Human interferon-γ induces expression of HLA-DR on keratinocytes and melanocytes

Summary Primary human epidermal cell cultures composed of keratinocytes and melanocytes were exposed to supernatants of phytohaemagglutinin (PHA)-stimulated T cells, various lymphokines and interferon-, and checked for the emergence of HLA-DR antigen using immunofluorescence and immunoelectron microscopy. HLA-DR expression was induced by the supernatants and human recombinant interferon- (rIFN-), whereas recombinant ₂, interleukin-2 and non-recombinant human interferon- had no such effect. The threshold concentration of rIFN- required to induce this phenomenon was 10 IU/ml; no further increase of reaction intensity was observed using doses of more than 100 IU/ml. Maximum reaction intensity was achieved after 72 h of incubation; a minimum of 3 h of incubation with rIFN- followed by 72 h incubation in rIFN--free medium proved sufficient to induce HLA-DR expression. The inductive effect of the supernatants and rIFN- could be completely abrogated by pretreatment with excess doses of the monoclonal antibody GZ4 specific for human IFN-. Keratinocytes and melanocytes reacted in an identical fashion both qualitatively and quantitatively in all experiments. These data indicate that IFN- possesses specific signal functions in the induction of HLA-DR expression on epidermal cells.Abbreviations IFN- interferon- - rIFN- recombinant interferon- - r IFN-₂ recombinant interferon-₂ - nrIFN- nonrecombinant interferon- - IL-2 interleukin-2 - EC epidermal cells - K keratinocytes - M melanocytes     

Permeability barrier disruption alters the localization and expression of TNFα/protein in the epidermis

Previous studies have shown that (1) epidermal TNF mRNA levels are increased following acute disruption of the cutaneous permeability barrier; (2) this increase is maximal at 1 h and decreases to control levels by 8 h; and (3) in essential fatty acid-deficient (EFAD) mice, a chronic model of barrier perturbation, TNF mRNA levels are also elevated several-fold over controls. In the present study we determined, using immunocytochemical procedures, epidermal TNF protein levels following either acute of chronic barrier disruption and the localization of any increase. Frozen, paraffin and Antibed sections of skin were incubated with polyclonal anti-mouse TNF antisera and detection was accomplished by either immunoperoxidase or fluorescence procedures. We found that (1) TNF-immunoreactive protein was present in normal mouse epidermis, and was primarily localized to the upper nucleated layers where it displayed a diffuse cytosolic pattern; (2) acute disruption of the barrier with acetone or tape-stripping resulted in TNF staining that was more intense throughout all of the nucleated epidermal cell layers in comparison with normal epidermis; (3) the increase in TNF staining occurred as early as 2 h after barrier disruption; and (4) increased TNF staining was also observed in the stratum corneum of EFAD mice. These results indicate that epidermal TNF protein levels increase after both acute and chronic barrier disruption, and are consistent with the hypothesis that TNF may signal and/or coordinate portions of the cutaneous response to barrier disruption.     

Absence of tumor necrosis factor-α in suction blister fluids and stratum corneum from patients with psoriasis

Summary Tumor necrosis factor (TNF)- is a cytokine with multiple biological properties, particularly proinflammatory, apart from the induction of tumor necrosis. In order to elucidate the role of TNF- in the pathogenesis of psoriasis, we have carried out bioassay and enzyme-linked immunosorbent assay for TNF- in suction blister fluids and horny tissue extracts from psoriatic skin. Although bioassay showed some activities in the suction blister fluids and horny tissue extracts, there were no significant differences between the levels of activities from normal and psoriatic skin. They were at the background level and pretreatment of the samples with anti-TNF- antiserum failed to abrogate the activities. ELISA confirmed the absence of TNF-. Therefore, the present study could not verify that TNF- plays a major role in the pathogenesis of psoriasis.     

