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T M Zollner

Publications and source records attributed to T M Zollner.

At least 19 recordsLinked to original sources
PubMed1999

[The role of bacterial superantigens in pathophysiology of the skin].

In contrast to conventional antigens, bacterial superantigens activate a large percentage of an organism's total T-cell repertoire. This has clinical implications particularly in the case of infections with Gram-positive bacteria. Unravelling the molecular mechanisms of superantigen-mediated T-cell activation has yielded new insights in the pathogenesis of a number of diseases, in the field of dermatology namely atopic dermatitis and psoriasis. Moreover, therapeutic applications of superantigens have begun to emerge.

Dermatitis, Atopic↗
PubMed1997

[Nail polish allergy. An important differential diagnosis in contact dermatitis].

HISTORY AND CLINICAL FINDINGS: Case 1. A 34-year-old woman presented with a recurrent, itching and erythematous plaque on her right cheek. Case 2. A 27-year-old woman reported itching erythema on her fingertips from time to time recently. Inspection revealed dyshidrosiform blisters. Both patients had been using nail varnish and varnish remover. Case 3. A 49-year-old woman had, for about 5 years, repeatedly experienced itching erythema at the perionychium of several fingers on which she had placed artificial nails. Marked oedema and erythema was noted. INVESTIGATION: Extensive epicutaneous tests were performed on these patients. They showed sensitisation against important allergens in nail varnish (toluolsulphonamide-formaldehyde resin), nail varnish remover (benzophenone-2) and artificial nails (ethylacrylate), respectively. The three patients also showed type IV sensitisation against other substances. DIAGNOSIS, TREATMENT AND COURSE: Epicutaneous tests documented type IV allergies to important constituents of nail varnish, nail varnish remover and artificial nails. Symptoms and skin changes disappeared when these three items were no longer used. CONCLUSION: Allergies against nail varnish and its remover and against artificial nails should be included in the differential diagnosis of skin allergies, even when patients have additional type IV sensitizations against common allergens. As the causative allergen can be easily avoided, knowledge of the particular problems associated with these allergies is of a great practical significance.

Adult↗
PubMed1997

Induction of psoriasiform inflammation by a bacterial superantigen in the SCID-hu xenogeneic transplantation model.

Psoriasis is a chronic skin disease affecting about 2% of the Caucasian population, characterized by co-existing inflammation and epidermal hyperproliferation. A T-lymphocyte-mediated autoimmune reaction induced by bacterial superantigens might be central in its pathogenesis. To model psoriasiform inflammation, we transplanted clinically uninvolved skin from psoriatic patients onto SCID mice. Repetitive intradermal injections with a bacterial superantigen and simultaneous intraperitoneal injections with the patients superantigen-stimulated peripheral mononuclear blood cells resulted in an inflammatory reaction exhibiting some of the hallmarks of psoriasis, e.g. epidermal hyperproliferation, papillomatosis, focal neo-expression of ICAMI, and an exocytotic T-lymphocytic infiltrate characterized by the expression of the cutaneous lymphocyte-associated antigen. These observations document the potential of superantigens to trigger psoriasiform dermatitis and provide a model to study lymphocyte homing.

Animals↗
PubMed1997

Alopecia areata but not androgenetic alopecia is characterized by a restricted and oligoclonal T-cell receptor-repertoire among infiltrating lymphocytes.

Although the etiology of alopecia areata is still unknown, evidence has accumulated to support an autoimmune pathogenesis for this disease. To evaluate the role of T cells in alopecia areata the T-cell receptor VB-repertoire was investigated in lesional skin and blood of 5 patients by means of a semiquantitative technique based on the reverse transcriptase polymerase chain reaction. Three patients with androgenetic alopecia served as controls. Amplification products were screened for clonality by temperature gradient gel electrophoresis. Four of 5 patients with alopecia areata exhibited a lesional T-cell receptor-repertoire characterized by an almost exclusive utilization of variable regions beta 2, 4, and 13. Temperature gradient gel electrophoresis revealed the oligoclonal constitution of the infiltrate. The restricted nature of the lesional T-lymphocytic infiltrate in alopecia areata strongly suggests that an antigen-specific T-cell response plays an important role in the pathogenesis of this disease.

Adult↗
PubMed1997

Superantigens but not mitogens are capable of inducing upregulation of E-selectin ligands on human T lymphocytes.

