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Biomedical subjects

A Kapp

Publications and source records attributed to A Kapp.

At least 181 records · Page 10Linked to original sources
PubMed1993

Granulocyte activation in bullous diseases: release of granular proteins in bullous pemphigoid and pemphigus vulgaris.

BACKGROUND: Eosinophil and polymorphonuclear granulocytes may be involved in the formation of blisters in bullous dermatoses, particularly bullous pemphigoid. OBJECTIVE: Our purpose was to evaluate the role of granulocyte activation in the pathogenesis of pemphigus vulgaris and bullous pemphigoid. METHODS: Levels of eosinophil cationic protein (ECP) and neutrophil-derived myeloperoxidase (MPO) in blister fluid and serum and levels of serum IgE were determined in patients with bullous pemphigoid (n = 12), those with pemphigus vulgaris (n = 9) and healthy volunteers (n = 12). RESULTS: In blister fluid and serum of patients with bullous pemphigoid, significantly elevated concentrations of ECP, MPO and IgE were detected as compared with controls. In contrast, ECP, MPO, and IgE levels in blister fluid and serum of patients with pemphigus vulgaris did not significantly differ from controls. Moreover, the MPO/ECP ratio in serum of patients with bullous pemphigoid was significantly decreased as compared with controls, whereas the MPO/ECP ratio in pemphigus vulgaris did not differ from controls, indicating a preferential activation of eosinophils in bullous pemphigoid only. In patients with bullous pemphigoid, serum levels of ECP and MPO significantly decreased during immunosuppressive therapy to levels similar to those of controls. CONCLUSION: Activated granulocytes, releasing their granular contents such as ECP and MPO, may be of importance for blister formation in bullous pemphigoid and may be useful for monitoring disease activity.

Aged↗
PubMed1993

The role of cytokines in the psoriatic inflammation.

Psoriasis represents an inflammatory skin disorder which is characterized by a marked hyperproliferation of keratinocytes in association with vascular expansion, fibroblast activation, leukocyte infiltration, alterations of eicosanoid metabolism and of cytokine production. However, it is unclear at present whether these changes may be a cause or a result of the significantly increased keratinocyte turnover. More than one mechanism is involved in triggering active psoriasis, particularly a genetic predisposition and environmental factors affecting the immune system. Most of the therapeutic regimes used for the treatment of psoriasis are immunosuppressive. Therefore, it is tempting to speculate that a specific defect of the immune system represents an important pathogenic principle in psoriasis. There are several lines of evidence that changes in cytokine production by keratinocytes and immunocompetent cells in the skin of the patients (particularly of interleukin-6 and TGF-alpha) may play an important role in the propagation of the inflammatory response in psoriasis. Further studies are required to reveal the role of a local T-cell activation as a basic mechanism for initiation and maintenance of the psoriatic inflammatory response. Accordingly, parameters, such as the evaluation of cytokine production in vitro and in vivo, as well as the measurement of cellular activation products, may be useful tools for diagnosis and monitoring of psoriasis.

Autoimmune Diseases↗
PubMed1993

Phorbol-12-myristate-13-acetate-treated human keratinocytes express B7-like molecules that serve a costimulatory role in T-cell activation.

In previous studies, Phorbol-12-myristate-13-acetate (PMA)-treated human keratinocytes (PMA-HNK) were shown to induce T-cell proliferation via a major histocompatibility complex (MHC)- and antigen (Ag)-independent mechanism, that was mediated in part by PMA-induced intercellular adhesion molecule (ICAM)-1 on HNK. Recently, the interaction of the B7 Ag on antigen-presenting cells with its ligand CD28 on T cells has been shown to deliver activation signals distinct from the interaction of MHC/Ag with the T-cell receptor. These findings led us to assess whether B7-dependent signals play a role in T-cell proliferation induced by PMA-HNK. We first examined B7 expression on HNK by staining with three different monoclonal antibodies (MoAbs). When analyzed by fluorescence-activated cell sorter, untreated HNK stained only faintly. By contrast, PMA induced a dose-dependent upregulation of B7 staining. This staining identifies a molecule closely related to B7 because it was blocked by purified recombinant B7 immunoglobulin. Upregulation of B7 staining was first observed 16 h after PMA treatment and persisted for at least 48 h; it was protein kinase C dependent and required de novo protein synthesis. Anti-B7 MoAbs reduced specifically the capacity of PMA-HNK to trigger proliferation of allogeneic peripheral blood mononuclear cells and T cells. The combination of anti-B7 and anti-ICAM-1 MoAbs further reduced this response. We conclude that PMA upregulates on HNK the expression of a B7-like molecule that contributes in concert with ICAM-1 to the capacity of PMA-HNK to induce proliferation of allogeneic T cells.

