Rolipram inhibits staphylococcal enterotoxin B-mediated induction of the human skin-homing receptor on T lymphocytes.

The cutaneous lymphocyte-associated antigen defines T lymphocytes with cutaneous tropism under inflammatory conditions. Bacterial infections participate in cutaneous inflammations, such as atopic dermatitis or psoriasis. Bacterial superantigens, such as staphylococcal enterotoxin B, can activate peripheral blood mononuclear cells to induce effector T cells bearing the T cell skin homing receptor cutaneous lymphocyte-associated antigen via enhancement of interleukin-12 production. We have identified and characterized the anti-inflammatory effects of different phosphodiesterase inhibitors on this system. Our data indicate that the selective type 4 phosphodiesterase inhibitor rolipram inhibits the Staphylococcal enterotoxin B-mediated generation of cutaneous lymphocyte-associated antigen positive CD3+ cells from peripheral blood mononuclear cells by reducing interleukin-12 production in a concentration-dependent manner. Conversely, type 3 phosphodiesterase or type 5 phosphodiesterase selective inhibitors were not effective. The rolipram inhibitory effect was on interleukin-12 production, as exogenously added interleukin-12 could revert rolipram suppression. These results suggest that selective type 4 phosphodiesterase inhibition may have beneficial effects on T cell mediated skin inflammatory processes characterized by the presence of bacterial infections, that are thought to exacerbate ongoing skin inflammation.     

Proliferation of T lymphocytes from atopic dermatitis skin is enhanced upon anti-CD3, reduced upon mitogen and superantigen, and negligible upon tuberculin stimulation

Knowledge about the nature of lymphocytes infiltrating atopic dermatitis skin is restricted to allergen-specific T cells. We investigated the proliferative capacities of T lymphocytes cultured in an antigen-independent way from biopsies of atopic dermatitis skin. When compared with peripheral blood mononuclear cells (PBMC) from healthy donors or atopic dermatitis patients, the skin-homing lymphocytes proliferated more vigorously in response to stimulation with anti-CD3 antibodies (1 microglml), reflecting their high response capacity. When stimulated with phytohemagglutinin (10 microg/ml) or staphylococcal enterotoxin A (0.1 microg/ml) the skin-homing lymphocytes achieved significantly lower proliferation levels than PBMC. In contrast to normal and atopic PBMC the skin-homing lymphocytes did not respond to tuberculin purified protein derivative (10 microg/ml). In the mixed lymphocyte reaction the skin-homing lymphocytes did not stimulate autologous PBMC to proliferate. We conclude that skin-homing lymphocytes have more pronounced immune deviations than PBMC in patients with atopic dermatitis. They represent a valuable approach for further investigating the pathogenesis of the disease.     

T cells and T cell-derived cytokines as pathogenic factors in the nonallergic form of atopic dermatitis.

A subgroup of patients with atopic dermatitis are known to have normal serum total immunoglobulin E levels, undetectable specific immunoglobulin E, and negative skin prick tests towards allergens. This form of the disease has been termed nonallergic atopic dermatitis. In this study, we found that, among 1151 chronic atopic dermatitis patients, about 10% had normal serum immunoglobulin E levels with no evidence for immunoglobulin E sensitization. We investigated immunologic mechanisms of patients with "allergic" and "nonallergic" atopic dermatitis using peripheral blood and skin biopsy samples. Our data suggest that T cells are likely involved in the pathogenesis of both forms of atopic dermatitis. Skin T cells equally responded to superantigen, staphylococcal enterotoxin B, and produced interleukin-2, interleukin-5, interleukin-13, and interferon-gamma in both forms of the disease. Interleukin-4, however, was not detectable in the skin biopsies of both atopic dermatitis types and was secreted in very low amounts by T cells cultured from the skin biopsies. Moreover, skin T cells from nonallergic atopic dermatitis patients expressed lower interleukin-5 and interleukin-13 levels compared with allergic atopic dermatitis patients. Accordingly, T cells isolated from skin biopsies of atopic dermatitis, but not from the nonallergic atopic dermatitis, induced high immunoglobulin E production in cocultures with normal B cells that was mediated by interleukin-13. In addition, B cell activation with high CD23 expression was observed in the peripheral blood of atopic dermatitis, but not nonallergic atopic dermatitis patients. These data suggest, although high numbers of T cells are present in lesional skin of both types, a lack of interleukin-13-induced B cell activation and consequent immunoglobulin E production in nonallergic atopic dermatitis.     

