Immunologically mediated epidermal cell injury

Lichenoid Tissue Reaction/Interface Dermatitis: Clinical and Histological Perspectives

“…Lichenoid tissue reaction/interface dermatitis skin diseases have traditionally been subdivided into those clinical disorders that display a high-density (''cell-rich'') inflammatory infiltrate and those that display a low-density (''cell-poor'') infiltrate (Romero et al, 1977;Sontheimer and Gilliam, 1981). Clinical examples of a cell-rich LTR include lichen planus and its variants, lichenoid drug reactions, lichen nitidus, lichen striatus, and some forms of autoimmune connective tissue skin disease such as discoid LE.…”

“…Even this is a rather broad subject. For more indepth discussion of the primary observations relating to the etiopathogenesis of lichen planus, the reader is referred to other more in-depth treatments of this subject (Pinkus 1973;Sontheimer and Gilliam 1981;Shiohara et al, 1986Shiohara et al, , 1987Shiohara et al, , 1988aShiohara et al, , b, c, 1992Oliver et al, 1989;Bleicher et al, 1990;Bratel et al, 1998;Sugerman et al, 2002;Lodi et al, 2005;Shiohara and Mizukawa, 2005). This review will address some of the modern currents of thought in this area.…”

T-Cell-Mediated Injury to Keratinocytes: Insights from Animal Models of the Lichenoid Tissue Reaction

“…The lichenoid tissue reaction (LTR) or interface dermatitis is a specific pattern of skin injury that is common to multiple disease processes. Unifying concepts behind this injury reaction pattern were identified by careful histologic analysis and include (1) epidermal cell damage with prominent keratinocyte cell death most pronounced at the basal-cell layer; (2) the subsequent formation of Civatte bodies in the epidermis and colloid bodies in the dermis; and (3) a prominent mixed mononuclear cell infiltrate at the dermoepidermal junction that ''obscures the junction'' (Ragaz and Ackerman, 1981;Sontheimer and Gilliam, 1981;Weedon, 1982). The nomenclature and nosology of the LTR-interface dermatitis pattern is well described in an accompanying article by Sontheimer and Gilliam (1981).…”

“…Unifying concepts behind this injury reaction pattern were identified by careful histologic analysis and include (1) epidermal cell damage with prominent keratinocyte cell death most pronounced at the basal-cell layer; (2) the subsequent formation of Civatte bodies in the epidermis and colloid bodies in the dermis; and (3) a prominent mixed mononuclear cell infiltrate at the dermoepidermal junction that ''obscures the junction'' (Ragaz and Ackerman, 1981;Sontheimer and Gilliam, 1981;Weedon, 1982). The nomenclature and nosology of the LTR-interface dermatitis pattern is well described in an accompanying article by Sontheimer and Gilliam (1981). The diseases that share this histologic reaction pattern have been classified into those with a prominent cellular infiltrate at the dermoepidermal junction (termed ''cell rich'') and those with a sparse cellular infiltrate, despite evidence of basilar keratinocyte damage (termed 'cell poor').…”

Blockade of Granzyme B Remarkably Improves Mucocutaneous Diseases with Keratinocyte Death in Interface Dermatitis

“…Journal of Investigative Dermatology (2018) 138, 2079e2083; doi:10.1016/j.jid. 2018.03.1507 TO THE EDITOR Lichenoid tissue reaction/interface dermatitis (LTR/IFD) is a pattern of skin inflammation characterized pathologically by infiltration of the skin basement membrane by auto-aggressive T cells, causing keratinocyte death (Sontheimer and Gilliam, 1981). A wide spectrum of skin disorders exhibit this set of histological features and mucocutaneous lesions, including acute graft-versushost disease (aGVHD).…”