Animals↗
PubMed1993

Induction of intercellular adhesion molecule 1 (ICAM-1) expression in normal human eosinophils by inflammatory cytokines.

Intercellular adhesion molecule-1 (ICAM-1) functions as a ligand for lymphocyte function-associated antigen-1 (LFA-1), and thereby plays a crucial role in mediating cell-cell interactions in inflammatory reactions. Human eosinophils represent important effector cells in allergic skin diseases. To gain more insight into the capacity of eosinophils to physically interact with LFA-1-positive inflammatory leukocytes, in the present study ICAM-1 expression in eosinophils was investigated. Using fluorescence-activated cell sorter analysis, it could be shown that highly purified (> or = 95%) eosinophils from peripheral blood of non-atopic individuals do not constitutively express ICAM-1 molecules. However, stimulation of eosinophils with interferon gamma (IFN gamma), tumor-necrosis factor alpha (TNF alpha), or interleukin 3 (IL-3) markedly upregulated ICAM-1 surface expression in a time- and dose-dependent manner. Cytokine-induced ICAM-1 expression in human eosinophils was corroborated by Northern blot analysis. Accordingly, unstimulated eosinophils did not express significant amounts of ICAM-1 mRNA, but ICAM-1 mRNA expression could be markedly induced in these cells upon stimulation with IFN gamma plus TNF alpha. The combination of TNF alpha with either IFN gamma, IL-3, IL-5, or granulocyte/macrophage colony-stimulating factor (GM-CSF) increased ICAM-1 expression in a synergistic fashion, whereas IL-5 or GM-CSF by itself did not induce ICAM-1 expression. Cytokine-induced ICAM-1 expression was specific, because IL-1 alpha, IL-1 beta, IL-2, IL-4, IL-6, IL-7, IL-8, C5a, and platelet-activating factor did not significantly affect eosinophil ICAM-1 surface expression. In summary, these studies indicate that eosinophils may be activated to express the adhesion molecule ICAM-1 upon stimulation with selected inflammatory cytokines, which may allow adhesion-mediated cross-talk between eosinophils and LFA-1-positive cells. In addition, these data demonstrate for the first time a role for IL-3, IL-5, and GM-CSF in regulation of ICAM-1 expression in human cells.

Antigens, CD↗
PubMed1993

The involvement of eosinophils in the patch test reaction to aeroallergens in atopic dermatitis: its relevance for the pathogenesis of atopic dermatitis.

Atopic dermatitis (AD) is considered a T-cell mediated disease. Activated T-cells, mainly of the CD4-subtype, are abundantly present in lesional AD skin. Although not many intact eosinophils are present, deposits of eosinophil derived major-basic-protein (MBP) and eosinophil-cationic-protein (ECP) suggest eosinophil involvement. After patch testing AD patients with aeroallergens, an eczematous reaction develops after 24-48 hr at the site of application. This patch test reaction shows macroscopic resemblance to lesional AD skin and does not take place in normal individuals, asthma and allergic rhinitis patients. Lymphocytes together with eosinophils infiltrate into the dermis 2-6 hr after allergen application. Twenty-four to forty-eight hours after patch testing, eosinophils are in an activated state since they release ECP (being EG2-positive). At this point in time eosinophils have also infiltrated the epidermis. Here they are EG2-negative. Forty-eight to seventy-two hours after patch testing the eczematous reaction decreases. This coincides with disappearance of eosinophils from both the dermis and the epidermis; then, a dendritic staining pattern can be observed in the epidermis with anti-eosinophil peroxidase. Thus, eosinophils infiltrate the dermis and epidermis after patch testing AD patients with aeroallergens and release part of their granular constituents. Recent in vitro investigations revealed that eosinophils from the circulation of AD patients react more powerfully in in vitro test systems such as chemiluminescence, chemotaxis and endothelial adherence and transmigration. It is very likely that this activated (= primed) state is caused by the influence of lymphocyte-derived cytokines like IL-3, IL-5 and GM-CSF, since activated lymphocytes in the circulation (and tissue) may release these cytokines. The primed state of the eosinophils may facilitate tissue infiltration. The subsequent activation of eosinophils within the tissue leading to mediator release and the function of these mediators need to be further elucidated. The close similarity between the cellular events after a patch test reaction to aeroallergens in AD patients and those present in lesional AD skin suggests that the patch test reaction may be a helpful in vivo model to study the pathogenesis of AD. The prominent involvement of lymphocytes and eosinophils in this reaction also suggests some similarity with late phase reactions (LPR) observed in the skin after intracutaneous allergen challenge.

