Allergic Contact Dermatitis Lesions Research Articles

Allergic contact dermatitis in pediatric practice.

Allergic contact dermatitis (ACD) is prevalent among pediatric population, adolescent and young adults. Patients with ACD experience a lot of sociopsychological and quality-of-life (QoL) difficulties. Children and their caregivers alike are vulnerable to the burden of ACD. We have, in this paper, provided an overview of ACD and discussed common and unusual causes of ACD. We performed an up-to-date literature review in the English language on "allergic contact dermatitis" via PubMed Clinical Queries, using the keywords "allergic contact dermatitis" in August 2022. The search included meta-analyses, randomized controlled trials, clinical trials, case-control studies, cohort studies, observational studies, clinical guidelines, case series, case reports, and reviews. The search was restricted to English literature and children. ACD may be acute or chronic and it affects more than 20% of children and adults with significant quality-of-life impairments. ACD is manifested by varying degrees of cutaneous edema, vesiculation, and erythema. The hypersensitivity reaction is one of the most prevalent forms of immunotoxicity in humans. Localized acute ACD lesions can be managed with high-potency topical steroids; if ACD is severe or extensive, systemic corticosteroid therapy is often required to provide relief within 24 hours. In patients with more severe dermatitis, oral prednisone should be tapered over 2-3 weeks. Rapid discontinuation of corticosteroids can result in rebound dermatitis. Patch testing should be performed if treatment fails and the specific allergen or diagnosis remains unknown. ACD is common and can be a physically, psychologically, and economically burdensome disease. Diagnosis of ACD is primarily based on history (exposure to an allergen) and physical examination (morphology and location of the eruption). Skin patch test can help determine the causative allergen. Allergen avoidance is the cornerstone of management. Topical mid- or high-potency corticosteroids are the mainstay of treatment for lesions on less than 20% of the body area. Severe cases of ACD may require treatment with systemic corticosteroids.

MR1 deficiency enhances IL-17-mediated allergic contact dermatitis.

Major histocompatibility complex (MHC) class Ib molecules present antigens to subsets of T cells primarily involved in host defense against pathogenic microbes and influence the development of immune-mediated diseases. The MHC class Ib molecule MHC-related protein 1 (MR1) functions as a platform to select MR1-restricted T cells, including mucosal-associated invariant T (MAIT) cells in the thymus, and presents ligands to them in the periphery. MAIT cells constitute an innate-like T-cell subset that recognizes microbial vitamin B2 metabolites and plays a defensive role against microbes. In this study, we investigated the function of MR1 in allergic contact dermatitis (ACD) by examining wild-type (WT) and MR1-deficient (MR1-/-) mice in which ACD was induced with 2,4-dinitrofluorobenzene (DNFB). MR1-/- mice exhibited exaggerated ACD lesions compared with WT mice. More neutrophils were recruited in the lesions in MR1-/- mice than in WT mice. WT mice contained fewer MAIT cells in their skin lesions following elicitation with DNFB, and MR1-/- mice lacking MAIT cells exhibited a significant increase in IL-17-producing αβ and γδ T cells in the skin. Collectively, MR1-/- mice displayed exacerbated ACD from an early phase with an enhanced type 3 immune response, although the precise mechanism of this enhancement remains elusive.

Protease‐ and cell type–specific activation of protease‐activated receptor 2 in cutaneous inflammation

BackgroundProtease‐activated receptor 2 (PAR2) signaling controls skin barrier function and inflammation, but the roles of immune cells and PAR2‐activating proteases in cutaneous diseases are poorly understood. ObjectiveTo dissect PAR2 signaling contributions to skin inflammation with new genetic and pharmacological tools. Methods/ResultsWe found markedly increased numbers of PAR2+ infiltrating myeloid cells in skin lesions of allergic contact dermatitis (ACD) patients and in the skin of contact hypersensitivity (CHS) in mice, a murine ACD model for T cell–mediated allergic skin inflammation. Cell type–specific deletion of PAR2 in myeloid immune cells as well as mutation‐induced complete PAR2 cleavage insensitivity significantly reduced skin inflammation and hapten‐specific Tc1/Th1 cell response. Pharmacological approaches identified individual proteases involved in PAR2 cleavage and demonstrated a pivotal role of tissue factor (TF) and coagulation factor Xa (FXa) as upstream activators of PAR2 in both the induction and effector phase of CHS. PAR2 mutant mouse strains with differential cleavage sensitivity for FXa versus skin epithelial cell–expressed proteases furthermore uncovered a time‐dependent regulation of CHS development with an important function of FXa‐induced PAR2 activation during the late phase of skin inflammation. ConclusionsMyeloid cells and the TF–FXa–PAR2 axis are key mediators and potential therapeutic targets in inflammatory skin diseases.

