Epidermal DR+T6- dendritic cells in inflammatory skin diseases

T lymphocyte and dendritic cell subpopulations were counted in three biopsies each of endogenous eczema and pityriasis rosea and two of lichen planus and compared with previous findings in psoriatic lesions. In common with psoriasis, proportionately more CD4 T cells than CD8 T cells were DR+ in both epidermis and dermis of all lesions. In addition, total numbers of epidermal dendritic cells were significantly increased in endogenous eczema and pityriasis rosea, and variably in lichen planus lesions. Interestingly, a DR+T6- subpopulation of dendritic cells was present in varying proportions in all three skin lesion types. Electron microscopy of DR+T6- dendritic cells from psoriatic lesions, using an immunogold staining technique, showed the cells to be of the Langerhans' cell lineage. DR+T6- dendritic cells are a subpopulation of Langerhans' cells which are not specific to psoriasis, but present in the lesions of other benign, inflammatory skin conditions in which CD4 T cells are preferentially activated.     

Decreased IL-10 production by psoriatic peripheral blood mononuclear cells stimulated with streptococcal superantigen

The strong association of acute guttate psoriasis and streptococcal throat infection has suggested a role for streptococcal antigens in the pathogenesis of psoriasis. We have reported that psoriatic peripheral blood mononuclear cells (PBMCs) showed significantly lower responses to cytoplasmic membrane-associated protein (CAP) isolated from group A beta-hemolytic streptococci, a kind of streptococcal superantigen. The objectives were to evaluate the abnormal cytokine production by psoriatic PBMCs to streptococcal superantigen, CAP. We compared the production of four different cytokines, i.e. IL-4, IL-5, IL-10, and IFN-gamma, by PBMCs between psoriatic patients and healthy controls after stimulation with CAP or two different staphylococcal superantigens, staphylococcal enterotoxin A (SEA) or E (SEE). When PBMCs were stimulated with CAP, the production of IL-10 was significantly lower by psoriatic PBMCs than by those from healthy controls, whereas those of IL-4, IL-5, or IFN-gamma were not different between the two groups. Such a significant decrease in IL-10 production by psoriatic PBMCs was not observed when they were stimulated with staphylococcal superantigens. Flow cytometric analysis of intracytoplasmic IL-10 demonstrated defective IL-10 production by psoriatic PBMCs in both CD3+ T cells and CD14+ monocytes. There was a significant positive correlation between IFN-gamma production by PBMCs and the proliferation of Vbeta8+ T cells preferentially stimulated by CAP. These data demonstrating the defective IL-10 production by psoriatic PBMCs stimulated with streptococcal superantigen seem to explain why only psoriatic patients evolve sustained and Th-1 deviated skin lesions after streptococcal upper respiratory infection.     

NAD and NADP dependent isocitrate dehydrogenase and fumarate hydratase activities in normal human skin and in some maculosquamous diseases of the skin

Summary Activities of the isocitrate dehydrogenases, ICDH(NAD) and ICDH (NADP), and of fumarate hydratase, FH,. were measured in subcorneal and basal epidermal layers in patients with psoriasis, neurodermatitis, lichen planus and pityriasis rosea and in healthy controls. Lowry's microtechniques were used. Since NADH formed by the ICDH reaction required high analytical sensitivity, this dinucleotide was measured photokinetically with the aid of bacterial luciferase. ICDH (NAD) and FH displayed similar activities in the skin of normal controls to those in the non-involved skin of the patients with various dermatoses. In the psoriatic lesion both enzymatic activities were markedly increased in the two layers studied. In neurodermatitis and lichen planus, however, the ICDH (NAD) activity was increased only in basal epidermis. FH activities were not increased over control levels in any of the three dermatoses. In epidermis ICDH (NADP) showed 20-fold higher activity than ICDH (NAD). The activity was similar in controls and in the non-involved skin of the patients with the 4 dermatoses as well as in the lesions of pityriasis rosea. It was increased 60% and 30% in basal layers of the psoriatic and the neurodermite lesions, respectively. The enzymatic activity was decreased 50% in subcorneal layers of lichen planus. In various tissues ICDH (NAD) is considered to be a strictly intramitochondrial enzyme, whereas ICDH(NADP) and FH are found also in the cytosol. If this also applies to epidermis, the results imply differences of mitochondrial function in psoriasis and the contrasted dermatoses. The high activity of ICDH (NAD) in parakeratosis (psoriasis) as compared to that in ortbokeratosis (lichen planus) was also discernable in neurodermatitis when para- and orthokeratotic epidermis were analysed separately.

