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Results for “Antigenic Modulation”

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PubMed2002

Human immune response in schistosomiasis: the role of P24 in the modulation of cellular reactivity to Schistosoma mansoni antigens.

Schistosome antigenic components are being tested as vaccine candidates with various degrees of success, but there are only few reports using multivalent antigens to stimulate an appropriate immune response that leads to resistance or granuloma modulation. We investigated the in vitro response of peripheral blood mononuclear cells (PBMC) from chronic intestinal schistosomiasis individuals to PIII, a multivalent antigen prepared from Schistosoma mansoni adult worm antigen, and response to P24, a single antigen obtained from PIII. Treatment of PBMC with either PIII or P24 caused significant decrease in cellular proliferation and granuloma formation induced by S. mansoni antigens, and a significant elevation in IL-10 and TNF-alpha but not in IFN-gamma production. Moreover, P24 promoted an elevation in TNF-alpha level on the in vitro granuloma reaction, when cocultured with polyacrylamide beads (PB) coupled to S. mansoni antigens. These findings suggest that, besides inducing protective immunity, PIII and P24 antigens seem to be important in the regulation of in vitro granuloma formation through stimulation of IL-10 and TNF-alpha production in human schistosomiasis. The more pronounced effect of P24 on reducing the in vitro granulomatous reaction could be associated with a balance between IL-10 and TNF-alpha production.

Animals↗

PubMed1993

Expression and modulation of a mononuclear phagocyte differentiation antigen (PAM-1) during in vitro maturation of peripheral blood monocytes.

Human macrophages obtained by in vitro maturation of peripheral blood monocytes express a surface antigen, PAM-1, recognized by a monoclonal antibody and typical of pulmonary alveolar and tissue macrophages. PAM-1, undetectable in freshly isolated peripheral blood monocytes, was expressed in monocyte-derived macrophages after 3 days of in vitro adherent culture and was maximal after 14-15 days (50%-60% of positive cells). Similar levels of PAM-1 positivity were observed in non-adherent monocyte-derived macrophages suggesting that cell adhesion was not a critical requisite for the expression of this antigen. Bacterial lipopolysaccharide and a monocyte chemotactic protein preparation respectively suppressed and upregulated PAM-1 expression in monocyte-derived macrophages. In contrast, interferon-gamma, although enhancing the levels of class II HLA-DR antigen in monocyte-derived macrophages, did not influence the kinetics of appearance and the levels of PAM-1 in these cells. Thus, expression of PAM-1, which is restricted to certain stages of the monocyte-macrophage differentiation pathway, is also differentially modulated by activation signals, which can be present in the micro-environment of inflammed tissues.

Antigens, Differentiation↗

PubMed1986

Valency of CD3 binding and internalization of the CD3 cell-surface complex control T cell responses to second signals: distinction between effects on protein kinase C, cytoplasmic free calcium, and proliferation.

We have studied the relationship of valency of CD3 stimulation and modulation of the CD3 receptor complex with biochemical and proliferative responses of T cells. Anti-CD3 Fab, as well as F(ab')2 and whole antibody caused rapid modulation of the CD3 antigen, whereas anti-CD3 conjugated to Sepharose did not. In the absence of monocytes, T cells stimulated with anti-CD3 Fab, F(ab')2, or F(ab')2-Sepharose showed differences in their ability to respond to second signals given by PMA, IL 1, IL 2, or antibodies to Tp67 and Tp44. None of the anti-CD3 signals alone caused resting T cells to produce IL 2, and only the Sepharose-bound anti-CD3 F(ab')2 caused T cells to express high levels of functional IL 2 receptors. Anti-CD3 F(ab')2-Sepharose-stimulated T cells produced IL 2 and proliferated in response to each of the second signals. Because anti-CD3-Sepharose did not cause modulation of the CD3 antigen, the ability of the Sepharose-bound antibody to induce T cells to express IL 2 receptors and to respond to individual second signals may be related to lack of modulation rather than valency of binding. Anti-CD3 Fab-stimulated T cells responded to PMA but required combinations of other second signals. T cells stimulated with unmodified anti-CD3 antibody or F(ab')2 fragments responded to PMA but did not respond to any other second signals alone or in combination. Stimulations that resulted in modulation (i.e., anti-CD3 whole antibody, anti-CD3 F(ab')2, or anti-CD3 Fab fragments) caused an increase in cytoplasmic calcium levels in resting T cells but blocked proliferation of T cells in response to mitogenic lectins or CD2 stimulation. Anti-CD3 F(ab')2 on Sepharose, however, did not block T cell proliferation. Whole bivalent anti-CD3 antibody or F(ab')2 fragments, but not monovalent Fab fragments, caused a rapid translation of protein kinase C activity from cytosol to membrane in the Jurkat T cell line. Because all of these modulate the receptor, these data indicate that the functional difference between monovalent and bivalent binding to CD3 is related to antibody valency and not to antigenic modulation. The use of Fab anti-CD3 stimulation that requires combinations of second signals for proliferation allowed an analysis of the functional relationships between IL 1, anti-Tp67, and anti-Tp44.

