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Biomedical subjects

B Volc-Platzer

Publications and source records attributed to B Volc-Platzer.

At least 37 records · Page 2Linked to original sources
PubMed1998

Improvement of physical fitness and muscle strength in polymyositis/dermatomyositis patients by a training programme.

In the present investigation, the benefit of physical training in patients with inflammatory myopathy was studied. In this prospective, randomized, controlled study, 14 patients with polymyositis (PM) or dermatomyositis (DM) were investigated. The training, consisting of bicycle exercise and step aerobics, took place over a 6 week period. Baseline and endpoint measurements included an 'activities of daily living' (ADL) score, peak isometric torque (PIT) generated by muscle groups in the lower extremities, peak oxygen consumption (VO2max), and creatine phosphokinase (CPK) levels. There was no significant rise in disease activity in the training group in comparison to the controls. The ADL score for the treatment group, in comparison to the control group, improved (P < 0.02), PIT rose (P < 0.05) and there was a statistically significant increase in oxygen uptake relative to body weight (P < 0.05). No rise in inflammatory activity, but significant improvement in muscle strength, oxygen uptake and well-being, were found in patients with inflammatory myopathy as a result of physical training. Besides medication, a physical training programme consisting mainly of concentric muscle contractions should therefore be an integral part of therapy, particularly in view of the cardiopulmonary risk of these patients.

Adult↗
PubMed1997

Complete remission of lichen-planus-like graft-versus-host disease (GVHD) with extracorporeal photochemotherapy (ECP).

A 45-year-old female patient with CML underwent allogeneic BMT and developed two episodes of acute GVHD. The first episode of acute cutaneous GVHD grade II (day +17) responded well to systemic CsA and steroids. During the second episode (around day +60) the patient developed erythroderma (grade III), and subsequently signs of lichen-planus-like GVHD. The patient did not respond to increased dosages of prednisolone and CsA. On day +89 extracorporeal photochemotherapy (ECP) was initiated. After four cycles, a significant improvement of erythroderma and lichen-planus-like lesions was documented, and after 12 cycles, a lasting complete remission was achieved. To our knowledge this is the first report of successful treatment of early-onset, lichen-planus-like GVHD after allogeneic BMT with ECP.

Acute Disease↗
PubMed1996

Expression of the monoclonal antibody HECA-452 defined E-selectin ligands in Langerhans cell histiocytosis.

The cutaneous lymphocyte associated antigen (CLA) recognized by the monoclonal antibody (moAb) HECA-452 plays a major role in the homing of lymphocyte subpopulations to the skin by binding to E-selectin on dermal microvessels. The factors responsible for the immigration of Langerhans cells (LC) and their precursors into the skin are still unknown, but because normal resting LC are also capable of expressing CLA, the antigen was proposed as a candidate LC-homing structure. To gain insight into these mechanisms, the expression of HECA-452 on neoplastic LC within and outside the skin was investigated in paraffin-embedded sections from 44 patients with localized and disseminated forms of Langerhans cell histiocytosis (LCH) presenting with proliferating cells positive for CD45, CD1a, S100 and HLA-DR. Irrespective of the clinical presentation or the type of organ involved, HECA-452 positive LC were detected in all biopsies tested (range 5->90%). The most prominent HECA-452 reactivity was observed in skin lesions and in areas with accumulations of eosinophilic granulocytes. Our data provide evidence for heterogeneous expression of sLex/sLea structures in various stages of activated and/or differentiated LCH cells. Remarkably, CLA-antigen expression on LCH-cells was not restricted to cutaneous sites. In view of recent findings on the expression of HECA-452 on resting epidermal LC, our data are compatible with the view that local cytokine production by keratinocytes or cells from the surrounding infiltrate induce and/or modulate CLA expression on LC in both cutaneous and extra-cutaneous sites.

Antibodies, Monoclonal↗
PubMed1994

Autoimmune-thrombocytopenia and SLE in a patient with 5q-anomaly and deletion of the c-fms oncogene.

Autoimmune-thrombocytopenia was the striking feature in a patient with typical clinical symptoms of systemic lupus erythematosus (SLE), complement C4 deficiency, and positive lupus serology. However, myelodysplasia was found in the bone marrow and chromosome analysis revealed a deletion of the long arm of chromosome 5 (5q-anomaly), which was confirmed by a hemizygosity for the c-fms oncogene (CSF-1-receptor) on Southern blot. Autoimmune phenomena reported in conjunction with myelodysplastic syndromes (MDS), e.g., an elevation of antinuclear antibodies, are usually regarded as nonspecific. This case report suggests that SLE can occur in patients with MDS and that a concomitant autoimmune-thrombocytopenia may mask the typical signs of the 5q- syndrome.