Role of tissue-resident memory T cells in the pathophysiology of allergic contact dermatitis.

We bring updated knowledge on tissue-resident memory T cells (TRM), underlining their major role in the recurrence and the severity of allergic contact dermatitis (ACD). ACD is a frequently encountered skin disease. It is defined as a delayed-type hypersensitivity reaction initiated by the recruitment of antigen-specific T cells into the skin of sensitized patients. ACD lesions tend to develop on already-exposed areas and worsen over time. That clinical observation has raised questions on the contribution of TRM to ACD recurrence and severity. TRM are memory T cells that persist in peripheral tissues, such as the skin, without recirculating through the blood. These cells provide effective immune memory against pathogens, but they may also participate in the development or exacerbation of numerous inflammatory diseases, including skin allergies. Recent works have demonstrated a major role for TRM in ACD pathophysiology. In ACD, TRM accumulate preferentially at the allergen contact site during the sensitization phase. Thereafter, these cells cause a rapid and intense response to any new allergen exposure. They also play a key role in flare-ups of ACD and the chronicity and severity of the disease. These aspects suggest that TRM may have an interest as therapeutic targets.

Irritant Contact Dermatitis.

Contact dermatitis accounts for 95% of occupational skin disorders. Irritant contact dermatitis (ICD) is often caused by cumulative exposure to weak irritants, accounting for 80% of all cases of contact dermatitis. ICD can co-exist with atopic dermatitis (AD) and allergic contact dermatitis (ACD). Patients with AD and ACD may have a lower inflammatory threshold for developing ICD. Therefore, it needs to be distinguished from lesions of AD and ACD. ICD Patients report stinging and burning in excess of pruritus. Pruritus is classically reported by patients with AD and ACD. ICD lesions are typically well-demarcated unlike AD and ACD. ICD is diagnosed by exclusion. Patients undergo testing to rule out type I and type IV hypersensitivity. Negative results suggest a diagnosis of ICD. Management consists of irritant identification and avoidance with regular emollient use. Although ICD is more common in certain occupations, genetics and environment play significant roles in its development.

Histomorphology and Immunophenotype of Eczematous Skin Lesions Revisited-Skin Biopsies Are Not Reliable in Differentiating Allergic Contact Dermatitis, Irritant Contact Dermatitis, and Atopic Dermatitis.

Lesions of allergic contact dermatitis (ACD), irritant contact dermatitis (ICD), and atopic dermatitis (AD) share similar clinical features and thus, their diagnosis can be challenging. The aim of this study was to reassess histopathology and immunophenotyping properties to distinguish between ACD, ICD, and AD. Charts of patients with eczema, who had undergone complete routine diagnostic workup (skin biopsies, patch tests, skin prick tests, and respectively or serum IgE levels), were reviewed. Thirty-five skin biopsy specimens of 28 patients (mean age 64 ± 15 years; ♀ = 13 ♂ = 15) with clear diagnosis of ACD (n = 15), ICD (n = 6), or AD (n = 14) were analyzed. Histomorphological and immunohistochemical (CD3, CD4, CD8, CD11c, CD34, CD123, S100, and IL-17) parameters were evaluated using Kruskal-Wallis test, Wilcoxon test, Fisher exact test, and decision tree analysis. Eosinophils were statistically significant (P = 0.0184), more often observed in AD than in ACD or ICD. No other statistically significant differences were found with regard to epidermal patterns, patterns of dermal infiltrates, or immunophenotyping. Using predictive modeling approaches, dermal eosinophils were found to be associated with AD, necrotic epidermal keratinocytes with ICD, and a focal type of parakeratosis with ACD. As an additional finding, pseudo-Pautrier microabscesses, which were present in the skin of 2 AD and 2 ACD patients, contained myeloid dendritic cells (CD11c). Differentiation of ACD, ICD, and AD should be based on clinical features and results of allergy tests. Histopathology does not reliably differentiate between ACD, ICD, and AD, but helps to exclude psoriasis, tinea, or T-cell lymphoma.