儿童特应性皮炎患者外周血单一核细胞IL-31与疾病严重程度相关性分析

目的 探讨IL-31在儿童特应性皮炎发病机制中的作用以及与特应性皮炎瘙痒的相关性。方法 22例特应性皮炎患儿与22例健康儿童外周血单一核细胞在葡萄球菌肠毒素B（SEB）刺激或非刺激状态下，应用实时PCR方法分析IL-31表达情况；酶联免疫吸附法测定其血清IgE水平；对患儿病情进行病情严重程度评分，分析IL-31 mRNA与IgE水平、疾病严重程度及瘙痒的相关性。结果 特应性皮炎患儿外周血单一核细胞IL-31表达显著增加，是对照组的23.2倍（P < 0.01）。特应性皮炎组和对照组外周血单一核细胞受SEB刺激后IL-31表达均有不同程度升高，以特应性皮炎组IL-31表达增加更显著，是对照组的20.44倍。患儿血清总IgE水平中位数为260.05 IU/mL（范围5.9 ～ 1131.01 IU/mL），对照组为17.7 IU/mL（范围5 ～ 140.7 IU/mL），两组比较，P < 0.01。IL-31与患儿病情严重程度以及血清总IgE水平无显著相关性（r = 0.07，P > 0.05；r = 0.22，P > 0.05）。结论 IL-31可能参与儿童特应性皮炎发病，其作用机制可能不依赖血清IgE；SEB能诱导正常人外周血单一核细胞快速表达IL-31，是IL-31产生的重要调节因素。     

Elevated cyclic adenosine monophosphate phosphodiesterase activity in peripheral blood mononuclear leucocytes from children with atopic dermatitis

We examined peripheral blood mononuclear leucocyte cyclic adenosine monophosphate phosphodiesterase (cAMP-PDE) activity in 80 children (aged 2-12 years) with atopic dermatitis. The enzyme activity (35.1 ± 18.6U) in children with atopic dermatitis was significantly higher than that (19.1 ± 12.6U) in age-matched non-atopic controls. There was no significant difference in the cAMP-PDE activity between children with mild atopic dermatitis and children with severe atopic dermatitis. These findings support the view that elevation of peripheral mononuclear leucocyte cAMP-PDE actvity in patients with atopic dermatitis is a gene-associated abnormality.     

Production of interleukin-2 by mononuclear cells in vitro in patients with atopic dermatitis and psoriasis. Comparison with serum interleukin-2 receptor levels.

Atopic dermatitis is associated with profound immunological alterations, in particular decreased lymphoproliferative responses upon stimulation with T-cell mitogens. T-cell blastogenesis involves the production of the soluble cytokine interleukin-2 (IL-2), which in turn upregulates the expression of its own receptor. To investigate the potential role of this cytokine for the pathomechanisms present in atopic dermatitis, 24-h supernatants of PHA-stimulated peripheral blood mononuclear cells from patients with atopic dermatitis (n = 30) of a moderate to severe disease activity were tested for IL-2 activity. In addition, serum concentrations of soluble interleukin-2 receptor (IL-2R) were measured. Non-atopic healthy controls (n = 19) and patients with psoriasis (n = 20), an inflammatory skin disorder with distinct pathogenesis, served as controls. In comparison with psoriasis patients and normal controls, PHA-stimulated mononuclear cells of atopic dermatitis patients released significantly less IL-2 into supernatants. Moreover, there was an inverse correlation between IL-2 concentrations and body surface involvement or serum IgE levels. In contrast, serum IL-2R levels were significantly elevated in both atopic dermatitis and psoriasis, as compared with healthy controls. Furthermore, IL-2R levels in atopic dermatitis patients showed a significant correlation with IgE levels and body surface involvement. The data indicate that T cell activation may occur in both skin diseases. Atopic dermatitis, however, is further characterized by the decreased capacity of mononuclear cells to release IL-2 upon stimulation in vitro.     

