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At least 109 records · Page 6Linked to original sources
PubMed1998

Expression of CD30 on T helper cells in the inflammatory infiltrate of acute atopic dermatitis but not of allergic contact dermatitis.

The CD30 molecule has been proposed as a marker for a subset of CD4+CD45RO+ (memory) T cells with potent B cell helper activity producing IL-5 and IFN-gamma and as a specific marker for Th2 cells. Recently, an association has been demonstrated between elevated serum levels of soluble CD30, which is shed by CD30+ cells in vitro and in vivo, and atopic dermatitis but not respiratory atopic disorders or allergic contact dermatitis. We studied the expression of CD30 in the inflammatory infiltrate of atopic dermatitis compared with that of allergic contact dermatitis, with special regard to skin disease activity (acute vs subacute/ chronic). Biopsies were obtained from 16 patients suffering from atopic dermatitis (acute n = 6, subacute/ chronic n = 10), from 7 patients with acute allergic contact dermatitis and from 5 positive patch-test reactions. Paraffin-embedded as well as snap-frozen material was stained with anti-CD30 and anti-CD45RO mAbs according to standard procedures. Double-staining procedures for CD30CD3, CD30CD4, CD30CD45RO and CD30CD68 were also performed. Abundant CD45RO+ cells were detected both in atopic dermatitis and in allergic contact dermatitis lesions. We found scattered CD30+ cells in only one of six formalin-fixed paraffin-embedded acute atopic dermatitis biopsies, but in all of the respective snap-frozen specimens, possibly because CD30 expression on atopic dermatitis infiltrating cells is weak and sensitive to formalin fixation and paraffin embedding. CD30CD3 and CD30CD4 double staining identified CD30+ cells to be helper T lymphocytes. No significant CD30 expression (either in paraffin-embedded or in frozen material) could be found in subacute/chronic atopic dermatitis lesions or in any of the specimens of allergic contact dermatitis. The results suggest a specific regulatory function of CD30+ T cells in acute atopic dermatitis. With respect to the view that CD30 is a marker for Th2 cells, our observations confirm previous findings that Th2 cells predominate in the infiltrate particularly of acute atopic dermatitis. CD30 expression in acute atopic dermatitis but not in acute allergic contact dermatitis might be helpful in the histological differentiation of these disorders and in the further characterization of atopy patch testing.

Acute Disease↗
PubMed1979

A new method for obtaining viable cells from dermal infiltrates. A study on 2,4 dinitrochlorobenzene induced contact dermatitis.

Experimental contact dermatitis has been induced in 2,4 dinitrochlorobenzene (DNCB) sensitized guinea pigs. The developing dermal infiltrate was excised and the infiltrating cells were obtained by mechanical extraction alone as well as by the combination with collagenase and elastase treatment. The most viable cells appeared in the elastase and mechanically extracted samples and the least in those subjected to mechanical treatment alone. The most cells in the enzyme-treated samples were present 24 h after re-exposure of the sensitized animals to DNCB consisting mainly of lymphocytes and of polymorphonuclear granulocytes. The optimum conditions for the action of enzymes including optimum duration of the treatment, buffer milieu, aspecific proteolytic effect on foreign substrate and action on T and B cell receptors have been elaborated. It was concluded that 80 min of collagenase treatment with gentle mechanical extraction under specified conditions does not affect any measurable immunologic properties of the liberated cells resulting in the second best yield. A comparison of these data with earlier reports and their significance is being discussed.

Animals↗
PubMedDate not supplied

Toilet seat contact dermatitis.

Allergic contact dermatitis to wooden toilet seats was a previously well-recognized pattern of regional dermatitis. We report a recent occurrence in a child that highlights a possible resurgence in this presentation, associated with the increasing popularity of wooden toilet seats.

Child, Preschool↗
PubMed1982

Actinic reticuloid via persistent light reaction from photoallergic contact dermatitis.

Photoallergic contact dermatitis developed in a patient who had used deodorant soaps containing tribromsalan. He persistently reacted to light, since the dermatitis persisted long after cessation of contact with the causative chemical. During this period, he experienced generalized, eczematous dermatitis on several occasions. On testing, the patient showed extremely severe photosensitivity extending through the ultraviolet to the visible spectrum. At that time, a skin biopsy specimen showed the microscopic findings of eczematous dermatitis. A diagnosis of actinic reticuloid was first made histologically nine years after the initial examinations, when the patient was 56 years old. This long-term follow-up study may support the view that photoallergic contact dermatitis, persistent light reaction, and actinic reticuloid could constitute various phases of a single disease.

Chronic Disease↗
PubMed1999

The epidemiology of occupational contact dermatitis.

Occupational contact dermatitis (OCD) ranks first of all occupational diseases in many countries. The incidence rate is believed to be around 0.5-1.9 cases per 1000 full-time workers per year. Epidemiological studies play an important role in observing disease trends, analysing risk factors, and monitoring the effect of preventive measures. In this review article the lack of truly epidemiologic data on OCD and the difficulties of those studies are illustrated. The following issues are highlighted: case ascertainment and bias, the distribution of allergic and irritant contact dermatitis in the working population, the interrelationship between exogenous (allergens, irritants) and endogenous factors, the prognosis, the social and economic impact, and the need for intervention studies.

Bias↗
PubMedDate not supplied

The role of CD4+ and CD8+ T cells in contact hypersensitivity and allergic contact dermatitis.