Adult↗
PubMed1994

Association between chronic cutaneous lupus erythematosus and HLA class II alleles.

CCLE, a disease entity at the benign end of the lupus spectrum, is characterized by marked photosensitivity and skin lesions in sun-exposed areas. The histopathology of lesions resembles hypersensitivity type IV reactions. We have asked whether an association between class II alleles and CCLE exists. RFLP analysis of HLA-DQA genes revealed a Taq I HLA-DQA1 allelic restriction fragment overrepresented in a group consisting of 26 patients as compared to healthy control individuals. This result was corroborated by typing with oligonucleotide probes. The presence of the DQA1*0102 allele in the patients' group led to a relative risk of 4.57, with a statistical significance of p < 0.05 after correction for 36 comparisons. Although not statistically significant, it is interesting that all patients possess in at least one of their HLA-DQA1 alleles a nucleotide sequence coding for the amino acid glutamine at position 34 of the DQ alpha molecule. The expected frequency of these alleles in the control population amounts to 82%. The HLA-DRB1*16 allele, which is found in linkage disequilibrium with the HLA-DQA1*0102 allele, is also observed at an increased frequency in the patient's group, though the association was not significant after correction for the number of comparisons. However, no associations of CCLE with alleles at the HLA-DPB1 locus was found. The association of CCLE with certain HLA class II alleles points to an involvement of HLA-DQ and/or -DR molecules in the pathogenesis of the disease. Alternatively, genetic loci in linkage disequilibrium may code for elements which contribute to the development of CCLE.(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1994

Constitutive expression of chimeric neo-Rev response element transcripts suppresses HIV-1 replication in human CD4+ T lymphocytes.

We have previously reported that chimeric neomycin phosphotransferase (neo)-Rev response element (RRE) transcripts suppress the function of the human immunodeficiency virus type 1 (HIV-1) Rev trans-activator protein in HeLa cells. In an extension of these experiments, human CD4+ CEM cells (G418-resistant cell populations and clonal isolates) stably expressing chimeric neo-RRE genes (2, 3, or 6 RRE copies) were generated using retroviral-mediated gene transfer. The transduced CEM clones were infected with the HIV-1 HTLVIIIB isolate and the following three phenotypes were observed: (i) the transduced CEM cells were readily infected with HIV-1 indistinguishable from the control CEM cells; (ii) the appearance of HIV-1 replication markers was significantly delayed; (iii) no signs of HIV-1 replication were detectable although proviral HIV-1 DNA sequences could be detected in these cells. Furthermore, HIV antigen expression was limited in neo-resistant CEM cell populations inoculated with the HIV-1 HTLVIIIB isolate. Only 10% of the CEM-pX17-3xRRE cells and 20% of the CEM-pX17-2xRRE cells displayed HIV-1 antigens 43 days after challenge and had retained CD4 surface expression on 47% and 64% of the cells, respectively. In sharp contrast, 80% of the CEM-pX17 or the CEM-pX17-6xRRE cells expressed HIV-1 antigens but no CD4 antigens were detectable in these cultures. These results clearly indicate that RRE decoys could be developed into an effective somatic gene therapy approach against HIV-1 induced acquired immunodeficiency syndrome (AIDS).

Base Sequence↗
PubMed1994

Expression of monoclonal antibody HML-1-defined alpha E beta 7 integrin in cutaneous T cell lymphoma.

Considering that integrins may play a major role in the localization in distinct biological features as well as in the dissemination of several types of lymphomas, we studied the expression of the monoclonal antibody HML-1-defined alpha E beta 7 integrin (CD103) in the clinically and histologically determined stages of 53 mycosis fungoides (MF) skin biopsies and in 16 affected lymph nodes. Immunoperoxidase staining revealed HML-1 immunoreactivity with T cells in the early stages of disease (patch and plaque stage MF). HML-1 expression was more pronounced on infiltrating epidermal than on dermal T cells. In contrast to early stages, tumor stage MF and lymph nodes affected in the course of cutaneous T cell lymphoma were HML-1 negative. We found a strong association between HML-1 expression, epidermotropism of infiltrating T cells, and the stage of disease. We provide evidence that: 1) the loss of the HML-1 antigen on T cells in MF is a marker of poor prognosis and 2) because the HML-1 antigen is selectively expressed on T lymphocytes of epithelial sites such as gut and skin, our results are compatible with the view that alpha E beta 7 integrins perform homing receptor functions for epitheliotropic T cells.