Animals↗

PubMed2006

ABH histo-blood group antigens in human thymus involution.

BACKGROUND: Human histo-blood group antigens (HBGA) are genetically determined glycoproteins supposed to participate in cell differentiation, adhesion, cancer metastasis and angiogenesis. In tissues, HBGA are mostly expressed in epithelial cells (EC). The EC comprising the thymocyte microenvironment play an important role in the ontogeny of the thymus. The aim of the present work is to investigate ABH HBGA in senile thymus and to characterize their expression pattern related to the process of aging. METHODS: Routine histology and immunohistochemical techniques were applied on thymus glands from senile and young individuals. RESULTS: Involuted thymus exhibited large areas of adipose tissue containing scattered EC, all positive for HBGA. Stromal EC revealed different morphology and intrathymic localization but uniform cytoplasmic staining for ABH antigens. Endothelial cells of blood vessels and red blood cells were intensely stained for HBGA. Only single scattered lymphocytes possessed HBGA. In contrast with senile thymus, most lymphocyte populations in the gland of young individuals, as well as the Hassall's corpuscules, expressed HBGA. CONCLUSIONS: The epithelial framework reorganization during age-related thymus involution involves modulation in ABH antigen expression in EC. These molecules are required by thymic EC to maintain the reduced but important crosstalk with lymphocytes during involution. The diminished reactivity for ABH antigens in the lymphocytes of aged thymus might reflect the impaired communication between these two cell types. We present novel evidence for permanent presence and modulation of ABH antigen reactivity in senile thymus, supporting the view that these molecules might be developmentally regulated.

ABO Blood-Group System↗

PubMed1988

Modification of bronchial blood flow during allergic airway responses.

Ascaris suum antigen effects on mean airflow resistance (RL) and bronchial arterial blood flow (Qbr) were studied in allergic anesthetized sheep with documented airway responses. Qbr was measured with electromagnetic flow probes, and supplemental O2 prevented antigen-induced hypoxemia. Aerosol challenge with this specific antigen increased RL and Qbr significantly. Cromolyn sodium aerosol pretreatment prevented antigen-induced increases in RL but not in Qbr. Intravenous cromolyn, however, prevented increases in Qbr and RL, suggesting a role for mast cell degranulation in both bronchomotor and bronchovascular responses to antigen. Antigen-induced increases in Qbr were not solely attributable to histamine release. Indomethacin pretreatment attenuated the antigen-induced increase in Qbr, thus suggesting that vasodilator cyclooxygenase products contribute to the vascular response. Antigen challenge significantly decreased Qbr after indomethacin and metiamide pretreatment, which suggests that vasoconstrictor substances released after antigen exposure also modulate Qbr; however, released vasodilators overshadow vasoconstrictor effects. Thus antigen challenge affects Qbr by locally releasing histamine and vasodilator prostaglandins as well as vasoconstrictor substances. These effects were independent of antigen-induced changes in systemic and pulmonary hemodynamics.

Airway Resistance↗

PubMed1983

Antigen-specific human B-cell responses: modulation by immunoregulatory T-cell subsets.