Effects of interferon-γ treatment on the cutaneous DTH reaction in rats

Summary The capacity of interferon- (IFN-) to induce class II histocompatibility antigens on different cell types including keratinocytes, is well known, but the impact of IFN- on the immune response is still unclear. Lewis rats sensitized with dinitrofluorobenzene (DNFB) were injected with recombinant rat IFN- (10⁵ U) or phosphate-buffered saline (PBS) once daily on 3 successive days at the bases of the ears either before or after they were challenged on the ears. As expected, the PBS-treated animals showed about a 30% increase in ear thickness and there was an induced expression of class II antigens on the keratinocytes as judged by immunohistochemistry 72 h after challenge. Exogenously added IFN- prior to DNFB challenge resulted in a significantly reduced ear swelling at 24 (p<0.01) and 48 h (p<0.05) after challenge. In this case the keratinocytes expressed class II antigens already at the time of challenge. When IFN- injections were given during the contact allergic reaction there was no significant reduction of ear swelling until 72 h (p<0.01). At that time point there was a more pronounced expression of class II antigens on the keratinocytes compared with PBS-injected animals, due to the IFN- treatment. These in vivo data support our previous observations that IFN- may play a self-limiting role in certain immune responses.     

The fatty-acid spectrum in plasma and adipose tissue in patients with psoriasis

Summary The long-chained fatty acids, which are precursors of prostaglandins and leukotrienes, were examined in plasma lipid esters and adipose tissue obtained from 20 male psoriatic patients and 36 matched controls. The fatty-acid composition of the plasma lipid esters (cholesterol esters, triglycerides and phospholipids) and adipose tissue was assayed using thin-layer and gas chromatography. In comparison with healthy controls, the patients' plasma lipid esters contained significantly lower levels of linoleic acid (18:2 6) and -linolenic acid (18:3 3), and higher levels of dihomo--linolenic acid (20:3 6). In the adipose tissue of the patients, the amount of -linolenic acid was significantly decreased, while that of arachidonic acid (20:4 6) was increased. The observed changes were more pronounced in patients with severe psoriasis than in those with a milder form of the disease. Our results suggest that psoriatic patients differ from healthy controls with regard to the distribution of several of the essential long-chained fatty acids involved in the biosynthesis of prostaglandins and leukotrienes. The relevance of these findings to the development of psoriasis remains to be established.     

Der Einfluß von Δ 1-Dehydro-Hydrocortison auf das Verhalten proteingebundener Kohlenhydrate im Blutserum bei Neurodermitis diffusa

Zusammenfassung Bei 14 Patienten mit Neurodermitis diffusa wurde das Verhalten der Serumeiweißzucker nach Applikation von ₁-Dehydro-Hydrocortison untersucht. Deutlich war den Befunden eine Verminderung von Glucosamin an Albumin, -und -Globulin. Die proteingebundenen Hexosen stiegen unter der Therapie an und zeigten sich zumeist an Albumin, -und -Globulin vermehrt.     

Effect of tumour necrosis factor alpha in vivo on human granulocyte oxidative metabolism

Summary Tumour necrosis factor alpha (TNF) effectively stimulates the oxidative metabolism of human PMN in vitro. Moreover, preincubation of PMN with TNF has been shown to result in an altered response of the target cells to subsequent stimulation. In the present study the response of PMN to stimulation in vitro was investigated in patients with metastasizing malignant melanoma receiving bolus injections of recombinant human TNF as therapy. TNF was given daily for 5 days. Blood samples were taken prior to TNF administration on days 1 to 4 and on day 8. Lucigenin-enhanced chemiluminescence (CL) was used as a sensitive measure of granulocyte oxidative metabolism. PMN were stimulated with TNF, TNF, GM-CSF, PMA, opsonized zymosan and f-met-leu-phe. A significant increase in CL responses was detected upon stimulation with TNF, TNF and PMA from day 1 to day 3, whereas no significant changes were observed for the background activity or when GM-CSF or opsonized zymosan were used as stimuli. On day 4 all CL responses returned to the day 1 starting level. A further significant decrease was observed on day 8 upon stimulation with TNF, TNF and GM-CSF. In contrast, the effect induced by f-met-leu-phe reached a maximum on day 4, but the CL response was found to be at the starting level on day 8. The results indicate that TNF induces significant changes in PMN response to distinct stimuli in vivo. Moreover, it may be possible that continous daily infusions with TNF induce a hyposensitization of PMN oxidative metabolism.     

