Effector pathways during eczematous dermatitis: where inflammation meets cell death
Article first published online: 7 JUL 2009
© 2009 John Wiley & Sons A/S
Volume 18, Issue 10, pages 893–899, October 2009
How to Cite
Kerstan, A., Leverkus, M. and Trautmann, A. (2009), Effector pathways during eczematous dermatitis: where inflammation meets cell death. Experimental Dermatology, 18: 893–899. doi: 10.1111/j.1600-0625.2009.00919.x
- Issue published online: 11 SEP 2009
- Article first published online: 7 JUL 2009
- Accepted for publication 26 May 2009.
- allergic contact dermatitis;
- atopic dermatitis;
- T cell
Abstract: During eczematous skin inflammation, the main constituents of the skin, keratinocytes (KC), play an important role in inducing and shaping the immunological response to environmental stimuli. This review focuses on the epidermal inflammation caused by keratinocyte-T cell interactions arising from a disturbed barrier function of the skin. In eczematous dermatitis, activated dermis- and epidermis-infiltrating T cells target KC for apoptosis. In turn, damaged KC respond by secreting inflammatory mediators, thus effecting further recruitment of immunocytes to inflamed skin. Further advances will come from identification of the immunoregulatory mechanisms involved in the pathogenesis of eczematous dermatitis. Potential therapeutic interventions are discussed.