Bs. Baker et al., ABSENCE OF GLUTEN-SPECIFIC T-LYMPHOCYTES IN THE SKIN OF PATIENTS WITHDERMATITIS-HERPETIFORMIS, Journal of autoimmunity, 8(1), 1995, pp. 75-82
Dermatitis Herpetiformis (DH) is an immunobullous skin disease with an
associated gluten-sensitive enteropathy. Withdrawal of gluten from th
e diet leads to the resolution of both the skin lesions and the entero
pathy. A T cell-mediated immune response to gluten has been implicated
in the damage to the gut; the possible gluten specificity of the T ce
ll infiltrate in DH skin lesions has not, however, been investigated,
T cell lines (TCL) were therefore established from the skin lesions of
eight patients with DH by culturing skin fragments for 11-17 days wit
h a medium supplemented with 20 U/ml of IL-2. In three cases, gliadin
(fraction of gluten toxic to the DH gut) and irradiated, autologous pe
ripheral blood mononuclear cells were also added. The TCL were stained
for CD3, CD4, CD8, TCR alpha beta and gamma delta expression by indir
ect immunofluorescence, and their proliferative responses to mitogens
and gluten fraction III (a peptic-tryptic digest of gluten) investigat
ed. Of the eight CD3(+) TCL, four were predominantly CD4(+) (82.1-98.8
%), three predominantly CD8(+) (92.6-98.6%) and one TCL contained both
87.6% CD4(+) and 95.2% CD8(+) T cells, a substantial proportion of wh
ich were presumably double-labelled CD4(+), CD8(+) T cells. All eight
TCL, which were almost exclusively TCR alpha beta(+), proliferated in
response to PHA whilst six out of the eight were stimulated by Concana
valin A. None of the TCL proliferated to gluten fraction III alone; ho
wever, two TCL showed increased proliferation to the antigen in the pr
esence of exogenous IL-2 or IL-4 (10 U/ml) compared to cytokine alone.
All eight TCL proliferated strongly in the presence of IL-2 alone, bu
t only two out of seven showed a moderate response to IL-4. These find
ings suggest that gluten-specific T cells are absent from DH skin lesi
ons.