Liliane Didierjean

Graft versus host reaction and lichen planus-like eruption in man.

Lichen planus-like eruptions can be seen in various circumstances, but graft versus host reactions (GVHR) occurring in bone marrow transplanted patients have never been reported as an aetiological factor. The sequence of histological events in lichen planus (LP) seems to include initial epidermal basal cell damage (Pinkus, 1973). The mechanism of this damage is unknown (Black, 1972). Skin lesions of GVHR in man appear to be related mainly to basal cell damage (Slavin & Santos 1973). Because of the similarity of the initial lesions in LP and in GVHR, lichenoid eruptions in GVHR could be expected. Nevertheless, GVHR skin eruptions have never been reported to be clinically lichenoid j maculopapular or dry scaling scarlatiniform rashes and even toxic epidermal necrolysis (Peck, Herzig & Elias, 1972) have been noted in the acute stage of GVHR, or atrophy and pigmentation in the quiescent phase (Slavin & Santos, 1973). Slavin & Santos (1973) first drew attention to the similarity between the histology of lichen planus and of GVHR j this similarity was observed mainly during a secondary phase of GVHR called by these authors: florid phase of aggressor lymphocytes destructive lesion. The following is the history of a patient whose acute GVHR skin eruption was initially maculopapular and subsequently became chronic with clinical and histological features of an extensive lichen planus-like eruption. This 13-year-old boy was admitted for post-hepatitis aplastic anaemia. Transplantation was performed with the marrow of his matched sister. On day 7, the first signs of engraftment were observed and the immediate course was uneventful. On day 11, he developed a diffuse maculopapular rash. Two days later, high spiking fever, diarrhoea and a rise of SGOT appeared. A skin biopsy on day 11 showed a grade H GVHR without any lymphoid infiltrate. From day 18 to day 52 he received a total dose of 280 mg IgG/kg of anti-thymocyte globulin. The SGOT was normal by day 62, and diarrhoea and anorexia disappeared on day 75. The skin lesions persisted with scaling and pigmentation. A second skin biopsy, on day 56, showed persisting grade II-HI GVHR, only sparse lymphoid cells were seen. On day 59, a cytomegalovirus (CMV) interstitial pneumonitis with viraemia was diagnosed. All immuno-suppressive therapy was discontinued and treatment with anti-CMV plasma, gammaglobulin and transfer factor was given. At that time there was a severe immunodeficiency (agammaglobulinaemia, vinresponsiveness of lymphocytes to phytohaemagglutin or to allogeneic lymphocytes). The clinical status improved progressively but skin lesions persisted and changed. Typical papular lichen planuslike lesions appeared. They were first observed on the extremities and progressively spread to the whole body. The buccal mucous membrane and nails were also involved. A skin biopsy, on day 90, demonstrated the characteristic lesions of lichen planus: basal epidermal cell damage with colloid bodies, and

Subcorneal pustular dermatosis and monoclonal IgA

A patient with subcorneal pustular dermatosis was found to have a circulating monoclonal IgA kappa immunoglobulin.

Immunohistochemical identification of interleukin 1α and β in human eccrine sweat-gland apparatus

Bouin‐fixed paraffin sections or acetone‐fixed cryostat sections were labelled with the avidinbiotin complex (ABC) or peroxidase‐antiperoxidase (PAP) method using three monoclonal antibodies (MAbs) and two polyclonal antisera to human recombinant interleukin i beta (IL‐iβ) and three polyclonal antisera to human recombinant interleukin iα (IL‐iα). In the secretory coil both IL‐α and β were detected in the clear, but not in the dark cells. Both luminal and basal cells of the coiled and straight ducts expressed IL‐iα and β, the IL‐i labelling being more intense in the luminal cells. IL‐i was not usually detected in the initial portion of the intraepidermal eccrine sweat duct, whereas intense labelling was seen in the upper part including through the stratum corneum. In skin biopsies of the palm, taken after exercise, there was only faint IL‐i labelling of the secretory cells, whereas the luminal cells of the dermal ducts showed intense labelling for both IL‐iα and β. In the acrosyringium, exercise did not alter the pattern for IL‐iα and β, except that in the palm, some of the antibodies to IL‐iβ produced a more intense immunolabelling of the acrosyringeal cells. This study identifies a distinct and similar distribution of the two forms of IL‐i throughout the eccrine sweat‐gland apparatus and indicates that part of the IL‐i epidermal pool originates from the sweat.

