Prevention of Cutaneous Penetration and CD1c+ Uptake of Pollen Allergens by a Barrier-Enhancing Formulation.

Recent studies have shown that pollen proteins can penetrate the impaired skin barrier of atopic patients and exacerbate their disease. In the presented study the effect of a topically applied barrier-enhancing formulation was investigated for its preventive effect on the uptake of pollen allergens into CD1c+ epidermal cells. The pollen proteins were fluorescence labelled and applied on barrier-disrupted excised human skin. CD1c+ cells were selected after magnetic cell sorting and analysed using laser scanning microscopy. In untreated disrupted skin, 81% of the CD1c+ cells contained the fluorescence-labelled pollen allergens. In formulation-pretreated skin only 12% of the CD1c+ cells showed an uptake of pollen allergens. These results encourage the treatment of atopic patients with barrier-enhancing formulations to reduce the impact of pollen on air-exposed skin areas and hence the exacerbation of cutaneous symptoms.

Human CD1d functions as a transplantation antigen and a restriction element in mice.

To study the potential functions of human CD1d (hCD1d), we developed transgenic (Tg) mice that ectopically express hCD1d under the control of H-2K(b) promoter. High levels of hCD1d expression were detected in all Tg tissues tested. Skin grafts from the K(b)/hCD1d Tg mice were rapidly rejected by MHC-matched non-Tg recipient mice, suggesting that hCD1d can act as transplantation Ags. Furthermore, we were able to elicit hCD1d-restricted CD8(+) CTLs from mice immunized with K(b)/hCD1d Tg splenocytes. These CTLs express TCR rearrangements that are distinct from invariant TCR of NK T cells, and secrete significant amounts of IFN-gamma upon Ag stimulation. Analysis with various hCD1d-expressing targets and use of Ag presentation inhibitors indicated the recognition of hCD1d by CTLs did not involve species or tissue-specific ligands nor require the processing pathways of endosomes or proteasomes. Additionally, the reactivity of hCD1d-specific CTLs was not affected by acid stripping followed by brefeldin A treatment, suggesting that CTLs may recognize a ligand/hCD1d complex that is resistant to acid denaturation, or empty hCD1d molecules. Our results show that hCD1d can function as an alloantigen for CD8(+) CTLs. The hCD1d Tg mice provide a versatile model for the study of hCD1d-restricted cytolytic responses to microbial Ags.

Efecto de la interleucina 1ß sobre la expresión de la molécula de adhesión ICAM-1 soluble tras una agresión endotóxica experimental / Effect of interleukin 1- on expression of the adhesion molecule ICMs-1 following experimental endotoxic shock

Introducción. Durante el síndrome de respuesta inflamatoria sistémica, la célula endotelial expresa en su membrana moléculas de adhesión, favoreciendo la acción lesiva local de los leucocitos polimorfonucleares de neutrófilos. En este trabajo estudiamos el efecto que ejerce la administración de interleucina 1ß murina sobre la expresión de la molécula de adhesión intercelular (ICAM-1) soluble tras una agresión endotóxica. Material y métodos. Se han dividido 72 ratones de la cepa CBA/H en tres grupos de 24: grupo 1 (simulado); grupo 2 (control, el shock endotóxico se provocó mediante la inyección de lipopolisacárido de membrana bacteriana de Escherichia coli serotipo 055:B5 a dosis de 125 mg/kg); grupo 3 (tratado con interleucina 1ß murina a dosis de 80 ng/ratón 24 h antes del lipopolisacárido de membrana). Se han determinado, mediante la técnica de ELISA, las concentraciones séricas de ICAM-1 soluble a las 1, 2, 4 y 24 h de inyectar el lipopolisacárido. Resultados. El tratamiento con interleucina 1ß provocó un significativo descenso de las concentraciones séricas de ICAM-1 soluble a las 4 y 24 h tras la agresión endotóxica respecto al grupo control. Conclusiones. La administración de interleucina 1ß disminuye las concentraciones séricas de ICAM-1 soluble, que aparecen elevadas tras una agresión endotóxica experimental (AU)