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Langerhans cells are MHC class II (Ia) positive antigen- presenting cells that play a crucial role in the induction of contact hypersensitivity (CHS). The topical application of a hapten modifies the cell surface moieties of Langerhans cells, and activates Langerhans cells to increase their size and Ia intensity. The haptenated and activated Langerhans cells emigrate from the epidermis and thus the in situ density of Langerhans cells usually decreases during 24-48h after the hapten application in CHS. To determine whether the early activation pattern of Langerhans cells is different between the afferent phase and the efferent phase of CHS, we compared the density and morphologic changes of Langerhans cells in CHS to trinitrochlorobenzene using nonsensitized and sensitized mice. We found that the application of a hapten induces more significant enlargement of Langerhans cell size in the afferent phase than in the efferent phase, whereas the reduction of Langerhans cell density is more marked in the efferent than in the afferent phase of CHS. Moreover, topical immunosuppressive drugs inhibit the in situ activation of Langerhans cells.

Background: Erythema multiforme is a polymorphous self-limited, often recurrent eruption that can follow herpes simplex virus (HSV) infection, hereby designated HAEM. Studies of relatively large groups of patients during one recurrent episode indicated that HAEM pathogenesis is associated with HSV gene expression, Vβ2 T cell infiltration of lesional skin and altered T cell receptor (TCR) repertoire usage by HSV-stimulated peripheral blood mononuclear cells (PBMC). However, HAEM recurrences are not always preceded by overt HSV eruptions and virus cannot be isolated from HAEM lesional skin. Therefore, it is unknown whether all HAEM recurrences experienced by a given patient are HSV related. Objective: The studies described in this report were designed to examine whether all HAEM recurrences experienced by a given patient are HSV related. Methods: We describe one patient who was studied longitudinally during 6 HAEM recurrences and in the intervening lesion-free periods. Lesional skin from all HAEM episodes was studied for HSV gene expression and infiltration by Vβ2 and Vβ3 T cells. PBMC obtained at these times were assayed for TCR repertoire usage upon HSV stimulation. Results: Lesional skin from all HAEM episodes was positive for HSV gene expression (RNA and protein) as well as Vβ2 T cell infiltration. HSV-stimulated PBMC obtained at these times had an altered TCR repertoire characterized by a predominance of Vβ2 cells. The duration of viral gene expression, Vβ2 cell infiltration and altered TCR repertoire usage correlated with the duration of clinical symptoms. Conclusion: The data suggest that HSV and a virus-specific immunopathology component are involved in the causation of all HAEM episodes experienced by the patient.

Exposure of herpes simplex virus (HSV) latently infected subjects to ultraviolet irradiation (UVR) (1 minimum erythema dose, 90% body surface) caused a significant inhibition of HSV and phytohemagglutinin-induced lymphoproliferation. The inhibition was observed on Day 3 post-UVR and lasted at least 9 days. UVR-induced downregulation of HSV-specific lymphoproliferation was associated with increased levels of activated transforming growth factor β However, the relationship between UVR-induced immune downregulation and the development of recurrent HSV lesions was incomplete.