PubMed Health⌕ Search

Biomedical subjects

T Dalianis

Publications and source records attributed to T Dalianis.

At least 37 records · Page 2Linked to original sources
PubMed1996

Loss of seroreactivity against human papillomavirus (HPV) in bone marrow transplant recipients.

Sera from 19 autologous and 35 allogeneic bone marrow transplant (BMT) patients at Huddinge University Hospital were analyzed by different ELISA assays before and 1 year after BMT for the presence of IgG antibodies towards human papillomavirus (HPV). One assay was a peptide-based enzyme-linked immunoadsorbent assay (ELISA). These peptides were derived from the amino acid sequences of the two major viral capsid proteins of HPV 16, p(31) L1 and (p49) L2. The other was an ELISA using HPV-type 16 virus-like particles (VLPs) as antigens. Before BMT 13/19 autologous and 14/35 allogeneic BMT patients were IgG positive towards p49 (L2). Reactivity to p31 (L1) was less frequent and was only observed in 7/19 autologous and 3/35 allogeneic BMT patients. One year after BMT 1/4 of the autologous and 2/3 of the allogeneic BMT patients who were IgG positive to p49 (L2) lost these antibodies as measured by the peptide ELISA assay. Regarding IgG reactivity to p31 (L1), one of the seven p31 (L1) positive autologous BMT patients and all three of the p31 (L1) positive allogeneic BMT patients lost this reactivity 1 year after BMT. Of all the 19 autologous and the 35 allogeneic BMT patients only two allogeneic BMT patients were weakly IgG reactive towards VLPs and 1 year after BMT this activity was lost in one of the two patients.

Adult↗
PubMed1995

Polyomavirus persists in CD4/8 double-knockout, but not in CD4 or CD8 single-knockout mice.

The effects of incomplete immunocompetence on possible persistence and reactivation of polyomavirus in adult mice were investigated by a polyomavirus-specific polymerase chain reaction (PCR). The presence of virus DNA was followed between 4 days and 2 months postinfection (p.i.) in polyomavirus-infected normal adult A/Sn mice and CD4-/- and CD8-/- single-knockout, as well as CD4-/-8-/- double-knockout BALB/c or C57BL/6 mice. The same study was performed in A/Sn mice immunosuppressed by thymectomy (THX), cytosine-beta-D-arabinofuranoside (Ara-C) treatment, and total body irradiation (TBI). Primary polyomavirus infection of CD4-/- or CD8-/- single-knockout mice was similar to that obtained in normal adult mice when followed by PCR. Viral DNA was detected in a limited number of organs during 4 weeks p.i., but was no longer observed after 1-2 months. In contrast, the virus could be detected in most organs of CD4-/-8-/- double-negative mice and in THX-, Ara-C-, and TBI-treated adult mice and was still present 1-2 months p.i. In polyomavirus-infected normal adult mice a later immunosuppression did not lead to reactivation of the virus. Furthermore, if a second challenge of polyomavirus was administered 4 weeks after primary infection in both normal or recently immunosuppressed mice no viral DNA could be detected by PCR.

Animals↗
PubMed1995

No association of JC virus with Alzheimer's disease or astrocytomas.

OBJECTIVES: To investigate if JC virus (JCV) can be involved in the pathogenesis of Alzheimer's disease (AD) and astrocytomas. STUDY DESIGN: A nested polymerase chain reaction (PCR) was used for the detection of JCV DNA in autopsy brain material (cerebral white matter) and cerebrospinal fluid (CSF) specimens from patients with AD and age-matched control patients without neurological diseases, together with biopsies from patients with astrocytomas (grades 3 and 4). Brain autopsy material from AIDS patients with progressive multifocal leukoencephalopathy (PML) was examined as positive control material. RESULTS: JCV DNA was detected by PCR in only one of the 17 brain autopsies from patients with AD, but in none of the 26 control patients without neurological diseases and in none of the 5 astrocytoma biopsies. JCV DNA was, however, detected in the brain material from two patients with PML. CONCLUSION: Our results show that JCV infection does not seem to be directly involved in the pathology of AD or in the development of astrocytomas. In addition, since no viral DNA was detected in CSF specimens from 43 patients without PML (17 with AD and 26 elderly controls), our results suggest that the finding of JCV DNA in CSF correlates to PML.