Overexpression of tIK ameliorates DNCB-induced allergic contact dermatitis in BALB/c mice

Abstract Allergic contact dermatitis (ACD) is a delayed type hypersensitivity reaction that is mediated by hapten-specific T cells. Dinitrochlorobenzene (DNCB)-induced contact hypersensitivity of the skin is a commonly-used mice model for studying the pathogenesis of contact dermatitis. IK cytokine is known to suppress IFN-γ induced expression of MHC class II molecules on B cells by increasing cAMP. Recently, we reported that truncated IK (tIK) cytokine-expressed transgenic (Tg) mouse ameliorated inflammatory arthritis symptoms by suppressing the differentiation of TH1 and TH17 cells and the activation of macrophages. However, there are still limited studies showing the functionality of this cytokine in inflammatory diseases such as ACD. Here, we investigated whether tIK cytokine expressing Tg mice are less susceptible for DNCB induced ACD. DNCB treatment caused severe dermatitis symptoms in wild type (WT) including weight loss, increased ear thickness and scratching behavior but those symptoms are significantly reduced in tIK Tg mice. The weights of draining lymph node (dLN) and spleen were also much less in tIKTg mice. In addition, tIK overexpression decreased IgE serum level, mRNA transcript of mast cell associated factors in Tg mice compared to WT mice. Analyzing T cell subpopulation in dLN revealed that Th2 and Th17 cell differentiation were suppressed by tIK expression while Tregs and Th1 differentiation were not affected. Taken together, our results presented here suggest that tIK expression effectively attenuate DNCB induced allergic contact dermatitis lesions by modulation Th cell differentiation. Futher studies are needed to elucidate immunological and molecular mechanisms by which tIK functions on this disease model.

Allergic Contact Dermatitis to Nickel: From Clinical Aspects to Therapeutic Measures

Nickel is the major cause of allergic contact dermatitis. It is a widely spread metal, being therefore very difficult to avoid. Nickel cutaneous allergy can occur in occupational and non-occupational contexts and can result from direct cutaneous contact, systemic as well as airborne exposure. Such allergy can manifest with typical lesions of allergic contact dermatitis or with peculiar features such as follicular erythemato-micropapularvescicular lesions. Diagnosis of allergic contact dermatitis to nickel is based on patch testing, employing nickel sulfate 5% in petroleum jelly. Reactions to patch test have to be assessed at 48-72 hours, and up to 6 days. Nickel contact dermatitis can be managed with the traditional therapeutic approach used in allergic contact dermatitis. As of today, hyposensitization therapy with oral nickel represents to be the only treatment acting on the pathogenetic mechanisms of nickel allergy. Keywords: Allergic contact dermatitis, nickel allergy, nickel sulfate, oral hyposensitization.

Serum osteopontin levels in disseminated allergic contact dermatitis

PurposeThe aim of the study was to evaluate serum osteopontin (OPN) concentrations in patients with disseminated form of allergic contact dermatitis (ACD), and to assess the relationship between serum OPN level and disease severity. Patients and methodsTwenty-four patients with numerous allergic contact dermatitis lesions and twenty-two age- and sex-matched healthy subjects as a control group were enrolled in the study. Serum osteopontin levels were measured in the ACD patients twice: in the acute stage and during disease remission by ELISA. ResultsSerum OPN concentrations were significantly increased in patients with disseminated ACD examined in the acute stage as compared to healthy subjects and ACD patients during remission (p<0.01 and p<0.001, respectively). In the ACD patients with extensive skin lesions (EASI>10), OPN serum levels were significantly higher than in those with mild disease (EASI<10). ConclusionsAcute disseminated ACD is characterized by elevated serum concentrations of osteopontin, with levels depending on ACD severity, which indicates its role in the elicitation phase of allergic contact dermatitis. The possibility of inhibition of OPN activity may create a new therapeutic perspective in severe forms of this troublesome skin disease.

Allergic contact dermatitis: clinical aspects.

The best way to be acquainted with the various facets of clinical lesions of allergic contact dermatitis (ACD) is to refer to the concept of the ACD syndrome. Obtaining differential diagnosis between irritant contact dermatitis and ACD based on clinical grounds is difficult. Moreover, hand eczema and photoalleregic contact dermatitis deserve special attention. The patch test remains the "gold standard" diagnostic tool, but many other very useful complementary tests have been developed in recent years.

