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Biomedical subjects

T Bieber

Publications and source records attributed to T Bieber.

At least 145 records · Page 8Linked to original sources
PubMed1991

Atopic eczema, Langerhans cells and allergy.

While the pathomechanisms of respiratory atopy are rather well established, the role of IgE-mediated hypersensitivity in the elicitation and maintenance of eczematous skin lesions in atopic eczema is still controversial. Few diseases are characterized by an equally elevated production of IgE antibodies as atopic eczema. Many authors, however, regard this only as epiphenomenon. On the other hand, there is clearcut clinical evidence for exogenous elicitation of atopic eczema by contact with aero or food allergens. A variety of hypotheses may help to explain the participation of IgE antibodies in the induction of eczema: vasoactive mediators secreted by skin mast cells or basophils after allergen contact may produce itch, contact urticaria or a 'late-phase-reaction' with consequent eczematous skin changes further maintained by scratch responses. Recent investigations stress a possible role of Langerhans cells in the epidermis with a low affinity receptor for IgE with possible function for antigen presentation, mediator release or regulatory interactions. Certain cytokines such as interleukin-4 or gamma-interferon are able to enhance the expression of the IgE-receptor on the surface of Langerhans cells. IL-4 and gamma-interferon act synergistically in this respect on Langerhans cells, contrary to B cells. Furthermore lymphocytes may act directly via certain cytokines (e.g. histamine releasing factor, chemotactic factors etc.) on mast cells or eosinophil granulocytes in a proinflammatory sense. Eosinophils seem also to be involved in the inflammatory response in atopic eczema by releasing products such as major basic protein (MBP) or eosinophil cationic protein (ECP) which has been found to be elevated in severe atopic eczema.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗
PubMed1990

Human epidermal Langerhans cells express only the 40-kilodalton Fc gamma receptor (FcRII).

In man, three distinct classes of receptors for the Fc fragments of IgG (FcRI, II, III) have been defined. The FcRI has a Mr of about 72 kDa, binds human IgG-coated E, and is recognized by mAb such as 32. The FcRII has a Mr of 40 kDa, binds murine IgG1-coated E, and reacts with the mAb IV.3 and CIKM5, which recognize CDw32 moieties. Lastly, the FcRIII has a Mr of 50 to 70 kDa and is recognized by anti-CD16 mAb. In the present study we have shown that i) only murine IgG1-coated E form rosettes with 49 +/- 1.5% (mean +/- SEM, n = 9) of CD1a+ epidermal cells (EC) (which represent Langerhans and indeterminate cells) and that ii) the mAb anti-FcRII CIKM5 prevents this rosette formation. Among the mAb reacting with the three different types of FcR, only those recognizing FcRII i) stain about 55 +/- 1.5% (mean +/- SEM, n = 9) of the CD1a+ EC and ii) reveal the presence of dendritic cells in epidermal sheets obtained by suction blister. Under the electron microscope i) apparently all the cells forming rosettes or reacting with the gold-labeled anti-FcRII mAb (CIKM5 or the F(ab) fragment of IV.3) contained Birbeck granules and ii) the gold-labeled mAb were internalized in unfixed Langerhans cells by receptor-mediated endocytosis and accumulated in lysosomes. Labeling by the anti-FcRII mAb of the CD1a+ cells in suspension disappears after 48 h of culture. All these observations strongly suggest that CD1a+ EC express only the FcRII. This conclusion was confirmed by immunoprecipitation experiments, whereas no specific immunoprecipitate was noted with the anti-FcRI or anti-FcRIII mAb, the anti-FcRII mAb immunoprecipitated a protein of Mr 40 kDa.

Antibodies, Monoclonal↗
PubMed1990

Fc receptors of human Langerhans cells.