In vitro T-cell requirements for and modulation of human B-cell responses were studied in individuals immunized in vivo to the protein antigen keyhole limpet hemocyanin or tetanus toxoid. T cells were required for antibody synthesis in both antigen-driven and pokeweed mitogen (PWM)-driven cultures. T cells were separated into T4+ and T8+ subpopulations using monoclonal antibodies, and their modulation of antibody synthesis was studied. T4+ cells functioned as helper cells in both antigen-driven and PWM-driven cultures in a dose-dependent manner. Whereas T8+ cells suppress both total and specific immunoglobulin secretion in PWM-stimulated cultures, in antigen-stimulated cultures T8+ cells do not suppress unless activated by another cell population present in peripheral blood mononuclear cells (PBMNC). This cellular requirement was further investigated by prestimulation of cells prior to addition to optimally stimulated antigen-driven cultures of PBMNC or B cells, monocytes, and helper T cells. No suppression of these optimally stimulated cultures was seen when T8+ cells were precultured with antigen or PWM. However, after 3-5 days preculture of total T cells with PWM or antigen and then selection of T4+ cells, these cells were able to induce fresh autologous T8+ cells to suppress optimally stimulated antigen-driven cultures. Addition of a precultured mixture of T8+ cells with 20% T4+ cells also resulted in antigen-induced suppression. These data indicate that T8+ cells can suppress antigen-driven cultures but require the presence of preactivated T4+ cells for induction of this suppression of antigen-specific T-cell-dependent human B-cell responses.

Antibody-Producing Cells↗

PubMed1993

Serum modulates mast cell responses to IgE antigen stimulation.

Serum induces the expression of the fos and jun gene families, which encode the transcription factor AP-1. Since we previously found that activation of mast cells by IgE-antigen (Ag) induces the mRNA accumulation of c-fos, c-jun, junB and junD proto-oncogenes, we were prompted to investigate whether serum could affect such accumulation in these cells. In addition, we investigated whether serum could modulate inhibition of DNA synthesis in immunologically stimulated mast cells. Mast cells, which were cultured in the presence of fetal calf serum (FCS), were characterized by a high proliferation rate and high accumulation of the mRNA of c-fos, junB and junD proto-oncogenes. After sustained FCS deprivation both DNA synthesis and the level of c-fos mRNA were significantly decreased, as expected, whereas the level of c-jun, junB and junD mRNA were not affected. As opposed to mast cells which were cultured in the presence of FCS, immunological stimulation of FCS-deprived cells resulted in DNA synthesis inhibition and an increase in c-fos expression. The results also show that the level of c-fos mRNA was increased by either IgE-Ag or FCS up to a similar level, while these two triggers could not act synergistically to enhance this expression further. Thus, changes in DNA synthesis, induced by FCS, block the ability of the immunological challenge to inhibit mast cell growth and to enhance c-fos mRNA accumulation.

Animals↗

PubMed1984

Modulation of Ia and leukocyte common antigen expression in rat glomeruli during the course of glomerulonephritis and aminonucleoside nephrosis.

We have investigated changes in the glomerular expression of two antigens, Ia and leukocyte common (LC) antigens, during the course of two models of glomerular injury in the rat. Acute glomerulonephritis induced by nephrotoxic, antiglomerular basement membrane antiserum is accompanied by a 3-fold increase in the number of glomerular cells expressing Ia and LC antigens. Acquisition of the Ia+ phenotype appears to occur in LC+ monocytes that have assumed subendothelial and intramesangial positions. Enhanced Ia expression is seen over a wide range of proteinuria. Decomplementation prior to nephrotoxic, antiglomerular basement membrane anti-serum administration abrogates both the proteinuria and the increased Ia expression; an increase in cells expressing LC antigen still occurs. The chronic phase of nephrotoxic, antiglomerular basement membrane antiserum-induced glomerulonephritis is associated with a persistent increase in glomerular Ia+ cells residing primarily in the mesangium. In the glomerulopathy induced by the aminonucleoside of puromycin, there are two phases of glomerular Ia modulation. In the first week, there is a decrease in Ia expression by LC+ cells. The second week is marked by infiltration by monocytes and an increase in Ia expression by both resident and infiltrating cells. Modulation of the Ia phenotype on resident and infiltrating marrow-derived cells carries implications with respect to the immunologic pathogenesis of both models of glomerular injury.

Animals↗

PubMed1988

Correlated expression of surface antigens in human thymocytes. Evidence of class I HLA modulation in thymic maturation.