Mast cell proteinases and cytokines in skin inflammation

The role of mast cells in provoking immediate-type hypersensitivity reactions is well established, but their involvement in chronic inflammation and immune reactions is not so clear. Mast cells synthesize and secrete large amounts of active proteinases, including tryptase, chymase, carboxypeptidase and cathepsin G, which can rapidly process numerous biologically active peptides and proteins or their precursors. Furthermore, mast cells are able to produce a variety of cytokines such as interleukin-4 (IL-4), IL-5, IL-6, tumour necrosis factor- (TNF-) and interferon- (IFN-) which are known to be intensively involved in modulating and directing inflammatory responses in the skin. In this review, the role of mast cell proteinases and cytokines in skin inflammation is discussed.     

Pro-inflammatory cytokines upregulate the skin immunoreactivity for NGF,NT-3, NT-4 and their receptor,p75NTR in vivo: a preliminary report

Skin and hair follicles are both source and target of various cytokines and neurotrophins (NTs). While several pro-inflammatory cytokines are recognized to alter the expression of NTs and their receptors (NTRs), for example, on brain cells and fibroblasts in vitro, it is unknown whether this also occurs in normal mammalian skin in vivo. As a first step toward exploring this, we studied in murine back skin (C57BL/6) whether intradermally injected interleukin-1 (IL-1), tumor necrosis factor- (TNF-), and interferon- (IFN-) altered the cutaneous immunoreactivity patterns of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin-4 (NT-4), Trk-A, Trk-B, Trk-C and p75NTR and their receptors (TrkA, TrkB, TrkC, p75NTR) on the protein level in situ. By immunohistology, IFN, IL-1, and TNF- as well as a cocktail of all three cytokines increased NGF immunoreactivity (IR) in the proximal outer root sheath and hair matrix of anagen VI pelage hair follicles. The cytokine cocktail upregulated NT-3 and NT-4 IR in the epidermis, increased NT-4 IR in selected cells of the proximal outer root sheath, and also enhanced IR of p75NTR, in the follicular dermal papilla. Therefore, this pilot study provides the first preliminary indications that proinflammatory cytokines upregulate the cutaneous immunoreactivity of NGF, NT-3, NT-4 and their receptor p75NTR in vivo. This raises the question to which extent several of the recognized cutaneous effects of IFN, IL-1 and TNF- are mediated indirectly via modulating the expression of selected NTs and/or NTRs.Holger Bläsing and Sven Hendrix have contributed equally     

Immunoelektrophoretische Untersuchungen an Hautkranken

Zusammenfassung Immunoelektrophoretische Serumanalysen bei 113 Patienten mit verschiedenen Hauterkrankungen ergaben bei Purpura hyperglobulinaemica Waldenström, Antikörpermangel-Syndrom und Xanthomatosen der Haut krankheitsspezifische Serumeiweißbilder.Die Waldenströmsche Purpura zeigt ein charakteristisches Makroglobulin im ₂-Bereich. Beim Antikörpermangel-Syndrom fehlt das -Globulinsystem ganz oder teilweise. Bei den Xanthomatosen der Haut findet sich eine massive Vermehrung von -und ₂-Lipoproteinen und eine Verstärkung des ₂-Makroglobulins. Das ₁-Lipoprotein erscheint unverändert. Es finden sich keine Unterschiede zwischen hyperlipidämischen und hypercholesterinämischen Formen.Entzündliche Erkrankungen der Haut und der HautgefÄße zeigen häufig eine Vermehrung von Proteinen aus der Gruppe der -Glykoproteine und des -Globulinsystems, und zwar vorwiegend des ₂-Makroglobulins und des ₂-Makroglobulins.     