Receptors for the Fc fragment of immunoglobulins (Fc R) exhibit specificities for a wide variety of immunoglobulin classes and subclasses. In humans, at least three distinct classes of receptors for the Fc fragments of IgG (Fc gamma RI, II, III) and two classes of receptors for the Fc fragments of IgE (Fc epsilon RI, II) have been characterized. These classes were largely defined on the basis of their affinities for different immunoglobulin subclasses and their reactivities with monoclonal anti-receptor antibodies. Among these FcR, in healthy individuals, epidermal Langerhans cells (LC) express only the Fc gamma RII/CDw32. This FcR--a member of the immunoglobulin superfamily--is only present on about 50% of freshly isolated CD1a positive cells, as determined by rosette assays. It has a Mr of 40 kDa, is trypsin resistant, binds polymeric human IgG and murine IgG1-coated erythrocytes, and reacts with anti-CDw32 monoclonal antibodies (MoAb). LC internalize Fc gamma RII by receptor-mediated endocytosis. After 48 h of culture, human LC loose their Fc gamma RII, as revealed by flow cytometry. While the function(s) of the Fc gamma RII on human LC remain(s) unknown, this receptor may be primarily involved, like the Fc gamma RII present on mouse macrophages, in the clearance of extra-cellular immune complexes. In patients with atopic dermatitis having an elevated IgE serum level, beside an increased expression of the Fc gamma RII by LC located on lesional skin, IgE-bearing epidermal and dermal LC are present, again essentially on lesional skin. Double immunolabeling on cryosections reveals that on lesional skin only about 50% of the epidermal CD1a positive cells bear IgE. This capacity of LC to bind IgE molecules appears to be due to the presence of a specific Fc epsilon R. While the class of this Fc epsilon R still remains unclear, it appears to have some particularities: i) an associated expression with the CD1a antigen, ii) an affinity for IgG, and iii) a trypsin resistance. In vitro, human recombinant interleukin (IL)-4 and/or interferon (IFN)-gamma are able to induce the synthesis and expression of Fc epsilon RII/CD23 on a percentage of normal human epidermal LC. This Fc epsilon RII seems to be functional since it binds IgE molecules, this binding being prevented by preincubation with anti-CD23 MoAb.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Platelets↗
PubMed1990

[Langerhans cells in the physiopathology of atopic dermatitis].

INTRODUCTION. Atopic dermatitis (AD), allergic rhino-conjunctivities and allergic asthma constitute the classical triad of atopic diathesis attended, in many cases, by high serum IgE levels. While the pathophysiology of IgE-mediated allergic respiratory diseases is now better understood, the pathophysiological significance of atopic phenomena in the genesis and control of AD is still far from being clear. Numerous clinical and laboratory data point to a pathophysiological relation between IgE-mediated reactions and AD, but no one yet knows by which mechanism this interaction takes place. Some recent studies suggest that Langerhans cells might well be the missing link. THE LANGERHANS CELLS. Langerhans cells (LC) are dendritic epidermal cells originating in the bone marrow and supposedly belonging to the monocyte lineage. Their circulating precursors, the mechanism of their migration into the epidermis and their relationship with other dendritic cells, such as the interdigitating follicular cells, are controverted. LC express numerous surface markers, such as class I and II HLA, CD1a, CD4 and receptors for complement and IgE Fc fragments. Under normal conditions, LC do not express IgE receptors. Ultrastructurally, LC are characterized by the presence of Birbeck granules in their cytoplasm. Among the presumed functions of LC in the skin, the best documented is the presentation of antigens to T lymphocytes in allergic contact dermatitis. LANGERHANS CELLS IN ATOPIC DERMATITIS. Quantitative studies. Modern immunohistological methods based on the reactivity of monoclonal anti-CD1a antibodies have given results that are sometimes conflicting due to differences in the quantification techniques utilized. However, morphometric enumeration of LC on cryostat sections have shown that their number is about the same in AD and in normal skin. PRESENCE OF IgE BEARING LANGERHANS CELLS IN ATOPIC DERMATITIS. The presence of IgE molecules on the LC surface has been demonstrated in subjects with AD. It must be noted that in atopic subjects IgE bearing Lc are only found in patients with high serum IgE levels. They are absent in asthma patients without eczema, irrespective of their serum IgE levels. Daily applications of corticosteroids on AD lesions result in a decrease of anti-IgE markers on LC after one week and in their complete disappearance after 2 weeks. IN ATOPIC DERMATITIS LANGERHANS CELLS EXPRESS A RECEPTOR SPECIFIC TO Fc FRAGMENTS OF IgE. The exact nature of the receptor for IgE expressed in situ in AD patients is still conjectural. Some authors have been able to demonstrate that the binding of IgE molecules by LC isolated from the skin of atopic patients is inhibited by a monoclonal antibody directed against the low affinity receptor (Fc epsilon R2) of eosinophils and macrophages. This strongly suggests that certain factors induce the expression by LC of an Fc epsilon R2 receptor. IN VITRO INDUCTION OF IgE RECEPTORS ON NORMAL LANGERHANS CELLS...