Antibodies, Monoclonal↗
PubMed1993

Accumulation of gamma delta T cells in chronic cutaneous lupus erythematosus.

Monoclonal antibodies (moAbs) that recognize common or variable determinants of the gamma delta T-cell receptor (TcR) were used to assess gamma delta T-cell distribution on biopsy specimens and/or peripheral blood leukocytes (PBL) from 30 patients suffering from chronic cutaneous lupus erythematosus (CCLE). CD3+/gamma delta TcR + T cells were evaluated in 15 biopsies from patients with CCLE lesions, their numbers varying from 0.5 to 15.0% of all intralesional CD3 +T cells present. In all specimens from lesional skin gamma delta TCR+T cells were BB3 + and/or Ti gamma A +, indicating predominant use of the V gamma 2/V delta 2 phenotype. In the CCLE lesions the intraepidermal V gamma 2/V delta +T cells were observed in close vicinity to the damaged basal keratinocyte (KC) layer, and also randomly scattered among the densely packed inflammatory infiltrate in the dermis. In contrast to the immunohistologic findings, no numerical increase of gamma delta TcR+T cells could be observed among PBL from 28 of 30 CCLE patients. Only one CCLE patient being treated with hydroxychloroquine for two months had 15% CD3 +/gamma delta TcR+T cells among the PBL. Based on the immunohistologic findings one may infer that in CCLE, a skin-restricted form of LE, V gamma 2/V delta 2 +T cells expand extrathymically to an as yet unknown stimulus. One may also propose that these gamma delta T cells--based on their cytotoxic capacity--may contribute to the epidermal damage. It remains to be determined whether the extrathymic expansion of V gamma 2/V delta 2 +Tells occurs within lesional skin or in the periphery within subsequent recruitment into skin lesions. The results obtained by fluorescence-activated cell sorter analysis favor the first possibility.

Alleles↗
PubMed1993

CD68 positive epidermal dendritic cells.

In a pilot study designed to investigate immunopathologic events in the evolution of cutaneous lesions in pemphigus foliaceus, we found that in this condition the epidermis is replete with CD68+ dendritic cells. The present study was designed to investigate the nature of this novel intraepidermal CD68+ cell population. For that purpose lesional skin of five patients with PF and, for comparison, of patients with another acantholytic autoimmune disease, pemphigus vulgaris, were examined using a panel of monoclonal antibodies in a three-step immunoperoxidase technique, in an immunofluorescence double-labeling technique, and by immunoelectron microscopy. We found epidermal CD1a+ Langerhans cells significantly decreased in pemphigus foliaceus compared to pemphigus vulgaris, but pemphigus foliaceus and not pemphigus vulgaris epidermis harbored large amounts of bone marrow-derived (CD45+) cells that expressed CD68, HLA-DR, and beta 2-integrin antigens, the most pronounced expression being observed for CD11c and CD18. These epidermal CD68+ cells were of dendritic shape, were CD1a-, and lacked Birbeck granules (BG); however, a small portion of CD68+ cells was also CD1a+ and exhibited BG as revealed by immunoelectron microscopy. These findings demonstrate that in certain conditions, i.e., in pemphigus foliaceus but not in pemphigus vulgaris, there is a shift from CD1a+/CD68- epidermal Langerhans cells towards CD1a-/CD68+ dendritic epidermal cells. The detection of a small number of CD1a+/CD68+/BG+ dendritic epidermal cells may identify these cells as a link between the CD1a+/CD68+/BG+ Langerhans cells and the CD1a-/CD68+/BG- cell population and suggests that these cells represent a transitional form of myelomonocytic cells during their phenotypic and morphologic transformation into resident epidermal Langerhans cells.

Adolescent↗
PubMed1991

Cyclosporin A suppresses ICAM-1 expression by papillary endothelium in healing psoriatic plaques.

