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Y N Liu

Publications and source records attributed to Y N Liu.

At least 37 records · Page 2Linked to original sources

Structure and composition of a family of human cytomegalovirus glycoprotein complexes designated gC-I (gB).

Murine monoclonal antibodies (MAbs) were made to the 52,000 (gp52) and the 93,000 to 130,000 Mr (gp93-130) glycoproteins from a human cytomegalovirus (HCMV) glycoprotein complex designated gC-I or the gB homologue. MAbs recognizing either gp52 or gp93-130 could immunoprecipitate unreduced gC-I complexes from non-ionic detergent extracts of HCMV. Western blotting was performed with immunoaffinity-purified gC-I complexes which were reduced prior to analysis. MAbs made against gp52 recognized gp52 and a 158,000 Mr glycoprotein (gp158). MAbs which recognized gp93-130 in a Western blot also reacted with gp158, which is a gC-I precursor glycoprotein. The origin of gp93-130 was demonstrated by the reactivity of our gp93-130 MAbs with a recombinant protein containing the N-terminal portion of the gB gene. These data are consistent with the hypothesis that gp52 and gp93-130 are generated from the same high Mr precursor by proteolysis. MAbs recognizing either gp52 or gp93-130 neutralized Towne strain HCMV, but MAbs recognizing gp52 required complement to neutralize whereas MAbs recognizing gp93-130 did not. It was also determined that gp93-130 and gp 158 have detectable amounts of O-linked glycans but gp52 does not, showing a difference in the glycosylation of these glycoproteins. Analysis of gC-I disulphide bonds showed that two types were present, one which was very susceptible to reduction and a second which was less susceptible. These complexes could consist of very susceptible inter-complex disulphide bonds and less susceptible intra-complex disulphide bonds.

Animals↗

Parrot breeder's lung: first case report in China.

The authors report the first case of parrot breeder's lung in China and the study of its immunology, respiratory physiology, as well as pathology. The main characteristics of this disease are progressive dyspnea after contacting parrots, patchy or reticular shadows in the lower lung fields on chest X-ray, the presence of alveolitis, accompanied by pulmonary interstitial fibrosis as demonstrated in lung biopsy, restrictive or mixed ventilation disorders with reduction of diffusing capacity and lung compliance. The results of specific ring precipitation test and counter immunoelectrophoresis were helpful in diagnosis. The importance of early diagnosis and treatment is also discussed.

Adult↗

General characterization of human cytomegalovirus-specific proliferative CD4+ T cell clones.

Over 80 human T helper cell (Th) clones reactive with human cytomegalovirus (HCMV) were generated using purified whole Towne strain HCMV as the in vitro antigen. These cloned T cells are CD3+, CD4+, CD8- and proliferate specifically to HCMV. All of the clones tested produce interleukin 2 and gamma-interferon and failed to show HCMV-specific cytotoxicity or natural killer (NK) activity. Most of the Th clones recognize multiple laboratory-adapted and wild-type strains of HCMV. The Th clones were also tested for their reactivity to a major envelope glycoprotein complex (gcI) and a 64,000 dalton internal matrix protein. Our results show that both proteins as well as other unidentified protein(s) are involved in Th responses to HCMV.

Antigens, Viral↗

Cytoplasmic suppression of tumor progression in reconstituted cells.

This report details studies of whether mouse NIH/3T3 TGr karyoplasts that are exposed to benzo[a]pyrene epoxide(trans) (BPDE) can progress to tumorigenicity when they are rescued with either mouse B10mtJ CAPr tumorigenic (experiment 1) or nontumorigenic (experiment 2) cytoplasts. The mitochondrial DNA of the B10mtJ cells has restriction fragment length differences that allow distinction from the mitochondrial DNA of the NIH/3T3 cells. The reconstructed clones in experiment 1 were all tumorigenic, while those from experiment 2 were all nontumorigenic. The clones in both experiments were passaged for an equivalent time. These findings reflect the presence of factors in mouse cytoplasm capable of suppressing the tumor phenotype of NIH/3T3-BPDE treated karyoplasts when rescued at an early stage of progression.

Animals↗

Human immune responses to major human cytomegalovirus glycoprotein complexes.

Sera from both human cytomegalovirus (HCMV)-seropositive adults and infants with congenital HCMV infection recognized two major HCMV glycoprotein complexes. However, proliferative responses of peripheral blood mononuclear cells to these complexes varied among seropositive adults and were not detected in any of the infants. Thus, these glycoproteins alone may not be sufficient to develop a subviral HCMV vaccine.

Adult↗

Immune mechanisms in congenital cytomegalovirus infection: activation of CMV-specific T helper cells (CMV-Th) by exogenous IL-2.