Effects of two novel cationic staphylococcal proteins (NP-tase and p70)and enterotoxin B on IgE synthesis and interleukin-4 and interferon-gamma production in patients with atopic dermatitis

We have characterized the cell-mediated and humoral immune response of patients with atopic dermatitis (AD) and healthy controls in response to two novel staphylococcal antigens (NP-tase, p70) and the superantigen staphylococcal enterotoxin B (SEB). The parameters studied were IgE, interleukin (IL)-4 and interferon (IFN)-gamma synthesis by peripheral blood mononuclear cells (PBMC) after stimulation with NP-tase, p70 and SEB in vitro. Both antigens, as well as SEB, induced IL-4 and IFN-gamma secretion in patients and controls. However, patients with AD showed a significantly diminished IFN-gamma production in response to NP-tase or SEB. Furthermore, we demonstrated a good correlation between antigen-stimulated IgE production and the IL-4/IFN-gamma ratio in vitro. A distinct subgroup of PBMC showed impaired IFN-gamma synthesis and enhanced IL-4 secretion after incubation with p70 or NP-tase. These data support evidence that a subgroup of patients with AD, synthesizing low levels of IFN-gamma after stimulation with staphylococcal antigens, may have impaired abilities to clear Staphylococcus aureus colonization. Persistent staphylococcal antigens could then be responsible for inflammatory and allergic skin reactions in patients with AD. We therefore conclude that, besides superantigens, staphylococcal antigens may also play a part in the pathogenesis of AD.     

CC chemokine receptor 4 expression on peripheral blood CD4+ T cells reflects disease activity of atopic dermatitis

Recent studies indicate that Th1 and Th2 cells differ in their chemokine receptor expression and their responsiveness to various chemokines. Therefore, selective Th2 cell recruitment in Th2-predominant inflammatory diseases such as atopic dermatitis may be under the influence of some chemokines. It is reported that CC chemokine receptor (CCR) 4 is selectively expressed on Th2 cells whereas CXC chemokine receptor (CXCR) 3 is selectively expressed on Th1 cells. In this study we examined CCR4 and CXCR3 expression on peripheral blood CD4+ and CD8+ T cells obtained from adult atopic dermatitis subjects, and compared the results with those from patients with psoriasis vulgaris and healthy controls. CCR4 was preferentially expressed on CD4+ T cells from atopic dermatitis subjects and CXCR3 was preferentially expressed on CD4+ T cells from psoriasis vulgaris subjects. This CCR4 expression was prominent especially in severe atopic dermatitis subjects. CCR4 expression on CD4+ T cells in severe atopic dermatitis subjects decreased on improvement of disease activity. CD25 was preferentially expressed on CCR4+CD4+ T cells but not on CXCR3+CD4+ T cells in atopic dermatitis subjects. Cutaneous lymphocyte-associated antigen was also preferentially expressed on CCR4+CD4+ T cells but not on CXCR3+CD4+ T cells in atopic dermatitis subjects. CD4+ T cells in atopic dermatitis skin lesions were predominantly CCR4+ cells. Taken together, this study strongly indicates that CCR4+CD4+ T cells reflect disease activity and suggests that CCR4 expression is important for T cell infiltration into atopic dermatitis lesions. Thus, CCR4 may be a possible target for therapy of atopic dermatitis in the future.     