To analyze the mode of action of Cyclosporin A (CsA) in psoriasis, we examined the phenotypic profile of resident and passenger skin cells in seven psoriatic patients before and after 2 weeks of CsA treatment using a large panel of monoclonal antibodies in a three-step immunoperoxidase technique. For comparison, skin biopsies from psoriatic patients receiving psoralen + UVA (PUVA) therapy were examined. Although both treatment protocols were equally effective in inducing resolution of psoriatic lesions, the phenotypic changes induced by CsA differed greatly from those seen after PUVA. In CsA-treated patients there was a dramatic reduction in the ICAM-1 expression by papillary endothelial cells, but density, pattern, and phenotype of infiltrating inflammatory cells remained essentially unchanged. In contrast, PUVA therapy had no visible effect on ICAM-1 expression by papillary endothelial cells, but resulted in a significant reduction of the hemopoietic resident and infiltrating mononuclear cells within the epidermis. These results favor, but do not prove, the assumption that the CsA regimen chosen in this study exerts its anti-psoriatic effect primarily at the level of the keratinocyte, i.e., by inhibiting events leading to keratinocyte proliferation as well as by interfering with the secretion of mediators responsible for ICAM-1 expression by papillary endothelial cells.

Adult↗
PubMed1991

Recombinant human interleukin 3 induces proliferation of inflammatory cells and keratinocytes in vivo.

In this preclinical study we investigated the effect(s) of recombinant human (rh) interleukin 3 (IL-3) on hemopoietic differentiation and attempted to evaluate possible clinical side effects of this hemopoietic growth factor. Rh IL-3, derived from either Escherichia coli or Chinese hamster ovary, was administered subcutaneously to 16 rhesus monkeys (by pairs) at different doses (11, 33, and 100 micrograms/kg/day) for 14 days. During the 2nd week of administration white blood cell counts increased 2- to 3-fold mainly because of a dose-dependent elevation of basophils (up to 40% of white blood cells) and eosinophils. In addition, moderate to marked elevations of plasma histamine levels were measured. Transient diarrhea and an erythematous skin rash with generalized cutaneous lesions that was not restricted to the injection sites were present in 3 of 6 animals treated with E. coli-derived rh IL-3 (1 of 2 animals that received 33 micrograms/kg and 2 of 2 that received 100 micrograms/kg) and 2 of 6 monkeys treated with Chinese hamster ovary-derived rh IL-3 (1 of 2 that received 33 micrograms/kg and 1 of 2 that received 100 micrograms/kg), respectively. Histopathologic and immunohistologic evaluation of skin specimens revealed a perivascular mononuclear cell infiltrate interspersed with numerous mast cells. Signs of vasculitis were absent. The density of the perivascular infiltrate correlated not only with the dose of IL-3 but also with the duration of the skin eruption. Moreover, hyperproliferation of basal keratinocytes resulting in acanthosis was observed in lesions persisting for 1 and 4 days as also evidenced by a significant (p less than 0.01) increase in Ki-67 (a proliferation-associated marker)-positive basal keratinocytes.

Animals↗
PubMed1990

Human epidermal T cells predominantly belong to the lineage expressing alpha/beta T cell receptor.

The epidermis of clinically normal-appearing human skin harbors a phenotypically heterogeneous population of T lymphocytes (TCs), the majority of which are CD2+/CD3+/CD5+ "memory" cells, but in an unactivated state, and express the TCR-alpha/beta. In contrast to murine skin, only a very minor subpopulation of CD3+ cells in the human epidermis bears the TCR-gamma/delta. Epidermal TCs primarily are distributed along the rete ridges in the basal keratinocyte layer and are often in close apposition to Langerhans cells (LCs). These TCs were propagated from epidermal cell suspensions after stimulation with TC activating agents (Con A, rIL-1, rIL-2), then evaluated for phenotypic features and TCR diversity. Similar to the in situ situation, most were CD4-/CD8+/TCR-alpha/beta+. In addition, two cultures contained TCR-gamma/delta+ cells; one of these determined to be an adherent CD4-/CD8+ population. Epidermal TCs were significantly (p less than 0.0001) more abundant in the sole than in the other body regions examined (i.e., 40 vs. 7 CD3+ cells/linear centimeter of epidermis) and seemed to have a particular affinity for the acrosyringial epithelium of eccrine sweat ducts. Moreover, the sole usually contained a greater number of CD8+ relative to CD4+ TCs, whereas the epidermal CD4/CD8 ratio in the trunk and extremities was quite variable, although the trend also was towards a slightly larger percentage of CD8+ cells. Collectively, our data suggest that the volar epidermis has a unique microenvironment which is responsible for both the higher density of TCs, preferentially CD8+, and lower number of LCs. This study has not only provided evidence for significant regional variability in the human epidermal TC population of normal skin, but also strengthens the concept for skin-associated lymphoid tissues (SALT), whereby memory TCs recirculate back to the epidermis and interact with resident antigen-presenting cells (i.e., LC).