Dermatitis, Atopic↗
PubMed1990

[Cutaneous amyloidoses].

Significant advances in basic research in biochemistry and immunology has tremendously increased our understanding of amyloidoses. The chemical structure of several amyloid proteins has been partly characterized. Specific antibodies may provide new methods for immunohistological diagnosis of amyloidoses. Cutaneous manifestations can affect the skin only or develop during the course of systemic amyloidoses. Although these conditions are so rare, dermatologists should be aware of the changing clinical manifestations of cutaneous amyloidoses if they wish to avoid diagnostic failures.

Amyloid↗
PubMed1989

Induction of Fc epsilon R2/CD23 on human epidermal Langerhans cells by human recombinant interleukin 4 and gamma interferon.

Human rIL-4 and human rIFN-gamma are able to induce the expression of the low affinity receptor for IgE (Fc epsilon R2/CD23) on normal human epidermal Langerhans cells, whereas IL-2 and PMA have no effect. A synergistic effect is observed when both cytokines are combined. These receptors are synthesized de novo by the LC since cycloheximide completely inhibits the appearance of Fc epsilon R2/CD23. Fc epsilon R2/CD23+ LC may have a major role in the pathogenesis of atopic eczema, as well as in the regulation of IgE synthesis.

Antibodies, Monoclonal↗
PubMed1989

Occurrence of IgE-bearing epidermal Langerhans cells in atopic eczema: a study of the time course of the lesions and with regard to the IgE serum level.

Uninvolved and lesional skin of untreated and treated patients with atopic eczema has been investigated immunohistochemically to determine the conditions in which IgE-bearing CD1a+ Langerhans cells/indeterminate cells (LC/IC) occur in this disease. IgE-bearing epidermal dendritic cells were present in patients with elevated IgE serum level (greater than 300 UI/ml) and the staining pattern was stronger in lesional skin. On double immunostaining, a subpopulation of CD1a+ LC/IC was found not to bear IgE molecules as determined by the ratio IgE+/CD1a+ cells on serial sections as well. The ratio IgE+/CD1a+ cells decreased in patients who underwent a local therapy with glucocorticosteroids. These results suggest that the expression of IgE receptors and/or binding of IgE molecules on epidermal LC/IC in atopic eczema may be controlled by a complex network of mediators from the epidermis or the inflammatory infiltrate, or both, and that this phenomenon could be down regulated by glucocorticosteroids.

Antigens, CD1↗
PubMed1989

Keratinocytes in lesional skin of atopic eczema bear HLA-DR, CD1a and IgE molecules.

Apparently normal, and lesional skin from patients with atopic eczema were investigated immunohistochemically with anti-HLA-DR, -CD1a and -IgE antisera. A CD1a+ intercellular pattern was observed in uninvolved skin in the majority of the patients whereas an HLA-DR+/CD1a+ network, mostly localized in basal and supra-basal areas, was shown in lesional skin of virtually all of them. Moreover, an HLA-DR+/CD1a+IgE+ intercellular pattern was observed in some of the patients only and was predominantly localized in those areas characterized by lymphocyte exocytosis, spongiosis or vesicle formation. Whether keratinocytes are able to synthesize CD1a antigen and Fc epsilon R or if these molecules are only produced and shed by CD1a+/IgE+ epidermal dendritic cells remains unclear.