Expression of guanine nucleotide binding proteins,Gs and Gi,in mRNAs in epidermal keratinocytes

Summary The stimulation or inhibition of adenylate cyclase by hormones and chemicals is mediated by the stimulatory or inhibitory guanine nucleotide-binding proteins, Gs and Gi respectively. Although the presence of these G-proteins in the epidermis has been suggested, no direct information regarding their nature has been available. Using cDNAs for these G-proteins as a probe, we investigated the nature of the G-proteins of various keratinocytes. FRSK cells, a cell line derived from fetal rat epidermal cells, and SV-40-transformed human epidermal cells, both of which are highly proliferative keratinocytes, contained mRNAs for both Gs- and two Gi- proteins (Gi-2 and -3). No evidence for the presence of Gi-1 or Go- was obtained. Normal human or pig epidermis had a relatively small amount of mRNAs for these G-proteins in the stable (hypoproliferative) condition. Tape-stripping-induced, and UVB-induced hyperproliferative epidermis contained an increased amount of these G-protein messages. However, all Gs-, Gi-2 and -3, as well as -actin mRNAs, were increased to a similar extent, and no specific expression of G-protein messages could be detected in the hyperproliferative epidermis.     

Effects of tumor necrosis factor-α on connective tissue metabolism in normal and scleroderma fibroblast cultures

Recent studies have demonstrated that tumor necrosis factor-(TNF-) selectively decreases production of collagens I and III, the major types of collagen in the dermis, and increases production of collagenase in cultured dermal fibroblasts. The effects of TNF- on collagens I, III and VI, fibronectin and collagenase gene expression by fibroblasts derived from normal individuals and patients with systemic sclerosis (SSc) were studied. SSc is characterized by excessive accumulation of collagen in the skin and in certain organs. TNF- inhibited collagen production and mRNA levels of collagens I and III and of fibronectin, and stimulated collagenase activity and collagenase mRNA levels in SSs fibroblasts. Levels of mRNA for 1(VI) and 3(VI) collagen and for -actin were unaltered in SSc fibroblasts incubated with TNF-. Similar results were observed for mRNA levels in normal fibroblasts incubated with TNF-. These results suggest that TNF- could be expected to be beneficial in the treatment of SSc. In addition, our results indicated that collagen-VI expression is regulated independently from expression of collagens I and III, and expression of fibronectin and collagens I and III are regulated in parallel in fibroblasts treated with TNF-.     

A fibroblast cell line cultured from a hypertrophic scar displays selective downregulation of collagen gene expression: barely detectable messenger RNA levels of the proα1(III) chain of type III collagen

The present study was designed to investigate the expression of type I, III and VI collagens by a fibroblast cell line initiated from a hypertrophic scar. The same tissue has previously been demonstrated to display markedly elevated expression of type I and III collagen mRNAs in vivo. Unexpectedly, slot-blot and Northern hybridizations revealed a barely detectable steady-state level of pro1(III) collagen chain mRNA in cultured hypertrophic scar fibroblasts. The levels of pro1(I) and 2(VI) collagen chain mRNAs were essentially the same in fibroblasts cultured from hypertrophic scar and in fibroblasts cultured from normal skin. However, Northern blot analyses indicated that the ratio of 5.8 kb to 4.8 kb species of pro1(I) collagen mRNA was slightly reduced in fibroblasts originating from the hypertrophic scar compared to that in normal fibroblasts. When normal fibroblasts were incubated in conditioned medium from hypertrophic scar cultures, the expression of pro1(III) collagen chain mRNA decreased to a markedly lower level. Our studies suggest that collagen synthesis by fibroblasts in hypertrophic scars is stimulated by humoral factors which are active only in vivo. Furthermore, the results suggest that fibroblasts cultured from hypertrophic scar display a selective downregulation of different collagen genes and that this downregulation is exerted through an autocrine mechanism.     