Bacterial infections can exacerbate immune mediated dermatoses, possibly via superantigens produced by these bacteria. Therefore, we asked whether superantigens induce the expression of adhesion molecules which may then facilitate invasion of highly activated T cells into different organs. The influence of exfoliative toxin (ET) and toxic shock syndrome toxin-1 (TSST-1) stimulation on the expression of a broad panel of adhesion and costimulatory molecules was investigated by flow cytometry. We found that only the E-selectin ligands cutaneous lymphocyte-associated antigen (CLA) and sialylated Lewis(x) (CD15s) are significantly upregulated by these superantigens but not by mitogen stimulation. In contrast, the mucosal lymphocyte-associated antigen (MLA) recognized by the monoclonal antibody Ber-Act8 was not differentially induced by mitogen or superantigen stimulation. Therefore, T lymphocyte stimulation by bacterial superantigens might directly influence their skin homing capacity. Furthermore, the superantigen-driven induction of CD15s-an adhesion molecule which is absent or only weakly expressed by resting or mitogen stimulated T cells-may indicate a role of this antigen for T cell skin homing. An additional adhesion pathway via E-selectin may thus be available to lymphocytes, comparable to granulocytes which constitutively express CD15s.

Antigens, CD↗
PubMed1997

Leg ulcers in Klinefelter's syndrome--further evidence for an involvement of plasminogen activator inhibitor-1.

An abnormality in platelet aggregability or fibrinolysis, namely elevated activity of plasminogen activator inhibitor-1 (PAI-1), has been recently documented in patients suffering from Klinefelter's syndrome associated with leg ulceration without underlying venous insufficiency. To determine whether increased PAI-1 activity is a general feature of Klinefelter's syndrome, or more specifically associated with leg ulceration, we investigated PAI-1 influencing parameters and PAI-1 activity in two groups of patients: (i) Klinefelter patients suffering from leg ulceration (n = 7); and (ii) Klinefelter patients without leg ulceration (n = 6). On analysing PAI-1 influencing parameters such as age, body mass index, triglycerides, C-reactive protein, testosterone, smoking behaviour, the presence of diabetes mellitus, and arterial hypertension, respectively, we found no statistically significant differences between the two groups. However, PAI-1 activity in group 1 was highly significantly elevated compared with that in group two patients (P < 0.005). We conclude that (i) PAI-1 activity is not elevated in Klinefelter's syndrome in general; (ii) elevation of PAI-1 activity in patients suffering from Klinefelter's syndrome does not appear to be secondary to PAI-1 influencing parameters; and (iii) elevation of PAI-1 activity may play a crucial role in the pathogenesis of leg ulceration in Klinefelter's syndrome. Therefore, a therapy for leg ulceration in Klinefelter's syndrome that aims to return the elevated PAI-1 activity to normal should be explored.

Arterial Occlusive Diseases↗
PubMed1997

The transformation of pityriasis lichenoides chronica into parakeratosis variegata in an 11-year-old girl.

Parakeratosis variegata is a rare disorder with unknown aetiology. In a few cases it arises from benign skin diseases such as pityriasis lichenoides et varioliformis acuta (Mucha Habermann disease) or pityriasis lichenoides chronica. However, transformation into malignant diseases such as cutaneous T-cell lymphoma has been observed. We report an 11-year-old girl with a 10-year history of pityriasis lichenoides chronica now presenting with parakeratosis variegata. Analysis of skin infiltrating T cells showed clonally rearranged T-cell receptor gamma chains occurring with a frequency of more than 2%. This finding is compatible with the clinical observation of parakeratosis variegata transforming into a malignant T-cell disorder. We therefore suggest that patients suffering from parakeratosis variegata and other diseases such as pityriasis lichenoides et varioliformis acuta or pityriasis lichenoides chronica should be continuously monitored.

Child↗
PubMed1996

The superantigen exfoliative toxin induces cutaneous lymphocyte-associated antigen expression in peripheral human T lymphocytes.

Several immune-mediated dermatoses including psoriasis and atopic dermatitis can be exacerbated by bacterial infections. Superantigen producing bacteria can be isolated from skin lesions of these dermatoses. Consistent with superantigen effects, skewed T cell receptor variable gene usage has been demonstrated within these lesions. Therefore, the question arises whether superantigen induce a skin-seeking phenotype within peripheral T cells. In this study, we investigated the in vitro influence of the V beta 2-selective superantigen exfoliative toxin from Staphylococcus aureus on the expression of the cutaneous lymphocyte-associated antigen on peripheral T lymphocytes of healthy donors. We demonstrate that exfoliative toxin dramatically upregulates cutaneous lymphocyte-associated antigen expression on T cell receptor V beta 2+ lymphocytes. Up to 69% of V beta 2+ lymphocytes expressed cutaneous lymphocyte-associated antigen after 5 days of in vitro culture. Additionally, exfoliative toxin also increased cutaneous lymphocyte-associated antigen expression in CD3+ T cell receptor V beta 2- lymphocytes indicating a different effect as caused by the superantigen-T cell receptor V beta 2 interaction. Our findings suggest influence of bacterial superantigens on T lymphocyte skin homing in vivo.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1995

T-cell-receptor repertoire in chronic plaque-stage psoriasis is restricted and lacks enrichment of superantigen-associated V beta regions.

