CD11b+ Cells and Ultraviolet-B-Resistant CD1a+ Cells in Skin of Patients with Polymorphous Light Eruption

Abstract

After ultraviolet exposure Langerhans cells (epidermal CD1a+ cells) disappear from the healthy skin, and CD11b+ macrophage-like cells, which are reported to produce interleukin-10, appear in a matter of days. These phenomena are related to the ultraviolet-induced local suppression of contact hypersensitivity reactions. A defect in this suppression might allow inadvertent immune reactions to develop after ultraviolet (over)exposure; i.e., it could cause ultraviolet-B-induced polymorphous light eruption. In order to test this we first exposed buttock skin of eight healthy volunteers to six minimal erythema doses from Philips TL12 lamps, and indeed observed a dramatic disappearance of CD1a+ cells 48 and 72 h later, at which time the number of CD11b+ cells increased in the dermis, and some occurred in the epidermis. The epidermis thickened and showed large defects, filled by CD11b+ cells, just below the stratum corneum. In 10 patients with polymorphous light eruption (five with a normal minimal erythema dose and five with a low minimal erythema dose) CD1a+ cells were present in the epidermis as well as in the dermis before exposure. Strikingly, these cells were still present in considerable number at 48 and 72 h after exposure to six minimal erythema doses. CD11b+ cells already present in the dermis before ultraviolet exposure, increased after ultraviolet exposure, and subsequently also invaded the epidermis. Despite the six minimal erythema doses, there were no apparent defects in the epidermis of the polymorphous light eruption patients. This deviant early response to ultraviolet radiation is likely to be of direct relevance to the polymorphous light eruption and is perhaps useful as a diagnostic criterion.

Ultraviolet B Radiation Induces a Transient Appearance of IL-4+ Neutrophils, Which Support the Development of Th2 Responses

“…Although macrophages also express CD11b and infiltrate UVB-irradiated skin, they are improbable candidates for the IL-4 ϩ cells because of the presence of CD36 and the absence of CD15. In connection to this, it was recently shown that the majority of the CD11b ϩ cells, which infiltrate UVB-exposed skin, lack the macrophage marker CD68 (23). Basophils and eosinophils also have a multilobed nucleus and express CD11b and CD15, but they are not known to infiltrate UVB-exposed normal human skin (24), and by means of specific mAbs we demonstrated that these two cell types are absent in irradiated skin.…”

Vitamin D3 Affects Differentiation, Maturation, and Function of Human Monocyte-Derived Dendritic Cells

“…Therefore, UV exposure induces a systemic and a local increase in 1␣,25-(OH) 2 D 3 in the skin. It is known that after UV exposure, Langerhans cells (epidermal CD1a ϩ cells) disappear from the healthy skin, and CD11b ϩ macrophage-like cells appear in few days (69). Moreover, UV radiation induces apoptosis and suppresses the immune function of epidermal Langerhans cells (70).…”

Photohardening of polymorphic light eruption patients decreases baseline epidermalLangerhans cell density while increasing mast cell numbers in the papillary dermis

“…A key cellular event in UV immunosuppression is the migration of Langerhans cells (LC) from the epidermis to the skin-draining lymph nodes (5) where they mediate the activation of immunoregulatory T cells (6). While LC migration and immune suppression is a normal response to UV in healthy human skin, this may not occur in PLE skin (7)(8)(9). Prophylactic UV photohardening in PLE patients restores the capacity for UVinduced LC migration which is thought to be one of the mechanisms of action of this therapy (10).…”