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Zusammenfassung Die Aktivit?ten der Enzyme Isocitrat Dehydrogenase ICDH (NAD) und ICDH (NADP) und der Fumarat Hydratase (FH) wurden in den subcornealen und basalen Epidermisabschnitten von Patienten mit Psoriasis, Neurodermitis, Lichen ruber und Pityriasis rosea sowie bei gesunden Kontrollpersonen bestimmt. Die Lowry-Mikrotechnik fand durchweg Verwendung, au?er dem Enzym ICDH (NAD), das eine hohe analytische Empfindlichkeit fordert. Das gebildete NADH in dieser Reaktion wurde photokinetisch mit Hilfe von bakterieller Luciferase gemessen.

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Kindly supported by the Swedish Medical Research Council (X19-2593), by the Foundations of Edvard Welander, of J?rgen Schaumann and of the Karolinska Institute and by the Swedish Psoriasis Association, Stockholm.     

Acute guttate psoriasis patients have positive streptococcus hemolyticus throat cultures and elevated antistreptococcal M6 protein titers

To further study the role of Streptococci hemolyticus infection and streptococcal M6 protein in the pathogenesis of acute guttate psoriasis, streptococcal cultures were taken from the throats of 68 patients with acute guttate psoriasis. PCR technique was applied to detect M6 protein encoding DNA from those cultured streptococci. Pure M6 protein was obtained by Sephacry/S-200HR and Mono-Q chromatography from proliferated Streptococcus hemolyticus. Antistreptococcal M6 protein titers were measured in the serum of patients with acute guttate psoriasis, plaque psoriasis and healthy controls by ELISA. A high incidence of Streptococcus hemolyticus culture was observed in the guttate psoriatic group compared with the plaque psoriasis and control groups. Fourteen strains of Streptococcus hemolyticus were cultured from the throats of 68 acute guttate psoriasis patients. Of these, 5 strains contain DNA encoding the M6 protein gene as confirmed by PCR technique. More than 85% purification of M6 protein was obtained from Streptococcus pyogenes. Applying our pure M6 protein with the ELISA methods, we found that the titer of antistreptococcal M6 protein was significantly higher in the serum of guttate psoriasis patients than in the control or plaque psoriasis groups (P < 0.01). We verified that patients of acute guttate psoriasis have a high incidence of Streptococcus hemolyticus in their throats and raised titers of antistreptococcal M6 protein in their sera.     

Monoclonal antibodies cross-reactive with group A streptococci and normal and psoriatic human skin

Infection with group A streptococci has been implicated as a factor capable of exacerbating psoriasis. In order to explore the possibility of cross-reactivity between streptococcal antigens and human skin in this phenomenon, skin from psoriatic patients and control subjects was reacted with 3 monoclonal antibodies against group A streptococci and antibody binding was estimated by the indirect immunofluorescence technique. Monoclonal antibody 54.2.8 stained the nuclei and cytoplasm of cells within the epidermis and epidermal appendages, as well as cells scattered throughout the dermis. In contrast, monoclonal antibodies 49.8.2 and 36.2.2 labeled the cytoplasm of epidermal cells and epidermal appendages but did not react with nuclei. No difference in the staining patterns of control skin and uninvolved skin from patients with psoriasis was observed. However, skin from psoriatic lesions contained large amounts of cross-reactive skin component(s). Sera from patients with guttate psoriasis did not react differently with normal or psoriatic skin when compared with normal sera. Western immunoblots of skin extracts demonstrated that monoclonal antibody 54.2.8 reacted with a family of proteins in the molecular weight range of 60-70K. The results indicate that component(s) in human skin share cross-reactive epitopes with group A streptococci. Immunologic cross-reactions between group A streptococci and human skin may play an important role in the exacerbation of certain skin disorders following streptococcal infections.     