Preferential usage of certain T-cell receptors by the lymphocytic infiltrate in psoriasis might indicate the involvement of an antigen in the pathogenesis of this disease. However, to date there are no data on the complete T-cell-receptor V alpha and V beta repertoire in psoriatic patients. We therefore compared the usage of T-cell-receptor variable regions in blood and skin of 10 patients with chronic plaque-stage psoriasis by means of semiquantitative polymerase chain reaction. Additionally, HLA class II alleles were analyzed by means of sequence-specific oligonucleotide typing. A considerable restriction of the T-cell-receptor repertoire was observed in the skin, where up to 20% of the variable regions present in the blood were not detectable. This was true for both alpha- and beta-chains. However, no interindividually constant pattern of T-cell-receptor restriction was deducible. Inconsistently, a certain preferential usage of some beta chains occurred within the cutaneous compartment. This report on the complete T-cell-receptor V alpha and V beta repertoire in psoriasis documents the restricted receptor repertoire of infiltrating T cells and a lack of enrichment of superantigen-associated V beta regions. Thus superantigens seem not to play a pathogenetically relevant role in chronic plaque-stage psoriasis.

Genetic Heterogeneity↗
PubMed1994

Differential expression of heat shock protein 70 (HSP70) and heat shock cognate protein 70 (HSC70) in human epidermis.

Autoimmunity and microbial agents have been suggested as playing a pathogenetic role in psoriasis. Since immune responses to microbial infections are often directed towards heat shock proteins (HSP), we investigated the expression of three HSP families in normal and inflamed human skin. Specimens from ten patients with psoriasis and three patients with positive patch tests for nickel and from five healthy volunteers were analysed by means of immunohistochemistry. The patterns observed were qualitatively similar in these conditions showing only minor quantitative differences. Psoriatic epidermis exhibited the highest level of expression. HSP27, HSP70 and heat shock cognate protein 70 (HSC70) were readily detectable. HSP27 was homogeneously distributed throughout the epidermis, whereas HSP70 was restricted to the basal layer and HSC70 primarily to the suprabasal layers. Other HSPs were detected to a lesser degree and showed a more irregular pattern. Thus, the qualitative expression pattern of HSPs seems to be constant between different skin conditions, but the expression of constitutive and inducible HSP70 depends on the differentiation state of keratinocytes.

Blotting, Western↗
PubMed1994

Enhancement of MHC-unrestricted cytotoxic activity of human CD56+ CD3- natural killer (NK) cells and CD3+ T cells by rhamnogalacturonan: target cell specificity and activity against NK-insensitive targets.

Rhamnogalacturonan-mediated enhancement of MHC-unrestricted cytotoxicity was studied with freshly isolated CD56+CD3- natural killer (NK) cells, interleukin-2 (IL-2)-activated CD56+ lymphokine-activated killer (LAK) cells und IL-2/anti-CD3-activated T cells as effector cells using NK-sensitive and NK-insensitive tumor cells as targets. The rhamnogalacturonan fractions IM, IP, and IQ were prepared from commercially available extracts of Viscum album. The dose/response relation of IM, IP, and IQ demonstrated the presence of various concentrations of cytotoxicity-enhancing compounds in all three fractions that were identified as rhamnogalacturonans by degradation studies with poly-alpha-D-galacturonidase (EC 3.2.1.15) and alpha-1,6-rhamnosidase (EC 3.2.1.40). Specific cytotoxicity of all three effector cell populations as well as the respective rhamnoagalacturonan-mediated cytotoxicity enhancement was readily inhibited in a dose-dependent manner by 60%-deacetylated mannose pentaacetate. Rhamnogalacturonan-mediated enhancement of cytotoxicity of fresh CD56+ NK cells was also observed with four of five NK-insensitive tumor cells as targets, indicating that the effector-cell/tumor-cell bridging activity of rhamnogalacturonans renders NK-insensitive targets susceptible to NK-mediated lysis. Moreover, the rhamnogalacturonan-mediated cytotoxicity enhancement became even more prominent when lymphokine-activated CD56+ LAK and CD3+ T cells were assayed with the NK-insensitive tumor cell targets.

Antigens, CD↗