Thalidomide upregulates macrophage inflammatory protein-1α in a herpes simplex virus-induced Behçet’s disease-like animal model

The mechanism of action of thalidomide in the treatment of patients with Behçets disease (BD) is poorly understood. There is some evidence to suggest that certain immunological abnormalities are associated with the pathogenesis of BD. A BD-like mouse model induced by herpes simplex virus (HSV) inoculation shows similar immunological abnormalities. In this study, thalidomide was administered in order to understand the mechanism for the improvement in symptoms in BD-like mice. Eight out of ten thalidomide-treated mice showed improvement but none of ten placebo-treated mice (P<0.005). The improvements were seen in mucocutaneous symptoms. The mice were sacrificed on the 6th day, and the spleens subjected to RT-PCR, FACS, Western blot and immunohistochemical analysis. IL-2, IL-4, IL-6, IL-10, IFN-, TNF, TGF, MCP-1, RANTES, perforin, IP-10, FasL, FasR and MIP-1 were determined. Among these, TNF, MIP-1, perforin and Fas were influenced by thalidomide treatment. These results suggest that thalidomide can attenuate HSV-induced BD-like symptoms in mice through the downregulation of TNF (P<0.005) and the upregulation of MIP-1 (P<0.005), perforin (P<0.05) and FasR (P<0.1).Abbreviations BD Behçets disease - COX Cyclooxygenases - FasL Fas ligand - FasR Fas receptor - MIP-1 Macrophage inflammatory protein-1 - HSV Herpes simplex virus - IFN Interferon - IL Interleukin - iNOS Inducible nitric oxide synthase - IP-10 Interferon-gamma-inducible protein-10 - LPT Lymphotactin - MCP Monocyte chemotactic protein - PI Propidium iodide - RANTES Regulated on activation normal T-cell expressed and secreted - TGF Tumor growth factor - TNF Tumor necrosis factor     

Ultrastructural localization of lectin binding sites in human melanocytes

Summary The ultrastructural localization of carbohydrate residues in human melanocytes of normal epidermis and of one compound naevus was studied. The following lectins were used in a post-embedding technique: 1. peanut agglutinin (PNA), which reacts specifically with N-acetyl-galactosamine; 2. Concanavalia ensiformis (Con A) indicating -d-glucose and -d-mannose binding sites; 3. Ulex europaeus agglutinin (UEA I) specific for -l-fucose; 4. Wheat germ agglutinin (WGA), reacting specifically with N-acetyl-glucosamine and neuraminic acid (sialic acid); and 5. Limax flavus agglutinin (LFA), also specific for sialic acid (Neu5Ac--2,3-Gal and Neu5Ac--2,6-Gal). When incubated with WGA, Con A and LFA strong labelling was seen within the cytoplasm and in the plasma membrane of melanocytes, whereas incubations with PNA and UEA I revealed an occasional gold particle only. The determination of the distribution of carbohydrate residues in normal melanocytes is a prerequisite for future studies of abnormal melanocytes.     

Effect of UVB radiation on the biosynthesis of HLA-DR antigens

Summary HLA-DR molecules on the surface of immunocompetent cells are thought to represent target structures for the immunomodulating effects of UV radiation during the induction of an immune response. We therefore investigated the effect of UVB radiation on the de novo synthesis of HLA-DR--chains in the cytoplasm and the expression of - and -chains on the surface of the human lymphoblastoid B-cell line Raji. Raji cells were UVB irradiated before biochemical experiments were performed. Cells were then metabolically labeled or radioiodinated and detergent lysates immunoprecipitated using antibodies directed against the - or the - and -chain of the HLA-DR molecule. Over a wide dose range, UVB-irradiated Raji cells were shown to still express HLA-DR determinants on their surface and, even more importantly, to be capable of synthesizing HLA-DR-, - and -chains in a normal fashion. Despite this, the functional capacity of Raji cells was impaired in a dose-dependent manner. UV radiation thus seems to exert its immunomodulating effects primarily at a different level than the incriminated immune-response-associated antigens, which are expressed as recognition structures on the surface of immunocompetent cells.     