Allergens↗
PubMed1993

The role of eosinophils in the pathogenesis of atopic dermatitis--eosinophil granule proteins as markers of disease activity.

Currently, there is a large body of evidence that atopic dermatitis (AD) has an immunologic basis. Atopy-specific helper T cells (Th2-like T cells) may play a pathogenetic role by producing and releasing cytokines relevant for the allergic inflammation, such as IL-4, IL-5, and other growth factors. Eosinophils are believed to be of major importance as effector cells mediating the pathogenetically relevant late-phase reaction which is associated with a significant destruction of the surrounding tissue. Accordingly, a significant preactivation of peripheral blood eosinophils was detected in AD patients, leading to an enhanced susceptibility of these cells to distinct stimuli such as IL-5. Toxic proteins, such as eosinophil cationic protein (ECP), contained in the matrix and the core of secondary granules of eosinophils, may play an important role by propagating the allergic inflammatory process and by modulating the immune response. The pathogenetic role of eosinophils in AD is further supported by the detection of these proteins in the eczematous skin of patients. Furthermore, recent data point to a significant correlation between disease activity and deposition of eosinophil granule content: ECP serum levels were significantly increased in AD patients. In addition, ECP levels correlated with the disease activity. Moreover, clinical improvement was associated with a decrease of both the clinical score and serum ECP levels. These data clearly indicate that activated eosinophils may play a major role in the allergic inflammatory process of AD. Therefore, modulation of eosinophil activation could prove to be an important pharmacologic modality for the treatment of AD.

Cytokines↗
PubMed1993

Lymphocyte subsets, sIL2-R and sICAM-1 in blood during allergen challenge tests in asthmatic children.

In order to study cell activation in peripheral blood on bronchial allergen provocation up to 24 h, we investigated 32 asthmatic children, sensitive to house-dust mites. Six healthy young adult volunteers served as controls. Lymphocyte subsets (CD3, CD19, CD4, CD8) and activation markers (CD25-T, HLADR-T, CD23) in peripheral blood as well as soluble IL2-R and soluble ICAM-1 in serum were evaluated. In terms of clinical reaction, 23 children exhibited a DAR, 6 an EAR, 6 a LAR and 3 children did not show a bronchoconstrictor response to allergen challenge with house-dust mite extract (NAR). In comparison to controls, asthmatic children showed a significantly higher expression of CD23 on B-lymphocytes (p < 0.05). Other subsets were in the same range in both groups. After provocation there was a significant increase of CD4/CD8-ratio only in asthmatic children. Serum levels of sIL2-R were significantly higher in asthmatic children compared to controls at baseline as well as at 12 and 24 h after provocation, without variation during observation period. No differences were noted for sICAM-1. Our results confirm the hypothesis that lymphocytes, as important cells in regulation of allergic immune response, are recruited into peripheral blood under allergen challenge conditions in sensitized asthmatic children.

Adolescent↗
PubMed1993

Human cell adhesion molecule uvomorulin is differentially expressed in various skin tumors.

The cell adhesion molecule uvomorulin is important in cell recognition processes, both during tissue formation in embryonic development and in the maintenance of adult epithelia. In addition, uvomorulin appears to play a crucial role in carcinogenesis. Therefore, in the present study, the expression of uvomorulin in normal human skin and several benign and malignant proliferative skin lesions was evaluated by immunofluorescence microscopy using affinity purified antibodies. In normal human epidermis, basal and suprabasal keratinocytes showed a strong and homogeneous staining of the cell membrane. In contrast, uvomorulin expression was decreased in squamous cell, as well as in solid basal cell, carcinoma. Interestingly, solid basal cell carcinoma showed a dimorphic staining pattern with a reduced fluorescence of the inner cell layers and normal staining of the peripheral basal cells. In contrast, no such dimorphic staining pattern could be observed in squamous cell carcinoma, in which uvomorulin expression was homogeneously reduced. Decreased expression of uvomorulin was not specific for malignant skin lesions, since it could also be observed in condylomata acuminata. These studies demonstrate that human uvomorulin is differentially expressed in proliferative skin disorders, which may account at least in part for the differences observed in the clinical course between squamous cell and basal cell carcinoma.