Allergic contact dermatitis (ACD) and contact hypersensitivity (CHS) are delayed-type hypersensitivity reactions which are mediated by hapten specific T cells. During the sensitisation phases, both CD4+ and CD8+ T cell precursors are activated in the draining lymph nodes by presentation of haptenated peptides by skin dendritic cells. Subsequent hapten skin painting induces the recruitment of T cells at the site of challenge which induces inflammatory signals and apoptosis of epidermal cells, leading to the development of a skin inflammatory infiltrate and of clinical symptoms. There have been major controversies on the respective roles of CD4+ and CD8+ T cells in the development of the CHS inflammatory reaction. Experimental studies from the last 10 years have demonstrated that, in normal CHS responses to strong haptens, CD8+ type 1 T cells are effector cells of CHS while CD4+ T cells are endowed with down-regulatory functions. The latter may correspond to the recently described CD4+ CD25+ regulatory T cell population. However, in some instances, especially those where there is a deficient CD8 T cell pool, CD4+ T cells can be effector cells of CHS. Ongoing studies will have to confirm that the pathophysiology of human ACD is similar to the mouse CHS and that the CHS response to weak haptens, the most frequently involved in human ACD, is similar to that reported for strong haptens.

CD4-Positive T-Lymphocytes↗
PubMed1988

Chronic, irritant contact dermatitis: mechanisms, variables, and differentiation from other forms of contact dermatitis.

Irritant dermatitis is an eczematous reaction to toxic chemicals contacting the skin. The mechanisms by which various chemicals elicit dermatitis are multiple. Strong irritants quickly elicit signs and symptoms of dermatitis, but weak irritants may not. Chronic cumulative exposure to weak irritants can elicit dermatitis which may mimic allergic contact dermatitis and mislead the physician and patient with respect to cause and preventative strategy. The skins of different people vary in susceptibilities to irritation. Susceptibility is also influenced by chemical properties, vehicles, concentrations, amounts applied to the skin surface, surface area, regional variations, length of exposure, method of exposure, age, sex, race, genetic background, environmental factors, hardening, concomitant disease, and the excited skin syndrome as well as treatment. Patch testing can help distinguish between allergens and irritants, but pitfalls may mislead.

Chronic Disease↗
PubMed1994

Is allergic contact dermatitis being overlooked?

Contact dermatitis is very common and is among the top 20 reasons for a patient to visit a physician. This article reviews the basic features of irritant and allergic contact dermatitis and provides case examples. We emphasize the use of patch testing to diagnose specific allergens in allergic contact dermatitis. Contact dermatitis is important to recognize since there are prevention and intervention strategies that may be of great help to the patient. Accurate diagnosis and prevention of contact dermatitis would have a positive impact on medical care costs and job productivity.

Adult↗
PubMed1988

[Aerogenic contact dermatitis].

Airborne contact dermatitis is caused by hypersensitivity of the delayed type (cell-mediated allergy). This contact allergy is brought about by airborne plant particles, which affect the unclothed skin, especially outdoors. In 2 patients, we found strong reaction to different plants of the compositae family, their mutual allergens being sesquiterpene lactones.

Aged↗
PubMed2001

Effector and regulatory T cells in allergic contact dermatitis.

Allergic contact dermatitis is a prototypic T-cell-mediated disease that has a socio-economic impact in industrialized countries. Here, Andrea Cavani and colleagues highlight recent developments in the T-cell-based effector and regulatory mechanisms of this common skin disorder.

Dermatitis, Allergic Contact↗
PubMed2002

Allergic contact dermatitis.

Allergic contact dermatitis (ACD) is a common occupational and environmental health issue. In common with other forms of allergy the disease progresses in two stages; an initial phase during which sensitization is acquired, followed later (after subsequent exposure to the same chemical allergen) by elicitation of a cutaneous inflammatory reaction. The development of skin sensitization is associated with, and requires, the activation and clonal expansion of allergen responsive T lymphocytes and it is these cells that orchestrate the cutaneous allergic reaction. In recent years, much has been learned of the characteristics of immune responses to skin sensitizing chemicals and of the roles played by dendritic cells, cytokines and chemokines. Some of the more interesting cellular and molecular mechanisms are reviewed briefly in this article. A more detailed appreciation of responses induced by chemical allergens has in turn facilitated the design of novel approaches to the toxicological evaluation of skin sensitization. Real progress has been made, not only in the development of improved methods for hazard identification and characterization, but also in the application of new paradigms for risk assessment. The newer methods now available and the opportunities that exist for further advances are considered. Finally, progress has been made in the characterization of skin sensitization in humans and in the clinical management of ACD. This article seeks to consider skin sensitization and ACD in holistic fashion, bridging experimental observations with clinical disease and basic mechanisms with practical toxicology.

Allergens↗
PubMed2003

[Pathomechanisms of the elicitation phase of allergic contact dermatitis].

Allergic contact dermatitis (ACD) is a T-cell mediated, antigen-specific inflammatory response to repeated epicutaneous exposure to haptens. Two immunologically distinct sequential steps are required to produce the clinical picture of ACD. In the sensitization phase, naïve antigen-specific T cells are primed and differentiate into memory or effector T cells. In the elicitation phase, reapplication of the same hapten leads to local recruitment of hapten-specific T cells which are cytotoxic, release cytokines and recruit other inflammatory cells. These events lead to clinically visible tissue inflammation characterized by edema, erythema, scaling, and blistering. For the clinician, the effector phase is especially important, because sensitization is generally asymptomatic, whereas elicitation produces the clinical picture of ACD. Detailed knowledge about the mechanisms of the elicitation phase of ACD is needed in order to develop novel therapeutic approaches.

Cytokines↗