Effects of recombinant human soluble interleukin-4 receptor on interleukin-4/staphylococcal enterotoxin B-stimulated peripheral mononuclear cells from patients with atopic eczema

In atopic eczema both in local inflammatory reactions and in peripheral blood high interleukin (IL) 4: interferon-γ (IFN-γ) production ratios have been demonstrated, indicating predominance of TH₂ cell subsets resulting in increased IL-4 production and high serum IgE. The in vitro immunomodulatory effects of recombinant human soluble IL-4 receptor (rsIL-4R) on IL-4-stimulated lymphocyte proliferation, IgE and IFN-γ production were studied in peripheral blood mononuclear cells from 10 patients with atopic eczema and seven healthy donors. In addition to control cultures (without any stimulus) and cultures with simultaneous application of rsIL-4R and IL-4, time-kinetic experiments were performed. We further investigated the influence of rsIL-4R on IL-4 production in staphylococcal enterotoxin B (SEB) stimulated peripheral blood mononuclear cells. Early addition of rsIL-4R to IL-4-stimulated peripheral blood mononuclear cells resulted in an increase in IFN-γ production and in suppression of IL-4 induced proliferation and IgE secretion. Unexpectedly, rsIL-4R in combination with SEB exhibited an IL-4 protective effect with a significant increase in detectable IL-4 in the culture supernatants. The present data support the assumption that rsIL-4R might be a promising new immunomodulatory substance in the treatment of atopic eczema.     

Lidocaine inhibits staphylococcal enterotoxin-stimulated activation of peripheral blood mononuclear cells from patients with atopic dermatitis

Atopic dermatitis (AD) is an inflammatory, chronically relapsing, pruritic skin disease and lesions associated with AD are frequently colonized with Staphylococcus aureus (S. aureus). Activation of T cells by staphylococcal enterotoxins (SE) plays a crucial role in the pathogenesis of AD. Previous studies have demonstrated that lidocaine could attenuate allergen-induced T cell proliferation and cytokine production in peripheral blood mononuclear cells (PBMCs) from asthma patients. The purpose of this study was to investigate the effects of lidocaine on SE-stimulated activation of PBMCs from AD patients. PBMCs were isolated from ten AD patients and stimulated by staphylococcal enterotoxin A (SEA) or staphylococcal enterotoxin B (SEB) in the presence or absence of lidocaine in various concentrations. Cellular proliferation and the release of representative T_H1- and T_H2-type cytokines were measured. The effect of lidocaine on filaggrin (FLG) expression in HaCaT cells co-cultured with SE-activated PBMCs was also examined. Our results demonstrated that lidocaine dose-dependently inhibited the proliferative response and the release of IL-4, IL-5, IL-13, TNF-α, and IFN-γ from SEA- and SEB-stimulated PBMCs and also blocked the down-regulation of FLG expression in HaCaT cells co-cultured with SEA- and SEB-activated PBMCs. These results indicate that lidocaine inhibited SEA- and SEB-stimulated activation of PBMCs from patients with AD. Our findings encourage the use of lidocaine in the treatment of AD.     

Natural killer cell function in atopic dermatitis

The natural killer (NK) cell function was examined in the peripheral blood mononuclear cells of 14 patients with moderate or severe atopic dermatitis. There were significantly impaired NK cell responses in the atopic patients as compared to the control group. This impairment showed a negative correlation with log IgE concentration in the scrum. These findings prompt consideration of a relationship between decreased NK cell activity and the familiar enhanced susceptibility to viral infections in patients with atopic dermatitis.     