Cadherins↗
PubMed1993

The 55-kD tumor necrosis factor receptor on human keratinocytes is regulated by tumor necrosis factor-alpha and by ultraviolet B radiation.

In previous studies we showed that cultured human keratinocytes expressed the 55-kD TNF receptor (TNFR) and that its expression the important for TNF alpha-mediated upregulation of intercellular adhesion molecule-1 (ICAM-1) expression on keratinocytes. Because factors that either reduce or enhance TNFR expression are likely to have a major impact on the biological effects of TNF alpha on keratinocytes, these studies were conducted to determine the factors that regulate its expression on keratinocytes. Using reverse transcriptase polymerase chain reaction, human keratinocytes were shown to lack 75-kD TNFR expression, indicating that TNF responsiveness of human keratinocytes critically depended on regulation of 55-kD TNFR expression. Human keratinocyte 55-kD TNFR surface and mRNA expression was found to be regulated in vitro by recombinant human (rh) TNF alpha. Stimulation of keratinocytes with rhTNF alpha initially decreased, but later increased, 55-kD TNFR surface expression. This biphasic modulation of 55-kD TNFR surface expression was associated with concomitant changes in 55-kD TNFR mRNA expression. Ultraviolet B (UVB) radiation, a well-known inducer of synthesis and secretion of TNF alpha by human keratinocytes, was found to mimic TNF alpha-induced modulation of 55-kD TNFR surface and mRNA expression via a TNF alpha-mediated autocrine regulatory mechanism. Production of soluble 55-kD TNFR by human keratinocytes remained unaffected by TNF alpha stimulation or UVB irradiation. These studies provide clear evidence that membrane expression of the human 55-kD TNFR may be regulated in human keratinocytes by the ligand itself: TNF alpha. Since in previous studies UVB irradiation transiently inhibited TNF alpha-induced human keratinocyte ICAM-1 expression, it is proposed that UVB radiation-induced biphasic modulation of human keratinocyte 55-kD TNFR expression may affect the capacity of these cells to respond to TNF alpha.

Base Sequence↗
PubMed1993

[The role of eosinophilic granulocytes for the pathogenesis of atopic dermatitis /neurodermatitis. Eosinophilic products as markers of disease activity].

Recent data provide increasing evidence for an immunological basis of atopic dermatitis (AD). Atopyspecific helper T cells (Th2-like T cells) may play a pathogenic role by producing and releasing cytokines that are relevant for the allergic inflammation, such as IL-4, IL-5 and other growth factors. It is suggested that eosinophils play a major role as effector cells mediating the pathogenetically important late-phase reaction, which is associated with significant destruction of the surrounding tissue. Accordingly, a significant preactivation of peripheral blood eosinophils was detected in AD patients, leading to enhanced susceptibility of these cells to distinct stimuli, such as IL-5. Toxic proteins, such as eosinophil cationic protein (ECP), which are contained in the matrix and the core of secondary granules of eosinophils, may play an important role by propagating the allergic inflammatory process and by exerting their direct immunomodulatory effects. A pathogenic role of eosinophils in AD is further supported by the detection of these proteins in eczematous skin of the patients. Furthermore, recent data indicate a significant correlation between disease activity and deposition of eosinophil granule content: ECP serum levels were significantly increased in AD patients. In addition, ECP levels correlated with the disease activity. Moreover, clinical improvement was associated with a decrease both in the clinical score and in serum ECP levels. These data clearly indicate that activated eosinophils are involved in the allergic inflammatory process in AD. Therefore, modulation of eosinophil activation could be an important pharmacologic modality for the treatment of AD in the future.

Allergens↗
PubMed1993

[The role of cytokines for the pathogenesis of psoriasis].

Psoriasis is an inflammatory skin disorder characterized by marked hyperproliferation of keratinocytes in association with vascular expansion, fibroblast activation, leucocyte infiltration, and alterations of eicosanoid metabolism and of cytokine production. However, it is unclear at present whether these changes are the cause or the effect of the significantly increased keratinocyte turnover. More than one mechanism is involved in triggering active psoriasis; genetic predisposition and environmental factors affecting the immune system have a particularly important role. Most of the therapeutic regimens used for the treatment of psoriasis are immunosuppressive. Therefore, it is tempting to speculate that a specific defect of the immune system is the major pathogenic principle in psoriasis. There are several lines of evidence suggesting that changes in cytokine production by keratinocytes and immunocompetent cells in the skin of the patients, particularly of interleukin-6 and TGF alpha, may play an important part in propagation of the inflammatory response in psoriasis. Further studies are required to find how far local T-cell activation is involved as a basic mechanism of initiation and maintenance of the psoriatic inflammatory response. Accordingly, parameters such as the evaluation of cytokine production in vitro and in vivo and the measurement of cellular activation products may be useful in the diagnosis and monitoring of psoriasis.

