle ORS (e.g. chemokines, defensins, TLR ligands). This may only lead to HS, if additional predisposing factors (e.g. genetically lowered threshold for activation, or defective suppression of, innate immune response loops; constitutive overexpression of TLRs or underexpression of immunoinhibitory signals) are present and once pro‐inflammatory stimuli are further up‐regulated, e.g. by microtrauma, (neuro‐) endocrine and/or local microbial signals. In this scenario, hyperkeratosis/hyperproliferation of ORS keratinocytes only represents the first visible sign of a primary imbalance of the intrafollicular controls of epithelial innate immune mechanisms. This chiefly calls for systematic exploration of the hair follicle innate immune system in as yet uninvolved intertriginous skin of HS patients versus normal controls as a key to unravelling the elusive pathogenesis of HS.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Paus, Ralf" sort="Paus, Ralf" uniqKey="Paus R" first="Ralf" last="Paus">Ralf Paus</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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