Antibodies, Monoclonal↗
PubMed1990

Photochemotherapy improves chronic cutaneous graft-versus-host disease.

We have used oral psoralen photochemotherapy (PUVA) to treat four patients with chronic graft-versus-host disease of the skin, oral mucosa, and liver, who had responded only partially to long-term immunosuppressive therapy (prednisolone, cyclosporine, azathioprine). PUVA therapy was delivered to the entire skin but not to the oral mucosa, and immunosuppressive therapy was continued in all patients. Two patients' skin lesions improved considerably; the oral lesions healed and did not recur in one. Immunosuppressive therapy could be reduced in these two patients. One patient with sicca signs did not improve. One patient had to interrupt PUVA therapy because of side effects attributed to 8-methoxypsoralen (nausea and vomiting). No flare of acute cutaneous graft-versus-host disease was noted during PUVA therapy. Chronic graft-versus-host disease of the liver did not improve in any patient.

Adolescent↗
PubMed1990

Restoration of defective cytokine activity within lepromatous leprosy lesions.

Immunohistological studies of tuberculoid leprosy lesions (TT-lesions) showed a dense, well organized granuloma consisting of a central area with epitheloid and giant cells containing interferon-gamma (IFN-Gamma) and CD3+, CD4+ T helper/inducer (Th/i) cells, a considerable proportion of which expressed the interleukin-2-receptor (IL-2 R). This central area was surrounded by round cells which consisted mainly of CD3+/CD8+ T cytotoxic/suppressor (Tc/s) lymphocytes. The overlying keratinocytes (KC) were strongly positive for HLA-DR antigens on the surface, indicating high intralesional IFN-Gamma activity. In contrast, lepromatous leprosy lesions (LL-lesions) showed a disorganized infiltrate composed by foamy cells and round cells, the latter mainly expressing the CD3+/CD8+ phenotype. IFN-Gamma activity could not be detected within the lesions. The KC overlying the infiltrate were consistently negative for HLA/DR reactivity pointing to a defective intralesional IFN-Gamma production in LL patients. Two out of four patients with LL leprosy could be sensitized with dinitrochlorobenzene (DNCB). The eliciting of DNCB skin reactions within the LL-lesion led to the recruitment of new infiltrating cells; the resulting infiltrate resembled a local reversal towards the tuberculoid pole of leprosy.

CD4-Positive T-Lymphocytes↗
PubMed1990

Autoantibodies in chronic GVHD: high prevalence of antinucleolar antibodies.

Sera from 32 bone marrow allograft recipients were screened for the presence of autoantibodies 4-61 months post-graft. Sera from 12 of 19 patients with extensive chronic graft-versus-host disease (c-GVHD) stained the nucleolar region strongly in immunofluorescence, indicating the presence of specific antinucleolar antibodies. In contrast, none of three patients with limited and none of 10 patients without c-GVHD had antinucleolar antibodies. Antibodies reacting with nuclear constituents other than nucleoli were found in five of the 12 antinucleolar positive patients. The appearance of antinucleolar antibodies coincided with early clinical symptoms of c-GVHD. We conclude that the appearance of antinucleolar antibodies after bone marrow transplantation is specific for patients with extensive c-GVHD. Furthermore, the development of extensive c-GVHD is paralleled by the emergence of these antinucleolar antibodies.

Adolescent↗
PubMed1989

Interstitial pneumonia as a cause of early mortality in allogeneic bone marrow transplantation: the Viennese experience.

A uniquely low incidence and death rate of interstitial pneumonia after allogeneic bone marrow transplantation for haemopoietic malignancy is described. Deduced from the comparison with results from a multicenter study, we conclude, that a) reduction of the dose rate to less than 5 rad/min, b) exclusion of CMV pos platelet donors and c) application of a CMV hyperimmune globulin are effectful means to reduce this most often deathly complication after BMT for haemopoietic malignancy.

Austria↗