Cytokines↗
PubMed1992

High-dose UVA1 therapy in the treatment of patients with atopic dermatitis.

BACKGROUND: Besides glucocorticosteroids, there is currently no known effective therapy for patients with acute atopic dermatitis. OBJECTIVE: The therapeutic effectiveness of high-dose UVA1 irradiation in the management of patients with acute exacerbation of atopic dermatitis was examined. METHODS: Patients in the high-dose UVA1 group (n = 15) were irradiated with 130 joules/cm2 UVA1; the control group (n = 10) was treated with UVA-UVB therapy in a minimal erythema dose-dependent manner (total number of treatments 15). RESULTS: High-dose UVA1 irradiation was found to induce a significant clinical improvement of atopic dermatitis (p less than 0.001). In comparison with UVA-UVB therapy, significant differences in favor of high-dose UVA1 were observed (p less than 0.01). High-dose UVA1, but not UVA-UVB treatment, significantly reduced the elevated serum level of eosinophil cationic protein in patients with atopic dermatitis (p less than 0.003). CONCLUSION: These studies indicate that high-dose UVA1 irradiation may represent a novel phototherapeutic modality for the treatment of patients with an acute exacerbation of atopic dermatitis.

Adult↗
PubMed1992

Ultraviolet radiation effects on human keratinocyte ICAM-1 expression: UV-induced inhibition of cytokine-induced ICAM-1 mRNA expression is transient, differentially restored for IFN gamma versus TNF alpha, and followed by ICAM-1 induction via a TNF alpha-like pathway.

Human keratinocytes (KC) during the course of inflammatory dermatoses strongly express the surface molecule ICAM-1, which plays an important role in the generation of the epidermal inflammatory infiltrate by mediating leukocyte-keratinocyte interactions. Accordingly, KC ICAM-1 expression is known to be induced in vivo and in vitro by cytokines either via the TNF alpha/TNF beta or via the IFN gamma-mediated pathway. In contrast, ultraviolet (UV) radiation previously has been found to potently inhibit cytokine-induced KC ICAM-1 surface expression by a sublethal mechanism. In order to further define this novel immunosuppressive effect of UV light, the effects of in vitro UV radiation on ICAM-1 mRNA expression in transformed human KC (KB cells) were examined. Accordingly, UV light (0-100 J/m2) inhibited IFN gamma- as well as TNF alpha-induced ICAM-1 mRNA expression, if KC were cytokine stimulated immediately after irradiation. After a 12-h incubation period, however, IFN gamma responsiveness was found to be restored in irradiated cells, whereas restoration of responsiveness to TNF alpha required at least a 24-h recovery phase. Moreover, UV light alone did not alter ICAM-1 mRNA levels after 4, 12, or 24 h. After 48 h, however, a significant increase in ICAM-1 mRNA and surface expression in UV-irradiated KC could be observed. In addition, this increase could be superinduced by stimulation of irradiated KC with IFN gamma, but not with TNF alpha. UV-induced upregulation of ICAM-1 expression could be mimicked by stimulating unirradiated cells with supernatants derived from UV-irradiated cells. Addition of biologically active anti-TNF alpha antibodies to UV-irradiated cells or to supernatants derived from UV-irradiated KC, however, did not even partially abolish this ICAM-1-inducing activity. UV light thus seems to affect KC ICAM-1 mRNA expression in a biphasic manner: an early period of inhibition of cytokine-induced ICAM-1 expression is transient and followed by restoration of responsiveness to ICAM-1-inducing cytokines. Moreover, UV itself is able to induce ICAM-1 mRNA expression at this later time point via a TNF alpha-like pathway. These studies identify UV irradiation as a potent modulator of cytokine regulated ICAM-1 gene transcription with the capacity to induce both inhibitory as well as enhancing effects.

Blotting, Northern↗
PubMed1992

Increased levels of inflammatory cytokines in human skin lymph derived from sodium lauryl sulphate-induced contact dermatitis.