The correlated expression of several surface antigens (CD 1, class I HLA, CD3) was examined in human unfractionated thymocytes or selected subsets by using single or double-color flow cytometry. Prethymocyte subpopulations expressed high levels of HLA. A high proportion of cortical cells expressed low levels of either HLA or CD 3 antigens. Most of these HLA+ cortical cells corresponded to the more immature cells and did not express HLA-B loci products. CD 1 a and CD 3 antigens were expressed in a high percentage of cells and the levels of expression of each antigen in individual cells were inversely correlated. These data and the contour of double-color histograms are suggestive of the existence of a single pathway of thymocyte differentiation in which class I HLA expression is switched off around the time of the initiation of CD 3 (and Ti?) expression. We suggest that the anti-major histocompatibility complex (MHC) specificity of the unselected Ti receptor may be incompatible with the expression of MHC products on the cell membrane. At this stage, CD 1 antigens, whose expression is inversely correlated with that of HLA, may fulfill the role of MHC antigens. The latter can be re-expressed later on, once the anti-MHC specificities of the Ti receptors have been selected against. Studies on in vitro modulation of HLA molecules by interferon-alpha did not reveal any correlation to the expression of CD 1 or CD 3 antigens.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1979

Effect of synthetic cyclic nucleotides on immunologic histamine release from calf granulocytes.

Sensitized bovine granulocytes release histamine when exposed to specific antigens. A unique modulation of histamine release by adrenergic agents has been shown in the bovine; beta-adrenergic agonists enhance and alpha-adrenergic agonists inhibit histamine release. This is an opposite response to that reported in other species. The present study was undertaken to determine the possible relationship between cyclic nucleotides and adrenergic agents in this species. Dibutyryl cAMP enhanced antigen-induced histamine release over the complete concentration range tested (10(-6)--10(-3)M); it also overcame, in a dose-dependent manner, the inhibition of antigen-induced histamine release produced by 10(-4) M phenylephrine. The 8-bromo cGMP AND 0-MONOBUTYRYL CGMP had no significant effect on antigen-induced histamine release nor did 8-bromo-cGMP have any significant effect on the enhancement of histamine release produced by 10(-4) M dibutyryl cAMP. These findings suggest that only cAMP has a role in the modulation of antigen-induced histamine release from bovine granulocytes.

Animals↗

PubMed2001

The transcriptional activity of cAMP response element-binding protein-binding protein is modulated by the latency associated nuclear antigen of Kaposi's sarcoma-associated herpesvirus.

A multifunctional transcription co-activator, cAMP response element-binding protein-binding protein (CBP)interacts with a number of cellular factors and participates in cell growth, transformation, and development. It is also targeted by many viral proteins for their transcriptional activity or for the regulation of cellular processes. Here, we report that the C/H3 region of CBP is targeted by the latency associated nuclear antigen (LANA) of Kaposi's sarcoma-associated herpesvirus (KSHV). LANA interferes with the interaction between CBP and c-Fos, a representative C/H3 region binding, cellular transcription factor, in vivo and in vitro. In addition, we found that LANA inhibits the transcriptional activity and the in vitro histone acetyltransferase activity of CBP, suggesting that LANA modulates the global transcriptional activities of infected cells through the interaction with CBP. These results indicate that KSHV follows one of the conserved strategies, which other viruses utilize for influencing the cellular processes.

Acetyltransferases↗

PubMed2006

Modulation of ABH histo-blood group antigen expression in normal and myasthenic human thymus.

The role of ABH histo-blood group antigens (HBGA) in intercellular communication during normal and pathological processes is still uncertain. The present work investigates the expression of ABH HBGA in epithelial cells and lymphocytes in normal thymus, and characterizes the modulation of their immunoreactivity during myasthenic transformation. Immunohistochemistry and immunoelectron microscopy were applied on normal young thymus and on myasthenia gravis-associated thymomas and thymic hyperplasias. The Hassall's corpuscules in the thymus of young individuals were homogeneously stained for HBGA, while in hyperplastic glands only their central part was positive. Stromal epithelial cells permanently expressed HBGA in all tissue samples. In thymomas, mainly the lymphocytes in close proximity to antigen expressing epithelial cells were positive, while in the hyperplastic gland the most intensely stained lymphocytes were those within Hassall's corpuscules. Novel evidence for modulation of ABH antigen reactivity in normal and myasthenic human thymus is presented. It suggests that HBGA might participate in the regulation of the cross-talk in the thymocyte microenvironment throughout the ontogeny, as well as during the myasthenic transformation.

