The sequence of events in psoriatic plaque formation after tape-stripping

Abstract

The sequence of events leading to the formation of a psoriatic plaque induced by tape-stripping was studied using light and electron microscopy. Among the earliest changes noted were increased mobility of the epidermal Langerhans cells across the basement membrane, evidence of Langerhans cell-lymphocyte interaction, and increased Langerhans cell 'activity' or 'cytotoxicity'. These changes were seen as early as 2 min after stripping and remained until the development of clinical psoriasis. Collections of epidermal lymphocytes showing the features of blastoid transformation while in contact with processes from activated Langerhans cells, suggest the involvement of la antigens in this process. We postulate that these findings are a manifestation of an increased immune responsiveness to trauma, controlled by genes located at the HLA-D locus of the major histoeompatibility complex, and mediated by enhanced cellular interactions. The appearance of basal keratinocyte herniations (BKH) at 1-3 weeks after stripping, coincided with the development of clinical psoriasis. Neutrophils made their appearance at the same time as, or slightly before, the appearance of BKH, and are suspected to play a role in the development of these structures. We believe that BKH maintain epidermal proliferation through the persistence of the epidermal-stromal interaction.

Lessons Learned from Psoriatic Plaques Concerning Mechanisms of Tissue Repair, Remodeling, and Inflammation

“…Tape stripping of symptomless skin has revealed that such superficial trauma initiates numerous cellular and molecular events. The sequence of events includes rapid (within 2 days) infiltration of the skin by T cells, macrophages, and DCs (Heng et al, 1985). Interestingly, the presence of CD8 þ T cells and CD11c þ mononuclear cells on day 7 correlated with the appearance of psoriatic lesions following tape stripping (Paukkonen et al, 1992).…”

Keratinocyte: A trigger or an executor of psoriasis?

“…Therefore, the early therapy for psoriasis is crude coal tar or a combination of coal tar and ultraviolet irradiation, both of which aim to inhibit keratinocyte proliferation and then restore normal epidermopoiesis. 1,2 Few years later, retinoids were also found to efficiently inhibit the proliferation of keratinocytes and then used to treat psoriasis. 3 Therefore, keratinocytes were originally consider as a main driver of psoriasis.…”

“…The histology of lesional skin from patients with psoriasis demonstrates that epidermal keratinocytes in lesional skin are hyperproliferative, and excessive immune cells infiltrate into the dermis and epidermis. Therefore, the early therapy for psoriasis is crude coal tar or a combination of coal tar and ultraviolet irradiation, both of which aim to inhibit keratinocyte proliferation and then restore normal epidermopoiesis 1,2 . Few years later, retinoids were also found to efficiently inhibit the proliferation of keratinocytes and then used to treat psoriasis 3 .…”

Psoriasis: Keratinocytes or Immune Cells – Which Is the Trigger?

“…In 1985, Heng et al [3] attempted to describe the microscopic sequence of events associated with psoriasis by studying the different stages of psoriatic plaques induced by tape-stripping. At the time, the research concluded that the proliferation of the epidermis was maintained and clearly identified.…”