A superficial peripheral lymph vessel draining the skin of the upper and medial part of the foot was cannulated on the lower leg of six healthy human volunteers. After 2 days an irritant contact dermatitis was induced by application of 10% sodium lauryl sulphate to the area of skin drained by the lymph vessel. Three days later the spontaneously regressing skin reaction was treated with clobetasol propionate. Lymph was collected twice daily for 7 days, and the levels of various cytokines (IL-1 alpha, IL-1 beta, IL-2 and soluble IL-2 receptors, IL-6, IL-8, TNF-alpha, GM-CSF) were determined by ELISA technique. In the majority of the volunteers all cytokines examined were detected in several lymph samples, with the exception of IL-1 alpha and IL-8. In parallel with the clinical symptoms of the contact dermatitis the levels of IL-6 and TNF-alpha increased 8-10-fold, whereas for IL-1 beta, IL-2, IL-2 receptors, and GM-CSF there was a delayed, 2-3-fold increase. These results suggest that cytokines, in particular IL-6 and TNF-alpha, may actively participate in the immunological reactions in the skin and in the regional lymph nodes during contact dermatitis.

Cytokines↗
PubMed1992

Serum eosinophil cationic protein (ECP) is a sensitive measure for disease activity in atopic dermatitis.

Atopic dermatitis (AD) is characterized by alterations in cellular and humoral immunity including elevated serum levels of IgE, IL-2 receptor (IL-2R) and eosinophil cationic protein (ECP). In order to evaluate the relevance of these serum parameters as indicators of disease activity, the concentrations of IgE, IL-2R and ECP were measured in serum samples of patients with an acute exacerbation of AD (n = 19) on admission to hospital and every 6 days up to discharge, and compared with those from normal non-atopic controls (n = 15). The severity of the disease in the AD patients was examined using an established clinical scoring system. On admission, AD patients showed significantly elevated serum levels of IgE, IL-2R and ECP compared with normal controls (P less than or equal to 0.0001). Clinical improvement was associated with a decrease of both the clinical score (P less than or equal to 0.001) and serum ECP levels (P less than or equal to 0.005). No significant changes in serum IgE and serum IL-2R were observed. In addition, there was a significant correlation between serum ECP and the clinical score (R = 0.67, P less than or equal to 0.001). These data indicate that serum ECP may be a helpful tool for monitoring disease activity in AD.

Acute Disease↗
PubMed1992

Human epidermal keratinocytes are a source of soluble ICAM-1 molecules.

A soluble form of the usually membrane-bound adhesion molecule ICAM-1 was detected in supernatants derived from human epidermal keratinocytes. Specifically, supernatants harvested from long-term cultured normal human keratinocytes, or from the spontaneously immortalized keratinocyte cell line HaCaT, did not contain significant amounts of sICAM-1, but shedding of sICAM-1 was found to be markedly induced upon stimulation of keratinocytes with rh IFN gamma. In contrast, cells from the two epidermoid carcinoma cell lines, KB and A431, constitutively shed significant amounts of sICAM-1 even without cytokine stimulation, and sICAM-1 contents in supernatants harvested from these cells were further increased upon stimulation of cells with rh IFN gamma. These studies indicate, that in addition to peripheral blood mononuclear cells and human melanoma cells, human epidermal keratinocytes constitute an important cellular source of sICAM-1. By binding to leukocyte LFA-1 molecules, keratinocyte-derived sICAM-1 may influence inflammatory responses in the skin. In addition, constitutive shedding of sICAM-1 by transformed human keratinocytes may represent a possible mechanism by which neoplastic keratinocytes escape from cytotoxicity.

Cell Adhesion↗
PubMed1991

[Pathogenesis of atopic dermatitis].

Atopic dermatitis shows a familial disposition and is characterised clinically by extreme pruritus, typical eczematoid pathology and distribution on the integument, a chronic relapsing course, and a personal or familial history of atopic diseases (allergic bronchial asthma, rhinitis and allergic conjunctivitis, atopic dermatitis), as well as numerous other stigmata and microsymptoms. Although numerous exogenous factors help trigger the disease, more recent findings point to an immunological basis. In recent years, numerous cellular malfunctions of immune cells have been reported, with disturbances in T-lymphocyte predominating. The latest investigations now suggest that the reported changes in the immune response are due to an imbalance in the cytokine network. Thus, it has been observed that disturbances of cytokine production depend upon the severity of the disease, and show an AD-characteristic pattern. The pathogenesis of atopic dermatitis however, is not yet fully understood.

Dermatitis, Atopic↗