Restricted T-cell receptor Vβ gene usage in the skin of patients with guttate and chronic plaque psoriasis

A strong association between acute guttate psoriasis and group A, β-haemolytic streptococcal infections is well established. Furthermore, streptococcal M proteins and toxins have been shown to act as superantigens, stimulating subpopulations of T lymphocytes expressing particular Vβ families. We have therefore studied the possible role of streptococcal superantigens in psoriasis by staining peripheral T lymphocytes and skin sections from patients with guttate or chronic plaque psoriasis for the expression of nine TCR Vβ families, using a range of monoclonal antibodies. A marked over-representation of Vβ2⁺ T lymphocytes was observed in the dermis and epidermis of patients in both groups, when compared with T lymphocytes in their peripheral blood. A less marked dermal increase in Vβ5.1⁺ T lymphocytes was also observed in these patients. These findings are consistent with the involvement of a superantigen, possibly streptococcal, in the pathogenesis of psoriasis.     

Different in situ distribution patterns of dendritic cells having Langerhans (T6+) and interdigitating (RFD1+) cell immunophenotype in psoriasis, atopic dermatitis, and other inflammatory dermatoses

Dendritic cells bearing Langerhans cell (OKT6+) or interdigitating cell (RFD1+) immunophenotype may be regularly detected within the dermis of chronic skin diseases characterized by a lymphohistiocytic (lymphoreticular) infiltrate. These 2 subsets of antigen-presenting cells within the dermis of lesions of exacerbating chronic plaque psoriasis, exacerbating nummular dermatitis (discoid eczema), atopic dermatitis, allergic contact dermatitis, pityriasis rosea, lichen ruber planus, and cutaneous lupus erythematosus were quantified using computer-assisted morphometry. The mean dendrite length per dermal dendritic cell was significantly higher for RFD1 than for OKT6 (74.4 +/- 0.98 microns vs 70.0 +/- 1.26 microns: p = 0.0023). The mean dendrite length per dermal dendritic cell was remarkably constant for each marker in the various diagnostic categories studied. Disease-specific patterns of total dendrite length and number (expressed per 100 infiltrating mononuclear cells) of these 2 dendritic cell types within the subepidermal infiltrates were obtained. Pityriasis rosea was characterized by its unique high percentage of OKT6+ Langerhans cells. Atopic dermatitis and psoriasis had relatively high percentages of both RFD1+ interdigitating cells and OKT6+ Langerhans cells. Nummular dermatitis had an intermediate number and total dendrite length for OKT6, but was relatively low in RFD1+ cells. Allergic contact dermatitis, lichen planus, and lupus erythematosus had low numbers and dendrite lengths for both dendritic cell subsets. It is suggested that pityriasis rosea is characterized by an abnormal migration pattern of Langerhans cells. Psoriasis and atopic dermatitis may be examples of diseases in which skin-localized antigen-presenting and T-cell-inducing events are continuously taking place. The other diseases may reflect inflammatory processes in which local antigen presentation is less relevant to the tissue reaction.     

The role of streptococcal infection in the initiation of guttate psoriasis.

BACKGROUND AND DESIGN--Although the association between streptococcal infection and guttate psoriasis is well known, to date there has been little information on whether only limited groups and/or serotypes of beta-hemolytic streptococci are involved. One hundred eleven patients with a sudden onset or deterioration of psoriasis were investigated for evidence of streptococcal infection. Of these patients, 34 had acute guttate psoriasis, 30 had a guttate flare of chronic psoriasis, 37 had chronic plaque psoriasis, and 10 had other types of psoriasis. RESULTS--Serologic evidence of recent streptococcal infection was present in 19 (58%) of 33 patients with acute guttate psoriasis compared with seven (26%) of 27 patients with guttate exacerbations of chronic psoriasis. Streptococcus pyogenes was isolated from 19 (17%) of all 111 patients (9 [26%] of 34 with acute guttate psoriasis, four [13%] of 30 with guttate exacerbations of chronic psoriasis, and five [14%] of 37 patients with chronic psoriasis) compared with seven (7%) of 101 of a control population of patients being seen for treatment of viral warts. Other beta-hemolytic streptococci were found with equal frequency in the study and control populations. Thirteen isolates of 10 different streptococcal serotypes were obtained from the 64 patients with guttate psoriasis. These serotypes were similar in distribution and prevalence to those present in the local community. CONCLUSIONS--This study confirms the strong association between prior infection with S pyogenes and guttate psoriasis but suggests that the ability to trigger guttate psoriasis is not serotype specific.     

