Lichenoid Tissue Reaction Induced by Local Transfer of Ia-Reactive T-Cell Clones

Desmoglein 3–specific CD4+ T cells induce pemphigus vulgaris and interface dermatitis in mice

“…It has been described that cytotoxic CD8 + T cells are capable of directly injuring keratinocytes and thus play a central role in interface dermatitis (24,25). Although there are very few reports that have studied the role of CD4 + T cells in interface dermatitis, one study has clearly demonstrated that CD4 + T cells alone can injure keratinocytes (26). The cytotoxic effector function of CD4 + T cells has been observed in other animal models, including EAE, with results that are also consistent with ours in terms of tissue injury by CD4 + T cells (27).…”

“…Although CD4 + T cells are likely involved in helping CD8 + T cells, the roles of CD4 + T cells in these models are unclear. Another report showed a local interface dermatitis model in which CD5 + CD8 -allo-Ia-reactive T cell clones were injected subcutaneously and demonstrated that the immune response against the allo-MHC class II antigen was capable of inducing interface dermatitis (26). The Dsg3-specific TCRs we used are MHC class IIrestricted, and these CD4 + T cells were also capable of inducing interface dermatitis.…”

Lichen planus

“…14 Further studies have shown that these cells produce Civatte bodies and basal layer degeneration characteristic of LP. 15 Both a temporal and spatial relationship between cytotoxic T cells and epithelial cell damage have been reported. 16 The intercellular adhesion molecule ICAM-1 has a widespread cellular G Marshman distribution and is probably involved not only in the recruitment of circulating inflammatory cells but also in their functional control and their retention within and migration through the skin.…”

Induction and control of lichenoid tissue reactions

“…To date, three types of approach have been used to elucidate the mechanism(s) by which T cells migrate into the epidermis: the adherence reaction between T cells and cultured KC in vitro by Nickoloff and colleagues [26,27]; and the use of an animal model by us [41][42][43][44][45], in which the LTR is experimentally induced by intradermal inoculation of CD4 + autoreactive T cell clones. Another approach is examination of diseased human tissues for expression of adhesion molecules and cytokines [16,48,56,65].…”

“…Thus, LFA-1 expression on T cells is primarily important in the adhesion of the T cells to epidermal KC in the LTR. Because all the epidermotropic T cells can produce IFN-3/and TNF-/3 [41,43], cytokines capable of inducing ICAM-1 expression on many cell types, it is likely that IFN-3, and TNF-/3 that are released by epidermotropic T cells upon antigenic stimulation induce KC to express (Fig. 3), while that of non-epidermotropic T cells induced only focal and weak ICAM-1 expression on KC even at 48 h, when the DTH reactions peaked.…”