Skip to content. | Skip to navigation

Advanced Search…
Personal tools
 
You are here: Home → For Faculty & Staff → Reference Search → 2001 References → Alard et al, Jun 2001, Hapten-specific tolerance induced by acute, low-dose ultraviolet B radiation of skin requires mast cell degranulation

Alard et al, Jun 2001, Hapten-specific tolerance induced by acute, low-dose ultraviolet B radiation of skin requires mast cell degranulation

Reference

Alard, P., Kurimoto, I., Niizeki, H., Doherty, J. M., & Streilein, J. W.  Hapten-specific tolerance induced by acute, low-dose ultraviolet B radiation of skin requires mast cell degranulation. Eur.J.Immunol., 31(6): 1736-1746. (Professional Student Author(s): Kurimoto,I.; Niizeki,H.) (2001).

Abstract

The deleterious effects of ultraviolet B radiation (UVR) on cutaneous immunity are mediated in part by cytokines released from cutaneous cells following radiation exposure. On the one hand, TNF-alpha has been advocated as the primary mediator of failed contact hypersensitivity induction, and, on the other hand, IL-10 has been held responsible for tolerance. While keratinocytes exposed to UVR have been found to produce both TNF-alpha and IL-10, there is reason to question whether these major cellular constituents of the epidermis are the relevant source of immunomodulatory cytokines after UVR. Dermal mast cells also produce TNF-alpha and IL-10, and we have recently reported that mast cell-derived TNF-alpha is required for UVR-induced impairment of CH induction. In this study, we have examined whether mast cells are also a relevant source of IL-10 in UVR-dependent tolerance. We found that (a) UVR fails to induce tolerance in mast cell-deficient mice, and (b) that tolerance occurs if mast cells are triggered to degranulate after ligation of the IgE receptor. Both types of tolerance were neutralized with anti-IL-10 antibodies, are hapten specific, and are associated with regulatory lymphoid cells. We conclude that mast cells are required in UVR-induced tolerance and may be one of the major sources of IL-10 that mediates the tolerance induced by acute, low-dose UVR
Document Actions
Personal tools