Epidermal cytoplasmic antibodies as detected by hrp-labelled antisera.
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Animals↗
Biomedical subjects
L Didierjean
Publications and source records attributed to L Didierjean.
[Differentiation antigens in keratinocytes II: cytoplasmic specificity expressed in the basal cell of the external root sheath of hairs but not in the basal cells of epidermis].
By means of indirect immunofluorescence with sera obtained from patients after bone marrow transplantation it has been demonstrated that antibodies were reacting with the cytoplasm of basal cells ((C.B.C.) in the external root sheath of hairs (E.R.S.). Some sera were found to react with C.B.C. of the E.R.S. but not with the C.B.C of the epidermis. The change in the antigenic properties of the basal cells was found to be situated at the orifice of the sebaceous gland duct.
Antibody Formation↗
Immunofluorescent tracing of cytoplasmic components involved in keratinocyte differentiation.
Sera with epidermal cytoplasmic antibodies (E.C.A.) produced by human subjects after bone marrow transplantation have been studied by indirect immunofluorescen on rabbit lip sections. These sections were used in order to give on a single specimen, areas of mucosa, of parakeratotic and of orthokeratotic epithelium. It has been demonstrated that E.C.A. distinguished the basal cell layer from the upper cell layers on the three areas. Moreover, E.C.A. were not found to react identically on mucosal, parakeratotic and orthokeratotic epithelium. These findings strongly suggest that the target antigens for E.C.A. are molecules involved in keratinocyte differentiation.
Animals↗
[Differentiation antigens in keratinocytes].
By means of indirect immunofluorescence with human sera it has been demonstrated that cytoplasmic components of the basal cell layer showed antigenic differences as compared to the upper cell layers. Moreover there were differences whether the cells were involved in a mucous, a parakeratinized or an orthokeratinized differentiation.
Animals↗
Cytoplasmic and HL-A antigens in the human epidermis.
HL-A antisera were found to react, in indirect immunofluorescence on human skin, with the cytoplasm of the upper cell layers of the epidermis. It has been established that this staining was not due to an HL-A-antigen-antibody reaction but rather to a contamination of HL-A antisera with non-HL-A epidermal cytoplasmic antibodies. These findings ruled out a previous hypothesis that HL-A antigens were expressed in the cytoplasm of the upper epidermal cell layers. The localization of HL-A antigens in the human epidermis has not been demonstrated by use of indirect immunofluorescence.
Cytoplasm↗
[Anticytoplasmic antibodies of human epidermal cells (author's transl)].
Antibodies reacting with the cytoplasm of epidermal cells (E. C. A.) were defected by indirect immunofluorescence (I.I.F.) studies of 255 sera in various dermatoses (8 p. 100) and significantly more frequently (46 p. 100) in bone marrow transplanted patients having skin lesions. Bound E.C.A. were only found in two cases. E.C.A. were found to be devoided of any diagnostic value. E.C.A. were interpreted as the result of a skin injury liberating skin antigens which stimulated their production. The reaction of E.C.A. in I.I.F. on human skins substrates showed three different patterns; in some cases only the basal cell layer was stained; in others only the supra basal layers were stained; in other all the layers were stained. A serum was shown to be able to give the three patterns of reaction (or no reaction at all) if different human skins were used as substrate. Autologous skins never gave a basal cell layer staining. These findings support the facts that (I) there is antigenic differences between the basal cell layer and the supra basal layers (with regard to the cytoplasmic antigens) (II) these antigens may be different from one subject to the other, supporting the allogeneic nature of this system. Therefore, E.C.A. are regarded as a useful marker of the human skin cytoplasmic antigens.
Animals↗
[Coexistence of lichen planus and bullous pemphigoid (an immunofluorescence study of a "lichen pemphigoides") (author's transl)].
A 35 year old black man presented with a generalized eruption of lichen planus; subsequently tense blisters appeared within the lichenoid lesions and on clinically normal skin. Histopathological characteristics of lichen planus were present in the papules, and those of bullous pemphigoid were seen in the bullae taken from non-lichenoid skin. Direct immunofluorescence studies revealed immunological characteristics of lichen planus in skin and mucosal lesions of L. P. Bound IgG and beta1 C/beta1 A with tubular patterns were detected at the dermo-epidermal junction in all the skin fragments (clinically normal skin, bullous lesions lichenoid skin and mucous lesions). Indirect immunofluorescence studies showed at several intervals that the patient had circulating antibasement membrane zone antibodies (IgG; titres 1/50). This is the third published case in which immunofluorescence studies have established the "pemphigoid" nature of some bullous lichen planus. These findings are in favour of an immune disorder in lichen planus.
Adult↗
Skin antibodies in bone marrow transplanted patients.
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Adolescent↗
The lichen planus-like eruption after bone marrow transplantation.
A lichen planus-like eruption was seen in four patients after bone marrow transplantation. The skin and mucous membrane appearance closely mimicked lichen planus. The histopathology was also very similar to lichen planus. The occurrence of a lichen planus-like eruption (LPLE) after an immune basal cell damage related to the graft-versus-host reaction raised the question of the immune nature of this eruption. The correlation found between biological signs of graft-versus-host reaction and the out-break or relapse of the lichen planus-like eruption supports the hypothesis that the skin changes could be a sign of a chronic immune response against recipient epidermis.
Adolescent↗
Spectral properties of topical retinoids prevent DNA damage and apoptosis after acute UV-B exposure in hairless mice.
We showed in a recent study that topical retinyl palmitate prevented UV-B-induced DNA damage and erythema in humans. Given that retinyl palmitate is a precursor of retinoic acid, the biological form of vitamin A that acts through nuclear receptors, we wondered whether these protective effects toward UV-B exposure were either receptor dependent or linked to other properties of the retinoid molecule such as its spectral properties. We determined the epidermal retinoid profile induced by topical retinoic acid in hairless mice and analyzed its effect on markers of DNA photodamage (thymine dimers) and apoptosis following acute UV-B exposure; we compared these effects to those induced by other natural topical retinoids (retinaldehyde, retinol and retinyl palmitate) which do not directly activate the retinoid receptors. We then analyzed the direct action of these retinoids on UV-B-induced DNA damage and apoptosis in cultured A431 keratinocytes. Topical retinoic acid significantly decreased (approximately 50%) the number of apoptotic cells, as well as the formation of thymine dimers in the epidermis of mice exposed to acute UV-B. Interestingly, the other topical retinoids decreased apoptosis and DNA damage in a similar way. On the other hand, neither retinoic acid nor the other retinoids interfered with the apoptotic process in A431 keratinocytes exposed to UV-B, whereas DNA photodamage was slightly decreased. We conclude that the decrease of apoptotic cells in hairless mouse epidermis following topical retinoids and UV-B irradiation reflects a protection of the primary targets of UV-B (DNA) by a mechanism independent of the activation of retinoid nuclear receptors, rather than a direct inhibition of apoptosis.
Animals↗