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A study of dendritic cell and MHC class II expression in dogs with immunomodulatory-responsive lymphocytic-plasmacytic pododermatitis

The term immunomodulatory-responsive lymphocytic-plasmacytic pododermatitis (ImR-LPP) has previously been proposed to denote a sub-population of dogs with idiopathic pododermatitis. The objective of this study was to investigate dendritic cell (DC) and MHC class II antigen expression in lesional ski...

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Published in:The veterinary journal (1997) 2008-09, Vol.177 (3), p.352-359
Main Authors: Breathnach, Rory M., Fanning, Shay, Mulcahy, Grace, Bassett, Hugh F., Jones, Boyd R.
Format: Article
Language:English
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Summary:The term immunomodulatory-responsive lymphocytic-plasmacytic pododermatitis (ImR-LPP) has previously been proposed to denote a sub-population of dogs with idiopathic pododermatitis. The objective of this study was to investigate dendritic cell (DC) and MHC class II antigen expression in lesional skin of dogs with ImR-LPP ( n = 47). Median epidermal CD1c + cell counts were 37.8 and 12.5 mm −1 in ImR-LPP dogs and healthy controls ( n = 27), respectively ( P < 0.01), while the corresponding dermal cell counts were 180.9 and 45.0 mm −2, respectively ( P < 0.01). Intra-epidermal clusters of DCs were observed in 18/47 dogs with ImR-LPP. Median epidermal MHC class II + cell counts were 32.5 and 10.5 mm −1 in ImR-LPP dogs and healthy controls, respectively ( P < 0.01), while the corresponding dermal cell counts were 216.9 and 46.9 mm −2, respectively ( P < 0.01). Dermal MHC class II + staining was primarily associated with DCs (47/47 dogs), mononuclear inflammatory cells (45/47), fibroblast-like cells (19/47) and vascular endothelium (14/47). The DC hyperplasia and increased MHC class II expression in lesional ImR-LPP skin are consistent with enhanced antigen presentation, and suggest that both parameters may contribute to the pathogenesis of ImR-LPP through the priming and activation of CD4 + T cells. Equally, it is possible that the enhanced DC numbers observed in this study may contribute to the immunoregulation of steady-state pathology in lesional ImR-LPP skin through additional expanded, although as yet unresolved, mechanisms.
ISSN:1090-0233
1532-2971
DOI:10.1016/j.tvjl.2007.05.013