Perianal Streptococcal Dermatitis Associated With Guttate Psoriasis and/or Balanoposthitis: A Study of Five Cases

Abstract: Perianal streptococcal dermatitis (PSD) is a recently described cutaneous entity caused by group A β-hemolytic streptococci. It is characterized by perianal erythema, sometimes associated with functional disturbances. We describe four children (2 boys, 2 girls) who had acute guttate psoriasis and also PSD. One of these patients also had balanoposthitis. A fifth patient experienced an association of PSD and balanoposthitis without psoriasis. To our knowledge, the association between guttate psoriasis and PSD has only been reported in five children, and the one with balanitis has not been previously reported.     

Lichen planus-like atopic dermatitis: expanding the differential diagnosis of spongiotic dermatitis

Spongiotic dermatitis represents a commonly encountered histopathological pattern seen by dermatopathologists. The differential diagnosis of lymphocyte predominant acute spongiotic dermatitis typically entails atopic dermatitis (AD), contact dermatitis, nummular dermatitis, pityriasis rosea and seborrheic dermatitis. Recently, our group has characterized a distinct subtype of spongiotic dermatitis occurring exclusively in heavily pigmented patients. Clinically, lesions of this subtype are nearly indistinguishable from lichen planus. However, the histology is contradistinctive to classic lichen planus. The purpose of this report is to raise awareness among dermatopathologists of this variant as a possible diagnosis in spongiotic dermatitis specimens submitted as lichen planus.     

Intraepidermal nerve fiber expression of calcitonin gene-related peptide, vasoactive intestinal peptide and substance P in psoriasis

In order to evaluate more fully the role of neuropeptides in the pathogenesis of psoriasis, skin biopsies were obtained from 36 patients with psoriasis to identify substance P (SP), vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP). Lesional and nonlesional skin was examined from these biopsies and the results compared with those from biopsies taken from patients with a variety of other inflammatory dermatoses, including lichen planus, lichen simplex chronicus, spongiotic dermatitis, and seborrheic dermatitis. Also studied was a series of nine biopsies taken from patients with no known skin disorders. We found an increase in the number of SP-positive nerve fibers within the epidermis in biopsies from lesional skin of psoriasis patients (8.4 nerves per 3-mm biopsy) compared with nonlesional psoriatic skin (2.6 nerves per 3-mm biopsy) and normal skin (2.0 nerves per 3 mm biopsy). Other inflammatory disorders also demonstrated fewer SP-positive nerves than lesional psoriatic skin; lichen planus (0 nerves per 3 mm biopsy) and lichen simplex chronicus (1.3 nerves per 3 mm biopsy). The difference in SP-positive nerve expression between lesional psoriatic skin and the group comprising nonlesional skin, normal skin, lichen planus, and lichen simplex chronicus attained statistical significance ( P < 0.013). SP-positive intraepidermal nerve fibers in lesional psoriatic specimens were fewer than in spongiotic dermatitis (17.4 nerves per 3 mm biopsy). There was no significant difference in numbers of VIP- or CGRP-immunopositive intraepidermal nerve fibers between psoriatic skin and the group comprising all other material tested. However, in five patients with psoriasis, there was a marked increase in the expression of intraepidermal CGRP (up to 10.7 nerves per 3-mm biopsy) and VIP (up to 8.3 nerves per 3-mm biopsy) which was not observed in control groups. These findings suggest that neuropeptides SP, CGRP, and VIP play a role in the pathogenesis of psoriasis. Received: 3 March 1997     