CD1d‐dependent, iNKT‐cell cytotoxicity against keratinocytes in allergic contact dermatitis

Conventional CD8+ T-lymphocytes are thought to be major effector cells in allergic contact dermatitis (ACD). However, previous work has demonstrated a significant population of invariant natural killer T-cells (iNKT-cells) in the elicitation phase of ACD. In this study, we investigate whether iNKT-cells have the capacity to serve as effector lymphocytes in ACD. Using in situ staining of skin biopsy specimens from ACD lesions, we observed intra-epidermal iNKT-cells. Presence of these cells provides the possibility of interactions with keratinocytes (KC), Langerhans cells (LC) and CD1d-bearing antigen-presenting cells (APC). Investigation into gene expression profiles of cytotoxic effector molecules in seven different cases of ACD found that the expression of perforin and granzymes A, B and K were significantly elevated in ACD relative to paired clinically normal skin. Immunostaining of ACD skin biopsy specimens revealed that these cytotoxic granules indeed localized to iNKT-cells. Studies of antigen presentation of KC to iNKT-cells show that these epithelial cells do not activate the expression of cytotoxicity effector genes in resting iNKT-cells, but had the capacity to serve as targets for activated iNKT-cells, which was dependent on CD1d expression. Mature LC were not able to present glycolipids to iNKT-cells and did not up-regulate CD1d in vitro to a variety of maturational stimuli or in vivo during ACD. These data suggest that iNKT-cells can serve as effector cells during human ACD and provide the rationale for developing inhibitory glycolipids as therapeutic agents for ACD.

Expression of lymphotoxin-β and its receptor in the skin of a mouse model of allergic contact dermatitis

Objective To investigate the expression of lymphotoxin-β and its receptor in the skin of a mouse model of allergic contact dermatitis (ACD).Methods BALB/c female mice at 6 to 8 weeks of age were randomly divided into the experiment group (n =15) and normal control group (n =10).Topical 2,4-dinitrofluorobenzene (DNFB,0.5％) was used to establish a model of ACD in the experiment group followed by challenge with DNFB (0.2％) at the right external ear on the 6th day.The normal control mice remained untreated.The right external ear was resected from all of the mice 24 hours after the challenge and divided into 2 parts for the measurement of mRNA and protein expressions of lymphotoxin-β and lymphotoxin-βreceptor by fluorescence-based real-time quantitative PCR and immunohistochemistry,respectively.Results The median mRNA expression levels of lymphotoxin-β and lymphotoxin-β receptor were 3.630 and 1.148respectively in the experimental mice,with the interquartile range being 1.187 and 0.617 respectively,and were both 1.000 in the control mice with the interquartile range being both 0.000.There was a significant difference between the experimental and control group in the mRNA expression levels of lymphotoxin-β and lymphotoxin-β receptor (P ＜ 0.01 ).Immunohistochemistry showed a significant increase in the expression of lymphotoxin-β and lymphotoxin-β receptor proteins in the experimental group compared with the control group (P ＜ 0.01 ).Conclusion There is an increment in the mRNA and protein expressions of lymphotoxin-β and lymphotoxin-β receptor in the lesions of ACD in mice.

Antigen-Specific Induction of Osteopontin Contributes to the Chronification of Allergic Contact Dermatitis

Allergic contact dermatitis is a T cell-mediated immune response, which in its relapsing chronic form is of high socioeconomic impact. The phosphoglycoprotein osteopontin (OPN) has chemotactic and Th1 cytokine functions and in various models is essential for robust T cell-mediated immunity. Here we demonstrate that OPN is abundantly expressed by both effector T cells and keratinocytes in allergic contact dermatitis lesions. T cells from nickel-allergic donors secrete high levels of OPN following antigen-specific stimulation. OPN may substitute for missing IFN-gamma secretion in T effector cells because low IFN-gamma-producing T cell clones secrete high levels of OPN, and OPN down-modulates their interleukin-4 expression. Furthermore, interferon-gamma from T effector cells augments OPN in allergic contact dermatitis by inducing OPN in keratinocytes, which in turn polarizes dendritic cells and attracts inflammatory cells. In the murine contact hypersensitivity (CHS) model for allergic contact dermatitis, OPN is strongly induced in antigen-specific proliferating T cells, and OPN null mice display a reduced chronic CHS inflammatory response due to a decreased influx of effector T cells. Importantly, because of its function for chronic allergic contact dermatitis, OPN may well be a therapeutic target, because anti-OPN antibody treatment in part suppresses established chronic CHS.