ABO Blood-Group System↗

PubMed1985

A lung perfusion technique for the detection of antigenic intrapulmonary bronchoconstriction and its mediation.

A guinea pig intraluminal perfusion model was used to assess the effects of antigen challenge of airway reactivity and its pharmacologic modulation. Increases in airway perfusion pressure, following antigen provocation, could be reproduced 60 min later without significant modification of the response. We found no change in lung volume nor observed tissue edema following antigen provocation, and suggest that rises in perfusion pressure are due to decreases in airway caliber. Pharmacologically, the antihistamines, mepyramine and chlorpheniramine, and the antiallergic agent, disodium cromoglygate (DSCG), failed to inhibit antigenic bronchoconstriction. Indeed, mepyramine produced some potentiation of allergic bronchospasm. Compounds reported to inhibit 5-lipoxygenase (phenidone, benoxaprofen, and noradihydroguiaretic acid (NDGA)) or antagonize SRS-A (FPL 55712), produced inhibition of antigen-induced bronchoconstriction. The cyclooxygenase inhibitor, indomethacin, produced biphasic modulation of antigenic bronchoconstriction, potentiation at low doses, and inhibition at high concentrations. Overall, drug-induced modulation of allergic bronchoconstriction suggests that this model more closely resembles the antigenic reactions observed in the parenchymal strip preparation than in the trachea.

Animals↗

PubMed1991

The uptake of inorganic iron complexes by human melanoma cells.

The human melanoma cell line, SK-MEL-28, expresses high levels of melanotransferrin. The uptake of inorganic iron (Fe) complexes compared to transferrin-bound Fe by these cells has been investigated to determine whether melanotransferrin has a role in Fe uptake. The mechanisms of Fe uptake have been characterised using 59Fe complexes of citrate, nitrilotriacetate, desferrioxamine, and 59Fe added to Eagle's minimum essential medium (MEM) and compared with human transferrin (Tf) labelled with 59Fe and iodine-125. Iron uptake from the Fe complexes of citrate, nitrilotriacetate and MEM were similar, and far greater than that from Tf at the same Fe concentration (2.5 microM). Ammonium chloride and a monoclonal antibody to the transferrin receptor (42/6), had no effect on the uptake of Fe from inorganic Fe complexes, suggesting that receptor-mediated endocytosis of Tf was not involved. The monoclonal antibody, 96.5, specific for melanotransferrin did not alter total Fe uptake but slightly increased the proportion of Fe internalised, possibly due to the modulation of the antigen by the antibody. However, from the time required for modulation to occur (approximately 2 h), the small increase in internalisation observed and the fact that no increase in total cell Fe occurred, it is suggested that melanotransferrin has little role in Fe uptake.

Ammonium Chloride↗

PubMed1989

Changes in cell surface antigen expression during murine bone marrow cell regeneration in vivo and proliferation in vitro.

Modulations in surface antigen expression during marrow regeneration in vivo, and proliferation in vitro in response to haemopoietic growth factors, were studied using a panel of monoclonal antibodies recognizing antigenic determinants expressed by primitive multipotential progenitor cells (Thy-1, Qa-m7), or lineage antigens restricted to committed progenitors and differentiated cells of the neutrophil/macrophage (7/4) and B lymphocyte (B220) lineages. These two categories of antigen exhibited differing responses to marrow perturbation and proliferation. Following administration of a cytotoxic dose of 5-fluorouracil, or lethal irradiation and transplantation of normal donor marrow, the levels of Thy-1 and Qa-m7 antigen expression rapidly increase, reaching a peak at the onset of regeneration: the nadir of marrow cellularity. Expression of these antigens returns to normal as regeneration proceeds and marrow is reconstituted. 7/4 and B220 antigen expression reflect the presence or absence of maturing cells bearing these markers: antigen expression declining following perturbation, and re-emerging during the course of regeneration. In vitro, when marrow cells taken from mice 8 days following treatment with 5-FU are grown in liquid culture in the presence of colony-stimulating factor-1 plus bladder cell carcinoma cell line 5637 conditioned medium, marrow cells are stimulated to proliferate and differentiate along the neutrophil/macrophage lineage. 7/4 antigen expression increases throughout the culture period, and B220 antigen is undetectable after the fifth day of culture. Thy-1 antigen expression also rises and remains elevated, and Qa-m7 antigen expression remains stable.

