here - Australian College of Veterinary Scientists

IgE-bearing cells have been demonstrated in the epidermis and dermis of lesional
skin from horses with IBH, together with increased numbers of mast cells, the
majority of which were tryptase-positive (van der Haegen et al 2001) and also
bearing IgE protein. No chymase-positive cells were found, similar to bovine skin,
but in contrast to human and canine skin where mast cells are both chymase and
tryptase-positive. IgE-mRNA and IgE-protein positive cells were found in the
dermis – likely B-lymphocytes and plasma cells – but also IgE-protein positive,
mRNA negative cells in both the dermis and the epidermis, which are likely to be
dendritic cells, including Langerhans cells. By comparison with samples from healthy
horses and horses with an infectious skin disease, this study was the first to provide
evidence demonstrating the role of IgE in the skin of allergic horses.
Epidermal Langerhans cells bearing IgE are thought to capture percutaneously
absorbed allergen, process and present to allergen-specific T-lymphocytes. In atopic
humans there is subsequent preferential expansion of T-helper cells of the Th2subset,
which release cytokines such as interleukin (IL)-4, with resultant stimulation
of IgE production by B-cells. The cytokine profile of the increased number of Tlymphocytes
demonstrated in the skin of allergic horses has yet to be elucidated.
The horse, in comparison to humans and dogs, shows a prominent late-phase
component 4-6 hours after intradermal challenge. As well as IgE-cross-linking
resulting in histamine release from mast cells, liberation of histamine from equine
basophils has also been demonstrated. Increased concentrations of a numbers of
inflammatory mediators has been documented during inflammatory reactions in the
horse, including eicosanoids, lysosomal enzymes, proteases, IL-1, leukotriene (LT)B 4,
prostaglandin (PG) E 2, histamine, serotonin, superoxides and tumour necrosis factor
(TNF).
In allergic skin disease in the horse the eosinophil is particularly important, together
with histamine, LTB 4 and platelet aggregating factor (PAF). Histamine injected
intradermally results in the ingress of numerous eosinophils and results in marked
oedema. Injection of LTB 4 and PAF also stimulates migration of eosinophils and
oedema, the number of eosinophils being proportional to the oedema. Foster and
colleagues at the Royal Veterinary College, London, studied cutaneous inflammation
in horses and demonstrated the importance of PAF and LTB 4 in horses with sweet
itch (IBH). PAF and LTB 4 induction of migration of eosinophils and neutrophils in
horses with allergic skin disease. PAF was shown to mimic antigen-induced
inflammatory responses and receptor antagonists to inhibit the responses.
Eosinophils are reported as the predominant inflammatory cells in skin biopsies
taken from atopic horses, as well as those with IBH. Eosinophils contain a range of
cytotoxic proteins and produce several potent inflammatory mediators and are
pivotal in the inflammatory process triggered by hypersensitivity reactions in the
horse.
ACVSC Proceedings Dermatology Chapter Science Week 2005 11