Evidence for the presence of bacteria in the blood of psoriasis patients

Evidence exists that microorganisms, particularly in the throat and skin, play a role in the pathogenesis of psoriasis. The aim of this study was to investigate whether evidence for the presence of bacteria, including Streptococcus pyogenes, can be demonstrated in the peripheral blood of patients with guttate and/or chronic plaque psoriasis. Peripheral blood samples from 20 patients with psoriasis, seven guttate, six chronic plaque and seven chronic plaque with associated guttate flare and from 16 control subjects were studied for the presence of bacteria by PCR using universal 16S ribosomal DNA primers and specific primers for S. pyogenes. Sequence analysis of amplified 16S rRNA sequences was used to determine taxonomic identity. Ribosomal bacterial DNA was detected in the blood of all 20 patients with psoriasis, but in none of the controls. Streptococci were detected in six of seven patients with guttate psoriasis, but none had staphylococci. In contrast, staphylococci were identified in 9 of 13 patients with chronic plaque psoriasis, whilst only 2 demonstrated streptococci. In three psoriasis patients, species other than streptococci and staphylococci were identified. These findings suggest that psoriasis is associated with bacteraemia, with distinct taxonomic groups present in guttate and chronic plaque psoriatic subtypes. The causes of the bacteraemia and its implications in psoriasis have yet to be determined.     

Peripheral blood lymphocytes from psoriatic patients are hyporesponsive to β-streptococcal superantigens

The strong association of acute guttate psoriasis and streptococcal throat infection, together with the preferential use of T cells expressing a particular T-cell receptor, has suggested a role for bacterial superantigens in the pathogenesis of psoriasis. We examined the proliferative responses of peripheral blood lymphocytes (PBLs), obtained from patients with psoriasis and from healthy controls, to streptococcal superantigens, cytoplasmic membrane-associated protein (CAP) and secretion-type CAP (SCAP), isolated from group A, β-haemolytic streptococci. PBLs from patients with psoriasis showed significantly less response to SCAP and CAP than those from healthy controls. Because there was no difference between psoriatic patients and controls in the proliferative response of PBLs to staphylococcal enterotoxin A or E (SEA, SEE) or the mitogen phytohaemagglutinin (PHA), these findings strongly suggest that the reduced reactivity to the streptococcal superantigens seems to reflect anergy of a population of PBLs to the superantigens. As the CAP used in the present study stimulates Vβ8 T cells selectively, we further examined the proliferation of Vβ8 T cells after such stimulation using flow cytometry. Vβ8 T cells obtained from three of four psoriatic patients failed to proliferate in the presence of CAP, whereas they proliferated vigorously in the presence of SEE, which activates Vβ8 T cells, confirming the specific hyporesponsiveness of PBLs from psoriatic patients to streptococcal superantigens. We then determined the effects of serum factors on the suppressed response of PBLs to the streptococcal superantigens with SCAP or CAP. It was partially restored when PBLs were cultured with sera obtained from healthy subjects, although the responses were still significantly lower than those of the healthy controls. In contrast, psoriatic sera markedly suppressed the proliferative response of PBLs from healthy controls to CAP or SCAP, but showed no suppression of the proliferative response of PBLs to SEA. Because these findings suggest the presence of specific inhibitory factors in psoriatic sera, we examined whether the inhibitory effect was caused by antisuperantigen antibody. However, no significant increase was detected in antibody titre to CAP in psoriatic sera, as has been noted in sera from patients with poststreptococcal glomerulonephritis. The present results show for the first time the hyporesponsiveness of PBLs to streptococcal superantigens and the presence of serum inhibitors that specifically inhibit T-cell response to the superantigens in psoriatic patients. These findings suggest a pathological role for streptococcal infections in the pathogenesis of psoriasis.     

Cellular localization of fractalkine at sites of inflammation: antigen-presenting cells in psoriasis express high levels of fractalkine.