Journal Article↗
PubMed1995

Similar incidence of graft-versus-host disease using HLA-A, -B and -DR identical unrelated bone marrow donors as with HLA-identical siblings.

Among 42 consecutive recipients of unrelated marrow were 39 HLA-A, -B, -DR identical, matched unrelated donors (MUD) and three with one HLA antigen mismatch. The majority were genomically typed for DRB, DQA, DQB and DPB. The recipients of MUD marrow were compared with 39 recipients of marrow from HLA-identical siblings with similar diagnoses, disease status and age. Each group included 24 patients with hematological malignancies, 6 with severe aplastic anemia and 9 inherited disorders. Immunosuppression consisted of anti-thymocyte globulin (ATG; pre-BMT mainly to recipients of unrelated marrow), CsA and four doses of MTX. Grade I acute GVHD was treated with prednisolone 2 mg/kg. In a comparison of MUD marrow recipients and HLA-identical siblings 34 of 39 and 36 of 39 of the patients engrafted, respectively. Recipients of MUD marrow and HLA-identical siblings achieved 0.2 x 10(9) WBC/l on day 16 (median) and 14, respectively (P = 0.03). Furthermore, the recipients of MUD marrow needed more platelet transfusions (P = 0.04). The incidence of acute GVHD grade II-III was 15% in the MUD marrow recipients compared with 11% among the HLA-identical siblings. The 2-4 year cumulative incidence of chronic GVHD was 29% and 22% in the two groups, respectively. The overall 2-year survival was 59 and 78%, respectively. Among patients with CML in chronic phase or accelerated phase (n = 26), 2-year relapse-free survival was 79% in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

T cell subsets involved in immunity against polyoma virus-induced tumors.

Lymphocyte subsets involved in the rejection of polyoma virus-induced tumors were studied. Depletion of CD4+ and CD8+ T cells as well as natural killer cells was performed in mice using monoclonal antibodies or anti-asialo GM1 anti-serum. Both CD4+ and CD8+ T cell subsets were found to be necessary for the rejection of polyoma virus-induced tumors, while natural killer cells played a minor, if any, role.

Animals↗
PubMed1993

Identification of H-2Kb-, Db- and Dd-binding peptides derived from amino acid sequences of polyoma virus T antigens.

Viral and tumor antigens are presented to cytotoxic T cells (CTL) in the form of short peptides. The peptide antigen is transported to the cell surface in conjunction with molecules encoded by the major histocompatibility complex (MHC). Different methods have recently been described for the analysis of the MHC-class-I binding ability of synthetic peptides. Here, we describe a protocol, based on intact RMA-S cells cultured at 26 degrees C in the presence of synthetic peptides, which gives an allele-specific peptide binding pattern with high resolution. This allowed an analysis of the H-2Kb-, Db- and Dd-binding capacity of a panel of synthetic peptides with amino acid (aa) sequences derived from polyoma (py) virus large-, middle- and small-T (LT, MT and ST) antigens, previously used in immunization experiments against py-virus-induced tumors. Eight single aa mutants and a deletion mutant of one peptide with an ability to bind both to H-2Kb and to Db were also analyzed. We foresee that the present protocol, or variants thereof, may serve as a simple and rapid assay for the systematic screening of the class-I binding ability of large sets of synthetic peptides in vitro. Such analysis may facilitate the search for viral or tumor peptide epitopes that are recognized by CTL.

Alleles↗
PubMed1993

Serological responses to human papillomavirus type 16 antigens in women before and after renal transplantation.