Systemic administration of etretin increases epidermal interleukin I in the rat

We have studied the effect of systemic administration of etretin (Ro 10–1670) on the epidermal interleukin I (ILI) pool in the rat. Hairless rats were given varying doses of etretin intraperitoneally for 21 days, or a fixed dose for 2, 8 and 16 days. Abdominal skin was taken and processed for light microscopy, autoradiography (using [3H]‐thymidine) and ILI assays. ILI was assayed in supernatants of epidermal extracts by both the lymphocyte activating factor (LAP) assay and the stimulation of prostaglandin E2 (PGE2) release from dermal fibroblasts. A significant increase in both LAF and PGE2 stimulatory activities was found during etretin administration. After 21 days’ treatment with varying doses there was a two‐ to three‐fold increase as compared to the controls, with a peak at 2 and 5 mg/kg. At a fixed dose a two‐fold increase was found after 2 days and a three‐ to four‐fold increase after 16 days; normal pretreatment values were restored 16 days after cessation of etretin.

Effect of topical retinoic acid on the interleukin Iα and β immunoreactive pool in normal human epidermis

The topical application of 0.1% retinoic acid (RA) on human skin over a period of 4 days, whether or not under occlusion, did not increase either IL‐iα or β immunoreactivity as determined by a sensitive enzymoimmunoassay. No down modulation was seen following the application of a potent topical corticosteroid. Occlusion increased the yield of IL‐iβ immunoreactivity. Immunoblot patterns of epidermal extracts revealed both the mature form of IL‐i (17 kDa) and the precursor (36 kDa) and were identical in amounts whether the specimens were from controls or from RA‐ or corticosteroid‐trcated skin. There was a slight modification in the pattern of high molecular weight proteins (52 kDa) probed by the anti‐IL‐iα and β sera. It appears that the IL‐1 epidermal immunoreactive pools are barely amenable to modulation because they represent a storage form linked to end‐stages of keratinocyte differentiation.

Calcium-binding proteins in rat skin

Skin Ca2+‐binding protein (SCaBP) was reported to be distinct from the Ca2+‐binding parvalbumin (PV), however, more recently its amino acid sequence was shown to be identical to PV. We purified a protein (M r 12 000; pI4.5) from isolated epidermis (free of other cell layers) of adult rats and whole skin (containing no PV) of newborn rats. This protein is referred to as epidermal protein (EP‐12), distinct from PV in its hydrophobicity, amino acid composition and immunological properties. Previously isolated SCaBP was shown to be a mixture of EP‐12 and PV. The localization and possible functions of EP‐12 and of PV in skin of adult and newborn rat are discussed.

Skin calcium-binding protein immunoreactivity in basal cell carcinoma

Skin calcium‐binding protein (SCaBP) is a low molecular weight protein of unknown function which is localized in the cytoplasm of epidermal basal cells. We have examined SCaBP immunoreactivity in basal cell carcinoma (BCC) since BCC cells retain some of the characteristics of basal cells, including the capacity for proliferation and migration from the dermo‐epidermal junction. We also examined immunoreactivity to basement membrane zone (BMZ) antigens (type IV collagen, laminin and bullous pemphigoid antigen) in BCC. We found that all BCC cells showed SCaBP immunoreactivity regardless of the histological type or position of the cells. BMZ antigens were expressed around tumourous buds, although bullous pemphigoid antigen may also present a cytoplasmic immunoreactivity. Our results suggest that SCaBP immunoreactivity is independent of the basal position of the cell, but may be related to the proliferative capacity and the undifferentiated state of the cell.

The Immunotracing of Keratinocyte Subsets

It is a well-established concept that mammalian cells may express antigenic properties linked to a given stage of their development or differentiation. Such a differentiation often runs parallel with the acquisition and/or the loss of functional properties by the cell. When an immunological marker becomes available for the tracing of a given cell line at a given stage of its differentiation it becomes easy, using simple immunotracing techniques, to recognize the corresponding cell subset in vivo within tissues, or in vitro in cultured cells. Moreover if the cell subset expressing the distinct antigen is involved in a specific function, the immunotracing technique provides a tool for investigating its function in physiologic and pathologic conditions.