2009
DOI: 10.1111/j.1600-0625.2009.00859.x
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New insights into the mechanisms of polymorphic light eruption: resistance to ultraviolet radiation‐induced immune suppression as an aetiological factor

Abstract: An abnormal immune response has long been thought responsible for the patho-aetiology of polymorphic light eruption, the most common photodermatosis. Recent evidence indicates that polymorphic light eruption patients are resistant to the immune suppressive effects of sunlight, a phenomenon that leads to the formation of skin lesions upon seasonal sun exposure. This immunological abnormality in polymorphic light eruption supports the concept of the biological significance and evolutionary logic of sunlight-indu… Show more

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Cited by 54 publications
(55 citation statements)
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“…56 The majority of these UV-recruited neutrophils home to the dermis 56 where they mediate immune suppression via IL-4 and IL-10 production. 56,79 Between days 3 and 5 after UV exposure, CD11b ϩ IL-10 -producing macrophages start to appear. 80 Macrophage phenotype can be altered by IL-33 81 suggesting that UV-induced IL-33 may also affect macrophage function, although further studies are required to determine whether this is the case.…”
Section: Discussionmentioning
confidence: 99%
“…56 The majority of these UV-recruited neutrophils home to the dermis 56 where they mediate immune suppression via IL-4 and IL-10 production. 56,79 Between days 3 and 5 after UV exposure, CD11b ϩ IL-10 -producing macrophages start to appear. 80 Macrophage phenotype can be altered by IL-33 81 suggesting that UV-induced IL-33 may also affect macrophage function, although further studies are required to determine whether this is the case.…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, UV phototherapy may augment the functional activity of Tregs in polymorphic light eruption in preseasonal photohardening. This activity is possibly associated with normalization of sun sensitivity in this presumably autoimmune-mediated condition (39). It is also worth mentioning that the infusion of expanded Tregs (e.g., by photopheresis) (25) has been suggested as a therapeutic concept to control immunity in graft-versus-host-disease after allogeneic bone marrow transplantation.…”
Section: Discussionmentioning
confidence: 99%
“…Additionally, a lack of skin infiltration by plasmacytoid dendritic cells may contribute to the pathogenesis of PLE (36). Photohardening works in PLE by restoring the normal UV immune suppressive pathways (10), allowing for the effective prevention of a Th1-driven immune reaction to potential UV-induced cutaneous photoantigens (37). Moreover, medical photohardening of PLE patients modulates baseline cytokine levels (38) and restores an impaired neutrophil responsiveness to the chemoattractant leukotriene B4 (LTB 4 ) (33) that is also a chemoattractant for bone marrow-derived mast cells progenitors (39).…”
Section: Or Induction Of Regulatory T Cells (Tregs) (22) Interestingmentioning
confidence: 99%