Antigens, CD↗
PubMed1989

Distribution of CD1a-positive cells in psoriatic skin during the evolution of the lesions.

Normal skin and psoriatic lesions from 35 patients were investigated immunohistochemically with regard to the CD1a+ cell population (Langerhans' cells and indeterminate cells) in the epidermis as well as in the dermal infiltrate. In the normal-appearing skin, we found the regularly typical pattern of CD1a+ dendritic cells in suprabasal position, but in lesional skin of chronic psoriasis the CD1a+ cells were scattered in the acanthotic epidermis. In initial lesions, CD1a+ cells represent up to 50-60% of the infiltrating cells of the dermal compartment, in several cases being preferentially localized in the upper part of the papillar dermis close up to the epidermal CD1a+ cells in basal position, whereas in chronic psoriasis they represent less than 10%. These results suggest that in psoriasis vulgaris, CD1a+ cells actively migrate between the epidermis and the dermal vessels.

Antigens, Surface↗
PubMed1989

[Chronic lichenoid keratosis: disease variant or disease entity?].

The presentation of a new case of keratosis lichenoides chronica (KLC) in a 61-year-old woman lead us to this comprehensive study of the cases already published in the literature. The clinical and histological substrate of KLC and its differential diagnosis and treatment are discussed in detail. The clinical appearance is mainly characterized by an eruption of (1) lichenoid, keratotic papules, (2) linear or plaque-like keratosis, and (3) psoriasis-like scaling lesions on the trunk and extremities. The course of the disease is chronic and progressive. Histopathological study shows variable features, which are similar to those of lichen planus only on rare occasions. This dermatosis does not show any pathological relationship with other dermatological conditions; we therefore suggest that KLC is a distinct entity.

Diagnosis, Differential↗
PubMed1988

Hemorrhagic bullous amyloidosis. A histologic, immunocytochemical, and ultrastructural study of two patients.

In patients with bullous hemorrhagic amyloidosis of the skin, the skin lesions were the first manifestations of a plasma cell dyscrasia. Both cases were characterized by similar clinical, histologic, and ultrastructural findings showing an intradermal blister within deposits of amyloid substances. Immunohistologic investigations with a panel of antibodies directed against amyloid fibril proteins showed reactivity of the amyloid deposits with an anti-A lambda serum in both patients.

Aged↗
PubMed1988

Comparison of different methods for enumeration of Langerhans cells in vertical cryosections of human skin.

We have quantified Langerhans cells (LC) in cryosections of normal human skin and lesional skin from patients with atopic eczema and psoriasis vulgaris using six different methods. The results from the different methods varied considerably and were sometimes contradictory, for example when LC numbers in psoriatic skin were compared with those in normal skin. Thus, in addition to the staining technique used and the selection of the dendritic cell type to be counted, the enumeration method used can also influence the quantitation of LC in normal and pathological skin.

Cell Count↗
PubMed1988

Antiallergic effects of the new histamine H1-receptor antagonist tazifylline in healthy atopic and non-atopic subjects.

Single oral doses (5, 10 and 15 mg) of the new H1-receptor antagonist 3,7-dihydro-7-[2-hydroxy-3-[4-[3-phenylthio) propyl]-1-piperazinyl]propyl-1,3-dimethyl-1H-purine-2,6-dione dihydrochloride (tazifylline, RS-49014) were administered at 7-day intervals to 12 atopic and 12 non-atopic volunteers in a double-blind randomised cross-over study. Antiallergic activity was evaluated from pre to 60 min post dose inhibitions of wheal and flare areas provoked by various cutaneous challenges. Atopic subjects showed greater skin reactivity than non-atopics to some challenges. Tazifylline was associated (in atopics and non-atopics) with statistically significant dose related inhibitions, of flare over 5-15 mg and of wheal (10-15 mg) induced by the more potent and reproducible challenges of codeine, 1% histamine and anti-IgE. Antiallergic activity of tazifylline in the 10-15 mg dose range was superior to 5 mg without the intervention of clinically significant sedative effects at any of the 3 dose levels tested.

Adult↗