Female renal transplant recipients have an increased incidence of human papillomavirus (HPV) associated lesions, such as cervical dysplasia and neoplasia [Schneider et al., 1983]. In this study we tested the serological responses by enzyme-linked immunoadsorbent assays (ELISA) to 3 different antigenic regions of HPV type 16. Sera from 35 female renal transplant patients collected before and at different times, up to 3 years, after transplantation were collected and tested. Before transplantation IgG antibodies against peptide 49, corresponding to the HPV L2 region, were found in 21/35 of the patients' sera. Of the L2 positive sera, 16 also demonstrated activity with the HPV L1 region derived peptide 31. All sera that were active against peptide 31 (L1) were also reactive with peptide 49 (L2). After renal transplantation, the antibody levels against these 2 peptides (peptides 49 and 31) dropped significantly (OD > or = 0.2) in all previously positive sera and remained so throughout the study, which lasted up to 3 years. The proportion of patients with IgA activity against the E2 region (peptide 245), which is common among patients with cervical neoplasia, increased from 9/35 before transplantation to 18/35 after transplantation. In parallel, we monitored 25 of these patients' sera before and after transplantation for antibody activity against measles, adenoviruses, and cytomegaloviruses (CMV). The majority of these sera--17/25 (68%) and 18/25 (72%), respectively--had no titer changes against measles and adenoviruses. Furthermore, the changes in antibody titers observed with CMV in these patients were not correlated with the fate of the antibodies against the HPV peptides.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoviruses, Human↗
PubMed1993

Persistence of polyomavirus in mice infected as adults differs from that observed in mice infected as newborns.

By using the polymerase chain reaction (PCR) technique, a technique more sensitive than Southern analysis, which allows detection of polyomavirus DNA only in newborn and nude adult mice, it has now been possible to monitor the persistence pattern of polyomavirus DNA after infection of normal adult CBA mice for the first time. Viral signs appeared gradually, showing variations in time course and organ distribution between mice, and reached a peak activity after 2 to 3 weeks, when they could be found in bone, heart, gonads, lymph node, and skin, but disappeared by 2 to 5 months. No virus DNA was detected in the kidneys or lungs, which is in contrast to what is observed after infection of newborn mice. This finding suggests that the persistence pattern of polyomavirus is age dependent.

Age Factors↗
PubMed1992

Modifications of an immunodominant peptide antigen induce different anti-polyoma tumor responses in two separate mouse strains.

An immunodominant polyoma peptide antigen MT162-176 was modified with regard to amino acid (aa) composition in an attempt to analyze its immunogenicity in detail. Twelve modifications of peptide MT162-176, 3 overlapping peptides and 9 peptides with point mutations, were synthesized and used for immunizations of (A.CA x C57BL/6)F1 and CBA mice against the syngeneic polyoma tumors SECA and SEBA. All 3 overlapping peptides MT162-176, MT165-174 and MT170-176, were immunogenic in (A.CA x C57BL/6)F1 mice against SECA, indicating that possibly more than one immunogenic epitope may be recognized within the MT162-176 sequence. In CBA mice, the 2 peptides covering the C-terminal half were immunogenic against SEBA, while the N-terminal peptide was possibly somewhat less efficient. The peptides with aa point mutations induced different anti-tumor responses in the 2 mouse strains. In CBA mice, only one mutant, MT162-176.28, was immunogenic. For (A.CA x C57BI)F1 3 different mutants, MT162-176.29, MT162-176.35 and MT162-176.36 were immunogenic against SECA, while the remaining 6 had lost their activity. These results suggest that a different emphasis of recognition of peptide MT162-176 exists with regard to the 2 mouse strains examined. Furthermore, different immunization procedures were tested. We found that repeated immunizations with peptide without Freund's adjuvant was the most efficient.

Amino Acid Sequence↗
PubMed1992

Immunization against polyoma tumors with synthetic peptides derived from the sequences of middle- and large-T antigens.