BACKGROUND: Chemokines play a key role in cell trafficking at sites of inflammation. The fractalkine CX3C chemokine is unique in several aspects. Fractalkine is expressed on activated endothelial cells and exists in two forms, either membrane anchored or in a soluble form. The soluble form is a potent chemotactic agent for T cells/monocytes and the anchored form functions as an adhesion molecule. In view of these specific functions fractalkine is capable of controlling the key regulatory mechanisms of cell trafficking at sites of inflammation. OBJECTIVES: Little is known about the significance of this important molecule in inflammatory diseases. We undertook this study to elucidate the role of fractalkine in inflammatory diseases of the skin. METHODS: We used a polyclonal antifractalkine antibody (immunoperoxidase and immunofluorescence stainings) in cryosections obtained from tissues of normal skin and that of selected cutaneous inflammatory diseases (psoriasis, lichen planus, eczema). RESULTS: Increased expression of fractalkine was observed in the dermal blood vessels of lichen planus, eczema and psoriasis tissues. The most striking finding was that the dermal dendrocytes in the papillary dermis of psoriasis tissues expressed high levels of fractalkine. Compared with 186.64 +/- 51.69 fractalkine positive dermal dendrocytes per mm2 of the upper dermis of psoriatic tissue, the number of positive cells in lichen planus, eczema, and normal skin were 17.29 +/- 12.50, 12.50 +/- 6.75 and 5.93 +/- 3.53, respectively. We also performed double label immunofluorescence staining with nerve growth factor receptor (NGF-R) antibody and fractalkine antibody. NGF-R-positive terminal cutaneous nerves were in close contact with the fractalkine-positive dermal dendrocytes in psoriatic lesions. CONCLUSIONS: The results of this study confirm that fractalkine is upregulated at sites of inflammation. Thus, it is likely that this molecule plays a key part in cell trafficking. An increased expression of fractalkine at the dermal papillae provides a plausible explanation for the migration and accumulation of T cells at these sites in psoriasis. Earlier studies have reported an increased number of dermal dendrocytes in psoriatic tissue; however, the functional role of these cells in the pathogenesis of psoriasis is largely unknown. Expression of fractalkine on the surface of dermal dendrocytes suggests an active role for these cells in localization and activation of lesional T cells.     

Phenotype and suppressor activity of T-lymphocyte clones extracted from lesions of oral lichen planus

Lymphocytes were extracted from six biopsy specimens of oral lichen planus. T-lymphocyte lines were expanded in culture with phytohaemagglutinin and interleukin 2, and cloned by limiting dilution. Fifteen T-cell clones were isolated with a probability of clonality of 96.3%. The majority of clones (n=13) expressed the αβ T-cell receptor, and of these, 11 were CD8⁺ and two were CD4⁺. Two clones were CD4^? and CD8^?, and expressed the γδ T-cell receptor. The ability of these clones (effectors) to suppress concanavalin-A-stimulated proliferation of autologous lesional T-cell lines (responders) was assessed. Maximum suppressor activity ranged from 17 to 100%. The majority of clones (n=12), including a CD3⁺ CD4⁺CD8^?αβ⁺ clone, displayed suppressor activity which was proportional to the effector to responder ratio. A CD3⁺CD4⁺CD8^?αβ⁺ clone and a CD3⁺CD4^?CD8^?γδ⁺ clone displayed substantial helper activity at higher effector to responder ratios. These results demonstrate differential helper and suppressor activity of T-lymphocyte clones extracted from oral lichen planus lesions. The balance between help and suppression may be a fundamental determinant of immunological activity within the lymphocytic infiltrate of oral lichen planus, and hence may dictate the clinical behaviour of the disease.     

Proteome analysis of skin distinguishes acute guttate from chronic plaque psoriasis

Psoriasis is a disease with considerable heterogeneity in clinical presentation. This is the first study using two-dimensional gel electrophoresis to compare global protein expression patterns in lesional and non-lesional skin from subjects with acute guttate psoriasis associated with streptococcal throat infection and chronic plaque psoriasis. Samples from experimentally induced contact eczema and normal skin from healthy controls were also included. Proteins with statistically significant differences in expression were used in hierarchical cluster analyses resulting in separation of the different samples into groups. Chronic plaque and guttate psoriasis samples were distinctly separated, indicating that they represent discrete phenotypes at the protein expression level. Interestingly, there was a trend in which guttate psoriasis lesions clustered closer to eczema than to chronic plaque psoriasis lesions, indicating that the duration of the inflammatory reaction may affect clustering. Several of the differentially expressed proteins were identified by mass spectrometry.     