Expression of neuropeptides and their degrading enzymes in ACD

Sensory neuropeptides such as neurokinin A or substance P modulate skin and immune cells the functions of neurokinin receptor activation during neurogenic inflammation. Zinc metalloproteases, such as neutral endopeptidase (NEP) and angiotensin-converting enzyme (ACE), effectively control the bioavailability of these neuropeptide mediators, which are released from sensory nerves, immune and skin cells during cutaneous responses to endogenous or exogenous noxious stimuli. Recently, studies have suggested that neuropeptides are one of the major pathogenetic fact in many dermatoses, such as allergic contact dermatitis (ACD), atopic dermatitis and psoriasis. To investigate the expression of major neuropeptides, SP and its degrading enzymes such as NEP and ACE, in the lesions of ACD. A skin biopsy was obtained from 10 patients with ACD. We analysed the expression of these molecules by immunohistochemical staining, confocal laser scanning microscopy, western blotting and reverse transcription PCR. There was a significant increase in expression of SP in keratinocytes from ACD lesions compared with those in control skin. There was also increased expression of ACE but not NEP in ACD. Neuropeptides and their degrading enzymes, particularly SP and ACE, have a significant role in the pathogenesis of ACD.

Allergic and irritant contact dermatitis

Irritant and allergic contact dermatitis are common inflammatory skin diseases induced by repeated skin contact with low molecular weight chemicals, called xenobiotics or haptens. Although both diseases may have similar clinical presentations, they can be differentiated on pathophysiological grounds. Irritant contact dermatitis (ICD) is a non-specific inflammatory dermatitis brought about by activation of the innate immune system by the pro-inflammatory properties of chemicals. Allergic contact dermatitis (ACD) corresponds to a delayed-type hypersensitivity response with a skin inflammation mediated by hapten-specific T cells. Recent progress in the pathophysiology of chemical-induced skin inflammation has shown that ICD and ACD are closely associated and that the best way to prevent ACD is to develop strategies to avoid ICD. The immunological diagnosis of ICD or ACD requires investigation of the presence (ACD) or absence (ICD) of antigen-specific T cells. The detection of T cells can be performed in the skin (collected from ACD lesions or positive patch tests) and/or in the blood, particularly by using the enzyme-linked immunospot assay (ELISPOT). This method, recently developed in ACD to metals, offers a new biological tool enabling the immunobiological diagnosis of ACD.

Evaluation of the effect of the specific CCR1 antagonist CP‐481715 on the clinical and cellular responses observed following epicutaneous nickel challenge in human subjects

The CC-chemokine receptor-1 (CCR1) is thought to be involved in recruitment of inflammatory cells in allergic contact dermatitis (ACD). CP-481715 is a specific antagonist of CCR1. To determine the inhibitory effects of CP-418 715 in ACD by evaluating the clinical signs and cellular infiltration in skin biopsies following epicutaneous nickel challenge in allergic subjects. In this phase 1/2 study, 40 subjects were randomized to 5 days of treatment in four parallel groups (placebo three times daily (TID), placebo once daily (QD), 1000 mg CP-418 715 TID, and 3000 mg CP-418 715 QD). Twenty-four hours after the first drug administration, nickel sulfate patches were applied on subjects' backs and removed 48 hours later. Pretreatment with 1000 mg CP-481715 TID resulted in significant reductions in visual scores of the nickel reactions (P = 0.01). Instrumentally measured erythema tended to decrease in the CP-481715 mg TID group (P = 0.06). No differences were noted between the 3000 mg CP-481715 mg QD group and pooled placebo. No significant differences were found for immunohistological cell counts. CP-418 715 was generally safe and well tolerated. Blocking of CCR1 only partly inhibited clinical manifestations of ACD. Several chemokine receptors are likely relevant for the cellular influx observed in ACD lesions.

Häufigste Auslöser allergischer Kontaktekzeme

The prevalence of allergic contact dermatitis is high. Patch testing is the standard procedure to detect contact sensitivity. More than 3000 allergens are known, today. On the basis of the data of this study the top allergens are presented. The retrospective analysis is based on the patch test results collected by the Information Network of Departments of Dermatology in 2004. Data of 9948 patients (6175 female und 3773 male) referred for the evaluation of suspected contact allergy were analysed to determine the frequency of sensitization to the 10 most common contact allergens. The top ten allergens were nickel sulphate (frequency of sensitization standardized for sex and age 17.2 %), fragrance mix (7.2 %), balsam of Peru (6.7 %), cobalt chloride (6.5 %), potassium dichromate (5.3 %), colophony (4.6 %), lanolin alcohol (4.3 %), p-phenylenediamine (4.2 %), ammoniated mercury (3.5 %) und methyldibromoglutaronitrile/phenoxyethanol (3.4 %) in 2004. Even after healing of the skin lesions of allergic contact dermatitis, it must be considered that sensitization persists indefinitely. Therefore, patients have to be informed exactly about their relevant contact allergens to ensure complete avoidance. To do so, physicians need a detailed knowledge of the most common contact allergens which are discussed in this paper.