We have used 9 synthetic peptides corresponding to sequences of polyoma virus small-T, middle-T and large-T antigens as immunogens in order to map antigenic epitopes that can induce polyoma-tumor-specific immunity in different mouse strains. We found that immunization of mice with synthetic peptides derived from amino acid (aa) sequences common to all 3 T-antigens (aa 1-19), or sequences common to only middle-T and small-T (aa 162-176), as well as synthetic peptides unique for middle-T (aa 269-282 and 371-381), or unique for large-T (aa 108-124, 316-333 and 436-449) can induce immunity against polyoma tumors. The synthetic peptides can be divided into 3 types with regard to immunogenicity; (i) peptides that immunize in more than one mouse strain and may represent immunodominant sites, (ii) peptides that may be immunogenic in only one strain, and thus strain-specific, and finally (iii) peptides that do not immunize in the strains tested so far.

Amino Acid Sequence↗
PubMed1992

One explanation for F1 antiparent responses.

The phenomenon of hybrid resistance, in which F1 offspring reject parental grafts, remains a perplexing problem. Here, Tina Dalianis and Lars Ahrlund-Richter propose that one component of the F1 antiparent response results from competition between the two sets of parentally derived major histocompatibility complex (MHC) molecules for 'promiscuous' peptides. Lack of tolerance in the F1 animal results from insufficient presentation of these peptides on the MHC molecule that has lower affinity for the peptides.

Animals↗
PubMed1990

Complete transformation of embryonal rat fibroblasts by polyomavirus occurs during passage in vitro.

The tumorigenicity of secondary rat embryo fibroblasts transfected with a plasmid harboring a replication origin-defective polyomavirus was found to increase during in vitro propagation. Thus, polyomavirus-transfected cells were found to be more than 10,000-fold more tumorigenic when injected into syngenic rats at 3 months after transfection compared to those injected at an earlier time point. Furthermore, most clones of polyomavirus-transfected cells did not grow in semisolid medium at 52 days after transfection but did grow at 95 days. Addition of glucocorticoid hormones, but not of 25% fetal calf serum, to the growth medium of the early passage cells resulted in limited anchorage-independent growth. An altered level of expression of a number of proteins was found in cells analyzed at different times after transfection. Notably, the expression of a component of the actin filament system, tropomyosin 2, was shown to decrease during growth in vitro. The development of a more fully transformed phenotype at late passages correlated with loss of the requirement for large T-antigen for growth. Thus, cells transfected with a polyomavirus mutant encoding a thermolabile large T-antigen did not grow at the restrictive temperature at 6 weeks after transfection, but grew well at 5 months after transfection. We suggest that these phenomena may be explained by assuming that establishment of rodent fibroblasts, and thereby sensitivity to transformation by middle T-antigen, is not an immediate consequence of expression of large T-antigen but occurs after a period of growth in vitro.

Animals↗
PubMed1989

Polyoma T-antigen-derived synthetic peptides induce polyoma-virus-specific macrophage migration inhibition.

Synthetic peptides, 2 derived from the sequence common to small, middle and large T-antigen, and I derived from the sequence unique for middle T, activated lymphocytes from polyoma-virus-immunized, but not from control mice, to release the lymphokine migration inhibitory factor (MIF). In contrast, purified, bacterially grown, full-length small T-antigen and a middle T-antigen mutant Py 1387T MT (lacking 37 C-terminal amino acids) did not induce lymphokine release, although they were capable of inducing an anti-polyoma TSTA response in vivo.

Animals↗
PubMed1989

A single peptide derived from the sequence common to polyoma small and middle T-antigen induces immunity against polyoma tumors.

Polyoma virus, an oncogenic virus, fails to induce tumors in immunocompetent rodents due to T cell-dependent mechanisms. The target recognized by the immune system has been functionally defined as polyoma tumor-specific transplantation antigen (TSTA) and has been postulated to be related to the virus three early proteins small T (ST), middle T (MT), and large T (LT) antigens. We show here that immunization with a synthetic peptide corresponding to amino acids 162-176 of polyoma MT and ST was able to decrease tumor progression of polyoma tumors, but not of nonpolyoma tumors. This indicated that these amino acids constitute an epitope of the polyoma tumor-specific transplantation antigen.

Animals↗