Animals↗

PubMed1997

Co-ligation of the antigen and Fc receptors gives rise to the selective modulation of intracellular signaling in B cells. Regulation of the association of phosphatidylinositol 3-kinase and inositol 5'-phosphatase with the antigen receptor complex.

Cross-linking of the Fc receptor (FcR) to surface immunoglobulin (sIg) on B cells inhibits the influx of extracellular calcium and abrogates the proliferative signal. The mechanism by which this occurs is not well understood. In this report we show that co-cross-linking the FcR to the antigen receptor gives rise to very selective modulation of signal transduction in B cells. Co-cross-linking sIg and the FcR enhanced the phosphorylation of the FcR, the adapter protein, Shc, and the inositol 5'-phosphatase Ship. Furthermore, phosphorylation of the FcR induced its association with Ship. Cross-linking of the FcR and sIg decreased the tyrosine phosphorylation of CD19, which led to a reduction in the association of phosphatidylinositol 3-kinase. In addition, the phosphorylation of several other proteins of 73, 39, and 34 kDa was reduced. Activation of the cells with either F(ab')2 or intact anti-IgG induced very similar changes in levels of tyrosine phosphorylation of most other proteins, and no differences in the activation of several protein kinases were observed. These results indicate that the inhibitory signal that is transmitted through the FcR is not mediated by a global shutdown of tyrosine phosphorylation but is, rather, a selective mechanism involving localized changes in the interactions of adapter proteins and the enzymes Ship and phosphatidylinositol 3-kinase with the antigen receptor complex.

Adaptor Proteins, Signal Transducing↗

PubMed1997

Rapid induction of Fas antigen mRNA expression in vivo by cycloheximide.

The effect of administration into rats of cycloheximide on the expression of genes, such as tissue transglutaminase, testosterone-repressed prostate message-2, Fas antigen, bcl-2, DNase I, and poly(ADP-ribose) polymerase, which were believed to be involved in the mechanism of apoptosis, was studied. While the effect of cycloheximide on the expression of genes other than Fas antigen was modest, only the expression of Fas antigen was elevated rapidly in most of the organs examined. A possible direct effect of cycloheximide on cells per se to induce Fas antigen mRNA expression was demonstrated by the tissue culture study using L929 fibroblast cells, although the magnitude of the induction detected in vitro was small compared with that in vivo. This induction of Fas antigen mRNA by cycloheximide is a first report on the modulation of Fas antigen mRNA expression in vivo.

Animals↗

PubMed1998

Interaction of the single-stranded DNA-binding protein Puralpha with the human polyomavirus JC virus early protein T-antigen.

Large T-antigen, the major regulatory protein encoded by polyomaviruses, including Simian Virus 40 (SV40) and JC virus (JCV), is a multifunctional phosphoprotein that is involved in many viral and cellular events. In addition to its integral role in viral replication and cellular transformation, T-antigen also regulates transcription of both viral and cellular genes. In particular, the viral late promoter has been used as a model for the analysis of T-antigen-mediated transcriptional activation. Earlier studies have demonstrated that the cellular protein Puralpha is able to attenuate the transcriptional activity of JCV T-antigen. We investigated the mechanism whereby Puralpha affects T-antigen function. Co-immunoprecipitation studies demonstrated that Puralpha and JCV T-antigen associate in vivo, and glutathione S-transferase affinity binding assays revealed that these two proteins interact in vitro. Moreover, we localized the sequences of Puralpha that are important for the interaction between Puralpha and JCV T-antigen. In addition, we demonstrated that Puralpha interacts with the SV40 T-antigen. Transient transfection studies demonstrated that Puralpha and JCV T-antigen interact functionally as well. More specifically, Puralpha and a deletion mutant that interacts with T-antigen attenuated T-antigen-mediated transcriptional activation. A Puralpha deletion mutant that is unable to interact with JCV T-antigen, however, was found to be incapable of abrogating JCV T-antigen transactivation. Taken together, these data demonstrate that Puralpha and T-antigen interact both physically and functionally and that this interaction modulates T-antigen-mediated transcriptional activation. The implication of these findings with respect to the cellular role of Puralpha is discussed.

Antigens, Polyomavirus Transforming↗