A Th2 chemokine, TARC, produced by keratinocytes may recruit CLA+CCR4+ lymphocytes into lesional atopic dermatitis skin

Atopic dermatitis is an inflammatory skin disease in which the inflammation is characterized by the influx of lymphocytes into the dermis. It is generally believed that atopic dermatitis is a Th2-type disease, i.e., the T lymphocytes produce interleukin-4, interleukin-5, interleukin-10, and interleukin-13, although it has become evident in recent years that the cytokine profile in the skin changes during the course of the disease towards a Th1-Th2 mixed cytokine profile (interferon-gamma, tumor necrosis factor alpha, and interleukin-2). The lymphocytes that home into the skin express cutaneous lymphocyte-associated antigen, and it has recently been shown that most of the lymphocytes in this population express the chemokine receptor CCR4. CCR4 is the receptor for the CC chemokine TARC (thymus and activation regulated chemokine), and this chemokine is expressed predominantly by keratinocytes in the basal layer of the epidermis of lesional atopic dermatitis skin in mice. In humans, however, it was shown to be expressed in the endothelial cells of the dermis. We have examined the peripheral blood mononuclear cells of atopic dermatitis patients for the expression of cutaneous lymphocyte-associated antigen and CCR4 and compared them with peripheral blood mononuclear cells from normal controls. We found that the proportion of CLA+CCR4+ lymphocytes is upregulated in atopic dermatitis patients. In addition we have examined skin biopsies of lesional and non-lesional skin from atopic dermatitis patients and found that the keratinocytes, but not the endothelial cells, produce TARC in the lesional but not in the nonlesional skin. To gain insight in the stimulatory mechanisms for TARC production in keratinocytes, as previously observed in mice, we cultured HaCaT cells and found that interferon-gamma and tumor necrosis factor alpha work synergistically to induce TARC production. These observations suggest that the induction of TARC production in keratinocytes plays an important role in the late phase skin invasion by CCR4+CLA+ Th2-type lymphocytes in atopic dermatitis.     

The atopic skin‐like microenvironment modulates the T‐cell‐polarising cytokine production of myeloid dendritic cells,as determined by laser scanning cytometry

Because it is not known exactly when or where myeloid dendritic cells (mDCs) acquire their atopic dermatitis (AD)‐specific T‐cell‐polarising ability in patients with this condition, we used laser scanning cytometry (LSC) to determine whether isolated peripheral blood mDCs from AD patients differed from cells from controls in their cytokine expression profiles de novo and after stimulation with Staphylococcus enterotoxin B (SEB) and thymic stromal lymphopoietin (TSLP), which represents an AD‐like microenvironment. Unstimulated mDCs from AD patients showed pluripotent T‐cell‐polarising capacity, and the surrounding skin microenvironment was essential for the distinctive, disease‐specific activity of mDCs (Th2‐Th22 bias). We also emphasise that LSC is an attractive technique to study the effect of new DC‐targeted therapeutic modalities in AD.     

特应性皮炎患者外周血表达不同细胞因子T细胞亚群的检测

目的 探讨特应性皮炎患者外周血表达不同细胞因子T细胞群的频数及其与疾病严重程度的相关性。方法 采用流式细胞仪，检测外周血表达不同胞质内细胞因子（包括IL-4、IL-5、IFN-γ、TNF-α）的CD4+ T、CD8+ T、CLA+ T细胞亚群的频数。利用特应性皮炎皮损面积严重度指数积分法方法，获取特应性皮炎患者病情严重程度积分，分析其与表达不同细胞因子的T细胞频数的相关性。结果 特应性皮炎患者外周血中，胞质内表达IL-4和IL-5的CD4+ T、CD8+ T、CLA+ T细胞频数均高于对照组，胞质内表达IFN-γ的CD4+ T、CLA+ T细胞频数低于对照组；差异均有统计学意义。患者组与正常人对照组中，TNF-α在不同T细胞亚群中表达差异无统计学意义。疾病严重程度与IL-4+CD4+ T细胞和IL-5+CLA+ T细胞群的表达频数相关。结论 患者外周血T细胞存在免疫偏移，表达某些细胞因子的T细胞亚群水平可能作为检测疾病严重程度的指标。     