银屑病患者血清中链球菌抗体的研究

为了进一步证实链球菌感染与银屑病的关系,我们应用免疫印迹法测试了银屑病患者血清中抗链球菌、抗金黄色葡萄球菌及抗白念珠菌抗体含量.发现点滴型银屑病患者的抗链球菌抗体含量不仅显着高于正常人对照组(P<0.01),亦高于慢性斑块型银屑病患者(P<0.05);但其抗金黄色葡萄球菌、抗白念珠菌抗体含量与对照组相比,结果均无显着性差异(P>0.05).本研究证明了链球菌感染与点滴型银屑病密切相关.     

Differential T-cell reactivity to the round and oval forms of Pityrosporum in the skin of patients with psoriasis

Pityrosporum yeasts have been implicated as a trigger for the initiation of scalp lesions in psoriasis. To determine whether Pityrosporum-reactive T cells are present in lesional psoriatic skin. T-cell lines (TCL) were cultured from the scalps of nine patients with psoriasis and seven with alopecia areata (disease controls), and from non-scalp lesions from six of the psoriatic patients. The psoriatic skin TCL were stained for CD3, CD4, CD8 and TCR αβ expression and tested in a proliferation assay with Candida albicans and purified protein derivative (PPD), and cytoplasmic and cell-wall extracts of P. ovale (oval) and P.orbiculare (round). The proliferative responses of corresponding peripheral blood mononuclear cells (PBMC) were also determined. All the PBMC samples responded to the Pityrosporum extracts to variable extents, but no significant difference in the response of the group to the two different forms of yeast was observed. The response was mediated by CD4⁺ T cells and inhibited by the addition of anti-HLA-DR antibody. In addition, all nine psoriatic scalp TCL, which were predominately CD3⁺, CD4⁺ TCR αβ⁺, responded to the cytoplasmic, and five of nine TCL to the cell-wall extract of P. orbiculare. In contrast, only three of the nine TCL proliferated to either extract of P. ovale. This difference was significant for both the cytoplasmic (P < 0.01) and cell wall (P = 0.01) extracts. Similarly, the TCL cultured from non-scalp psoriatic lesions also showed a more marked response to the P. orbiculare extracts (P = 0.05). Furthermore, four of seven and two of seven scalp TCL from lesions of alopecia areata responded to the P. orbiculare and P. ovale extracts, respectively; these responses did not differ significantly from those of the psoriatic scalp TCL. None of the skin TCL responded to either Candida albicans or PPD. These findings demonstrate that T cells with differential reactivity to the round and oval forms of Pityrosporum are present in, but are not specific for, psoriatic skin lesions. A role for these cells in the pathogenesis of psoriasis remains speculative.     

真菌荧光染色法检测健康皮肤和炎症性皮损的真菌定植

目的:利用荧光染色法检测健康皮肤和炎症性皮损的真菌阳性率及定植数量。方法:门诊收集正常皮肤及银屑病、特应性皮炎、湿疹和玫瑰糠疹患者,采集每位患者和健康对照组皮脂溢出部位(面部、胸部和背部)、干燥部位(双上肢)、潮湿部位(腹股沟、腘窝、肘窝)、头皮及足底部位的皮损皮屑,利用真菌荧光染色试剂快速染色,随机选择30个视野计数真菌(孢子)数量,数据使用R 3.5.3软件进行统计学分析。结果:共收集457例患者和888名健康对照,健康对照头皮和皮脂溢出部位的真菌检出率高分别为95%和96%,足底真菌检出率最低(44.29%)。湿疹组、银屑病组和玫瑰糠疹组皮脂溢出部位的真菌检出率分别为77.05%、66.67%、91.42%高于相应的干燥部位58.93%、47.62%、57.89%。在头皮、皮脂溢出部位、干燥部位,疾病组真菌检出率低于健康组,差异有统计学意义(均P<0.05)。健康组4个部位真菌分布的数量不同且差异有统计学意义(P<0.05)。皮脂溢出部位中,18～44岁年龄组孢子数量最多。结论:健康皮肤不同部位的真菌阳性率和孢子数量不同。特应性皮炎、湿疹、银屑病和玫瑰糠疹的皮损部位真...