Effects of adrenergic stimulating and blocking agents on the eccrine sweat secretion in atopic dermatitis and psoriasis

Summary Quantitative measurements of eccrine sweat secretion following stimulation with adrenaline and terbutaline sulphate, a-stimulator, have been performed in patients with atopic dermatitis and psoriasis by means of the electrolytic water analyzer, Meeco. Seasonal variations were demonstrated, the values being lower in the late autumn. The response to adrenaline could be blocked by phentolamine, an -inhibitor, while propranolol, a-inhibitor, had no effect.—The response to terbutaline was blocked by atropine and partly by practolol, a-inhibitor. Terbutaline induced a larger sweat response than isoprenaline, another-stimulator. A-receptor mechanism, in some way related to cholinergic receptors, is suggested.

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Zusammenfassung Die ekkrine Schweißabgabe nach intradermaler Infektion von Adrenalin und Terbutalin sulfat, einem-Stimulator, wurde mittels des elektrolytischen Wasser-Analysators Meeco quantitativ gemessen. Saison-abhängige Variationen wurden festgestellt, wobei eine signifikante Verminderung im Herbst beobachtet wurde. Die adrenalininduzierte Schweißabgabe wurde mittels Phentolamin, einem -Inhibitor, aber nicht mittels Propranolol, einem-Inhibitor, blockiert. — Das Terbutalin-induzierte Schwitzen wurde durch Atropin eindeutig, aber durch Practolol, ein-Inhibitor, nur teilweise blockiert. Terbutalin induzierte eine größere Schweißaktivität als Isoprenalin, ein anderer-Stimulator. Die Resultate deuten auf einen-Receptoren-Mechanismus in den ekkrinen Schweißdrüsen hin, der vielleicht in engem Zusammenhang mit cholinergischen Receptoren steht.

     

Arzneimittelexanthem durch pegyliertes Interferon-α<Subscript>2b</Subscript>

Zusammenfassung Im Vergleich zu rekombinantem "Standard"-Interferon-_2b führt die Anwendung von pegyliertem Interferon-_2b zu einer signifikant erhöhten Ansprechrate in der Therapie der chronischen Hepatitis C. Häufige Nebenwirkungen der Interferontherapie sind lokale, entzündliche Hautreaktionen an der Injektionsstelle. Wir beschreiben den Fall einer 57-jährigen, an Hepatitis C erkrankten Patientin, die im Rahmen einer Therapie mit pegyliertem Interferon-_2b ein generalisiertes, makulopapulöses Arzneimittelexanthem entwickelte. In der allergologischen Testung induzierten nur pegyliertes Interferon-_2b, nicht aber herkömmliches "Standard"-Interferon-_2b eine Hautreaktion vom Spättyp.

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Pegylated interferon-_2b-induced drug eruption

In comparison to recombinant "standard"-interferon-_2b, treatment with pegylated interferon-_2b significantly improves the therapeutic response of patients suffering from chronic hepatitis C. The most common side effect of interferon-_2b therapy is localized inflammatory skin lesions at sites of injection. A 57-year-old woman with hepatitis C infection developed a generalized maculopapular exanthem during the treatment with pegylated interferon-_2b. In contrast to recombinant "standard"-interferon-_2b, only pegylated interferon-_2b induced a delayed-type skin reaction during allergy testing.