Increased “in vivo” lymphocyte blastogenesis in the peripheral blood of patients with atopic dermatitis and allergic contact dermatitis

Summary The spontaneous ³H-thymidine (³HT) labelling of some lymphocyte subpopulations has been studied in the peripheral blood of five patients with atopic dermatitis and five with widespread allergic contact dermatitis and compared with that in 10 healthy subjects. One hour after addition of ³HT to heparinized blood, lymphocytes were separated and processed with two different rosetting techniques (E-rosette test and Active-E-rosette test). The cell suspensions were cytocentrifuged and autoradiography undertaken.An increased number of ³HT labelled lymphocytes was observed in the peripheral blood of patients with dermatitis as compared to controls. These labelled lymphocytes were E-rosette-forming cells (T cells) and E-non-rosetteforming cells (non-rosette-forming T cells and non-T cells). The ratio between the labelling index (LI) of E-rosette- to the LI of non-E-rosette-forming cells was in favour of T cells in allergic contact dermatitis (ratio=3.09) whereas in atopic dermatitis (ratio=0.93) the DNA synthesis was relatively greater in the non-rosette-forming cells.It is suggested that this increased LI of peripheral blood lymphocytes could be related to the increased dermal mononuclear cell ³HT-labelling that has been reported previously in these inflammatory skin diseases.D. Van Neste is recipient of a grant from INSERM, Paris and Administration des relations culturelles internationales (ARCI), Bruxelles     

IMMUNE MECHANISMS IN ATOPIC DERMATITIS: STUDIES AND HYPOTHESIS

The pathogenesis of atopic dermatitis remains uncertain. The aim of this study was to correlate blood and skin findings with respect to analysis of immunoregulatory T cells in 18 patients with severe atopic dermatitis. Circulating T lymphocytes were characterised by flow cytometry, and in situ infiltrates of acute skin lesions identified by the immunoperoxidase technique. Analysis of peripheral blood T lymphocyte sub-sets failed to reveal any difference from normal controls. Skin infiltrates were strongly positive for T11 – the pan T lymphocyte marker. The majority of these cells both in the dermis and epidermis were of the T4 helper-inducer sub-set, while a smaller proportion of cells were of the T8 suppressor- cytotoxic T cell sub-set. T6 positive Langerhans cells were markedly increased in the dermis of affected skin, compared with normal skin. The finding of increased numbers of helper-inducer T lymphocytes' in association with increased numbers of Langerhans cells, which function as antigen presenting cells, suggests a strong immunological mechanism in disease pathogenesis, and may yield knowledge both with respect to origin of skin damage and elevation of IgE.     

Disturbances of antimicrobial lipids in atopic dermatitis

Patients with atopic dermatitis exhibit an increased susceptibility to cutaneous infections, especially to pathological colonization with superantigen‐secreting Staphylococcus aureus. Recent attention has been focused on antimicrobial peptides, especially on cathelicidin and human β‐defensin‐2, which are under‐expressed in atopic skin. Antimicrobial lipids from the stratum corneum are also major contributors to cutaneous antimicrobial defense. Current aspects of biochemistry and function of antimicrobial lipids in atopic dermatitis are reviewed in detail. The major classes of stratum corneum lipids with antimicrobial activity are free fatty acids, glucosylceramides, and free sphingosines. Diminished levels of free sphingosines in the stratum corneum have recently been detected in atopic dermatitis and have been associated with the pathological colonization of atopic skin with Staphylococcus aureus. The superantigen staphylococcal enterotoxin B has been shown to reduce the suppressive effect of regulatory T cells on T‐cell proliferation, thus augmenting T‐cell activation in patients with atopic dermatitis. The killing of superantigen‐secreting bacterial strains with topically applied antimicrobial lipids offers new antiseptic and immunomodulatory options for the treatment and secondary prevention of atopic dermatitis.     