Safety of Blocking Vascular Adhesion Protein‐1 in Patients with Contact Dermatitis

Abstract: Vascular adhesion protein‐1 mediates leukocyte binding to vascular endothelia and migration to tissues. It is upregulated in inflammatory conditions. We studied the safety of vascular adhesion protein‐1 blockade by a single dose of the mouse monoclonal antibody vepalimomab in patients with nickel‐induced allergic contact dermatitis lesions. Vepalimomab, 0.05–0.50 mg kg−1 was safe and well tolerated. Four of nine patients reported adverse events of mild to moderate intensity. Human antimouse antibodies were detected after infusion in all the patients and they remained above the basal level for at least one month. Vepalimomab dose‐dependently labelled vascular adhesion protein‐1 in the inflamed skin. Luminal upregulation of vascular adhesion protein‐1 on the endothelium upon inflammation was demonstrated for the first time in patients in vivo. Vepalimomab was found on the endothelium up to 24 hr after dosing whilst it was cleared from the circulation with an apparent half‐life of 25–50 min. The results provide in vivo support for the concept of blocking vascular adhesion protein‐1 in human disease states and support previous proposals that vascular adhesion protein‐1 is a potential target molecule for inhibition of inflammatory reactions.

The Effect of Ciprofloxacin and Gentamicin on Spinal Morphine-Induced Antinociception in Rats*

Vascular adhesion protein-1 mediates leukocyte binding to vascular endothelia and migration to tissues. It is upregulated in inflammatory conditions. We studied the safety of vascular adhesion protein-1 blockade by a single dose of the mouse monoclonal antibody vepalimomab in patients with nickel-induced allergic contact dermatitis lesions. Vepalimomab, 0.05-0.50 mg kg(-1) was safe and well tolerated. Four of nine patients reported adverse events of mild to moderate intensity. Human antimouse antibodies were detected after infusion in all the patients and they remained above the basal level for at least one month. Vepalimomab dose-dependently labelled vascular adhesion protein-1 in the inflamed skin. Luminal upregulation of vascular adhesion protein-1 on the endothelium upon inflammation was demonstrated for the first time in patients in vivo. Vepalimomab was found on the endothelium up to 24 hr after dosing whilst it was cleared from the circulation with an apparent half-life of 25-50 min. The results provide in vivo support for the concept of blocking vascular adhesion protein-1 in human disease states and support previous proposals that vascular adhesion protein-1 is a potential target molecule for inhibition of inflammatory reactions.

La cellule de Langerhans : de la production in vitro à l’utilisation en immunothérapie cellulaire

Dendritic cells constitute a family of antigen presenting cells defined by their morphology and their capacity to initiate primary immune response. Langerhans cells are paradigmatic dendritic cells, described in 1868 by a young medical student, Paul Langerhans in Berlin. Langerhans cells are present with epithelial cells in the epidermis, bronchi and mucosae. After antigenic challenge, Langerhans cells migrate into the T cell areas of proximal lymph nodes where they act as professional antigen-presenting cells. Langerhans cells originate in the bone marrow and CD34+ hematopoïetic progenitors are present in cord blood or circulating blood. They are actively involved in skin lesions of allergic contact dermatitis or atopic dermatitis, in cancer immunosurveillance and are infected by HIV in AIDS. Since 1992, Langerhans cells may be generated in vitro from CD34+ cord blood or circulating blood progenitors by culture with GM-CSF and TNF alpha, as well as from peripheral blood monocytes by culture with GM-CSF, IL4 and TGF beta 1. The possibility to obtain from the blood, the circulating progenitors of dendritic cells and the subsequent possibility to harvest a large number of these cells through in vitro culture using growth factors, have given rise to several very interesting therapeutic perspectives, especially in the field of anti-cancer immunotherapy. In dermatology advanced studies have concerned malignant melanomas. Anti-melanoma immunization trials were performed in patients, through dendritic cells charged with melanoma antigens. Side effects appear to be limited. Injections of antigenically charged dendritic cells were performed subcutaneously, intravenously or in the lymph nodes. Positive clinical responses were obtained with, in some cases, complete remission of the metastasis. These results open a particularly interesting perspective in the field of cancer treatment.