     

Distribution of carbohydrate residues in normal skin

Summary Sections of biopsies of normal skin obtained from 11 individuals were incubated with 8 lectins using an avidin-biotin complex (ABC). All sections when incubated with the appropriate lectin showed the presence of the following carbohydrate residues: l-fucose, -(1–4)-d-GlcNAc)₂ (N-acetylglucosamine), acetylneuraminic acid, Gal--(1–3)-GalNAc (N-acetyl-galactosamine), -d-galactose, -d-glucose, and -d-mannose. In addition, sections of individuals with blood group A showed -d-GalNAc and sections of individuals with blood group B showed -d-galactose. In the stratum (str.) basale, carbohydrates were present in small quantities, but as the cells matured and moved upward, the incorporation of carbohydrates into the cell membranes increased considerably. In the str. granulosum, lectin reactivity was absent in many sections, probably due to masking by phospholipids. The dark cells in the eccrine glands showed reactivity with all lectins except in the one nonsecretor with blood group A₁, whose dark cells showed no l-fucose and -d-GalNAc. The endothelial cells of the blood vessels showed lectin reactivity except when incubated with concanavalin A. The sebaceous glands showed both cytoplasmic and membrane staining when incubated with various lectins.     

A Review of the Use of Infliximab to Manage Cutaneous Dermatoses

Background Infliximab is a chimeric monoclonal antibody that binds specifically to human tumor necrosis factor-alpha (TNF-), decreasing the effect of the cytokine in inflammatory diseases.Objective The aim of this study was to review the efficacy and safety of infliximab in the treatment of dermatological diseases.Methods A MEDLINE search (1966–January 2003), using the keyword infliximab was performed to find relevant articles pertaining to the use of infliximab in dermatology.Results Infliximab has been used in the following dermatological diseases: psoriasis, Behçets disease, graft versus host disease, hidradenitis suppurativa, panniculitis, pyoderma gangrenosum, SAPHO (synovitis, acne, pustulosis, hyperostosis and osteitis) syndrome, sarcoidosis, subcorneal pustular dermatosis, Sweets syndrome, toxic epidermal necrolysis, and Wegeners granulomatosis. There is a generally good safety profile for infliximab, which is similar to that when it is used to treat Crohns disease and rheumatoid arthritis.Conclusion Although not approved for use in dermatological diseases, there have been numerous reports of the efficacy of infliximab in cutaneous inflammatory diseases. The most promise lies in those diseases that have increased amounts of TNF- in the cutaneous lesions, such as psoriasis.

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SommaireAntécédents Linfliximab est un anticorps monoclonal chimérique qui se lie au facteur de nécrose des tumeurs alpha (TNF-), réduisant ainsi leffet de la cytokine dans les maladies inflammatoires.Objectif Passer en revue lefficacité et linnocuité de linfliximab dans le traitement des maladies de la peau.Méthodes Une recherche dans MEDLINE (de 1966 à janvier 2003) a été effectuée afin de trouver les articles pertinents à lusage de linfliximab en dermatologie, au moyen du terme clé « infliximab ».Résultats Linfliximab a été utilisé dans le traitement des affections suivantes: psoriasis, maladie de Behçet, maladie du greffon contre lhôte, hidrosadénite, panniculite, pyoderma gangrenosum, syndrome de SAPHO (synovite, acné pustulose palmo-plantaire, hyperostose et ostéite), sarcoïdose, dermatose pustuleuse sous-cornée, syndrome de Sweet, nécrolyse épidermique toxique et granumatulose de Wegener. Le profil dinnocuité de 1inflimixab est généralement bon, similaire au profil dinnocuité dans le traitement de la maladie de Crohn et de la polyarthrite rhumatoïde.Conclusion Bien que linfliximab ne soit pas approuvé pour le traitement des maladies de la peau, plusieurs rapports en prouvent 1efficacité contre les maladies inflammatoires cutanées. Le traitement à linfliximab semble le plus prometteur dans les maladies avec une forte présence de TNF- dans les lésions cutanées, telles que le psoriasis.

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Funding for the publication of this article was provided by Centocor, Inc., Malvern, PA, USA.