Peripheral natural killer cells exhibit qualitative and quantitative changes in patients with psoriasis and atopic dermatitis

Background Psoriasis and atopic dermatitis are the most recurrent skin inflammatory disorders. Despite their distinct aetiology and clinical aspects, these diseases share several immunological features. Besides the largely documented role of T cells, emerging literature supports a potential involvement of innate immune effectors, the natural killer (NK) cells, in both pathologies. In the peripheral blood, NK cells consist of CD3? CD56dim and CD3? CD56bright cell subsets, harbouring a distinct cell surface phenotype, but both endowed with the main NK‐cell effector functions: cytotoxicity and cytokine production. Objectives To determine whether the frequency, the cell surface phenotype and the functional properties of peripheral NK cells were affected in patients with psoriasis or atopic dermatitis. Methods Peripheral blood mononuclear cells were isolated from 11 patients with psoriasis, nine patients with atopic dermatitis and 16 healthy individuals. By using flow cytometry, we analysed the following parameters of peripheral NK cells: the frequency, the cell surface expression of several NK‐cell receptors (NKR) and the activation of the effector functions upon various in vitro stimuli. Results Peripheral NK cells were significantly reduced in both skin diseases. The cell surface expression of various NKR was differently modified in peripheral NK cells of the two cohorts of patients. Finally, NK‐cell natural cytotoxicity was affected only in atopic dermatitis, while interferon‐γ production was defective in both groups of patients. Conclusion Psoriasis and atopic dermatitis are associated with quantitative and qualitative changes of peripheral NK cells, mostly shared by both diseases, supporting a common process implicating these innate effectors in skin inflammation.     

Expression and function of CD43 and CDw60 on T cells from patients with atopic dermatitis.

Signalling via the CD43 and CDw60 epitopes has been reported as providing two novel pathways of T-lymphocyte activation. In Wiskott-Aldrich syndrome, which has atopic eczema-like skin symptoms, there is a defective expression of CD43, while CDw60 is strongly expressed on T cells from rheumatoid arthritis synovial fluid and from psoriatic skin lesions, and on blood mononuclear cells from patients with cutaneous T-cell lymphoma. We therefore studied the expression and function of these phenotypes on peripheral blood mononuclear cells and on CD4+ and CD8+ T-cell subsets from patients with atopic dermatitis. We observed a significant increase in the percentage of CD43+ cells among the blood mononuclear cells in patients with atopic dermatitis and an enhanced proliferation of CD4+ T cells following stimulation with anti-CD43 antibody. There were no changes in the CDw60 expression or function after stimulation with anti-CDw60 antibody. Thus, CD43 expression was not decreased but rather increased in blood mononuclear cells from patients with atopic dermatitis, whereas CDw60 expression did not differ from healthy controls.     

An in vitro study of depressed cell-mediated immunity and of T and B lymphocytes in atopic dermatitis.

Lymphocyte transformation tests, E binding(T) rosette assay and immunofluorescent preparations of B cells were studied in patients with atopic dermatitis, and also in healthy controls. Most of the patients were found to have high levels of IgE in serum. The patients were studied both during severe bouts of dermatitis and also when the dermatitis was almost healed. Lymphocyte transformation tests showed that patients were hyporeactive to PPD and herpes simplex antigen in vitro, both during periods of severe dermatitis and also when the dermatitis was in remission. The response to PHA in the patients was normal in vitro. No factors which could reduce cell-mediated immunity in vitro were found in patients' sera. A decreased number of T lymphocytes and a slight increase in the number of immunoglobulin-bearing lymphocytes (B cells) were demonstrated in the patients, both during remission and during recurrence of severe dermatitis. In 3 of 8 patients, increased numbers of IgE-bearing lymphocytes were found to be present when the patients had severe dermatitis. A possible correlation between high serum levels of IgE and depressed cell-mediated immunity in patients with atopic dermatitis is discussed.