Infants with congenital CMV infection have a specific defect in CMV-induced lymphocyte proliferation, providing a model for investigation of mechanisms of viral immune recognition and immune response. In the present study the possible role of a defect in lymphokine activation of CMV-specific T helper cells (Th) was examined. IL-1 activity was detected in supernatants of patient mononuclear cell (MNC) cultures stimulated with CMV. In contrast, no IL-2 activity could be detected in supernatants of CMV-stimulated MNC cultures, whereas PHA induced normal IL-2 production. Addition of low concentrations of either crude TCGF or recombinant IL-2 (rIL-2) resulted in 2-4 fold augmentation of CMV-specific lymphocyte proliferation; exogenous IL-2 had no effect on MNC responses to HSV. CMV-specific Th lines/clones were established from three congenital CMV patients by initial stimulation of MNCs with CMV antigen and 0.1 U/ml rIL-2, followed by repeated stimulation with CMV, HLA-matched allogeneic feeder cells and 10% TCGF. The resulting CMV Th lines/clones proliferated specifically in response to stimulation with CMV antigen and produced endogenous IL-2. Thus, the immune deficiency associated with congenital CMV may either be due to an intrinsic defect in CMV-Th activation or CMV-specific suppressor cell activity.

Adult↗

HLA class II restriction of T helper cell response to cytomegalovirus (CMV). I. Immunogenetic control of restriction.

All three HLA class II families (DR, DQ, and DP) are involved in restriction of helper T cell (Th) recognition of nominal antigens including CMV. Only limited studies have been described previously to determine whether restricting determinants of DR and especially DQ are subtypic to the serologically defined DR and DQ specificities, and to what extent restricting determinants are associated with Dw specificities defined in alloresponses. In the present report, we describe a large number of CMV-specific Th clones derived from two different individuals who are seropositive for CMV. Clones were classified as being DR-, DQ-, or DP-reactive based on blocking with monoclonal antibodies. DR- and DQ-restricted clones were then examined in panel studies using antigen-presenting cells (APC) expressing the Dw subtype of the restricting DR-DQ haplotype, as well as APC expressing different Dw subtypes associated with the serologically defined specificity. Unrelated specificities were also included. Our findings show that not only for DR but for DQ as well, the primary restricting determinants appear to be subtypic to the serologically defined antigen; furthermore, subtype restriction for both DR and DQ is very closely associated with single Dw specificities. In several cases in which cross-reactivity among restricting Dw specificities was observed in association with a given DR or DQ haplotype, a molecular basis could be suggested to explain the cross-reacting determinants. A small minority of the clones appeared to be CMV specific, but was restricted by a determinant(s) that is either monomorphic or minimally polymorphic.

Antigen-Presenting Cells↗

Epstein-Barr virus-transformed lymphoblastoid cell lines as antigen-presenting cells and "augmenting" cells for human CMV-specific Th clones.

The ability of Epstein-Barr virus-transformed lymphoblastoid cell lines (LCL) to present human cytomegalovirus (HCMV) antigen to a panel of HCMV-specific T helper (Th) clones was evaluated. Among the seven Th clones studied, only one clone (SP-CN/T3-16) proliferated well to HCMV presented by both autologous mononuclear cells (MNC) and LCL, and one clone (SP-CN/T3-9) proliferated significantly better to HCMV presented by autologous LCL than by autologous MNC. The majority of the HCMV-specific Th clones tested (five out of seven) responded much better to HCMV presented by MNC than to HCMV presented by LCL. The mechanism(s) responsible for the inefficiency of LCL to present HCMV to certain clones was studied. Our results suggested that the defect of LCL is not due to insufficient interleukin 1 production, insufficient MHC class II molecule expression, nor an inhibitory mechanism or factor. In this report, we also demonstrate that by adding a minimum amount of LCL along with MNC as antigen-presenting cells (APC), one can restimulate and expand Th clones much more efficiently than by using MNC alone as APC.

Antigen-Presenting Cells↗

Inhibition of lymphoid cell growth by a lipid-like component of macrophage hybridoma cells.

Previous studies have shown that plasma membranes of murine lymphocytes and lymphoid tumor cells can reversibly inhibit the growth of both normal and transformed lymphocytes. The inhibitor can be extracted with organic solvents and has properties consistent with it being a lipid or lipid-like component of the membrane. This report identifies a series of cloned macrophage hybridoma cell lines, obtained by fusion of splenic adherent cells and the P388D1 line, which have very high levels of lipid-like growth-inhibitory molecules. Furthermore, a survey of seven cloned lines indicated that the macrophages fell into two distinct groups with regard to their level of growth-inhibitory activity. Group 1 lines had little or no inhibitory activity when cells were examined for their effect on a B lymphocyte proliferative response. Organic extracts from these macrophages had inhibitory activity (on a per cell basis) comparable to that seen with extracts of the P388D1 parental cell line and lymphoid tumor cells. In contrast, relatively low numbers of Group 2 macrophages could profoundly inhibit B macrophage proliferation. The growth-inhibitory activity was quantitatively recovered in organic extracts of the macrophages. Although the precise nature of the lipid moiety remains undefined, the data argue against the involvement of oxidized cholesterol. These findings indicate that lipid-like inhibitors of cell growth are present and functional in these macrophage cell lines. In addition, the results demonstrate that the inhibitory activity found in plasma membranes and liposomes is present and active in the membranes of intact cells, which is in contrast to the possibility that the inhibitor is an artifact generated during subcellular fractionation. Thus, the inhibitor is likely to have a physiologic role in growth control and in macrophage-mediated immunoregulation, probably acting via a mechanism involving cell-cell contact.

Animals↗

Functional analysis of macrophage hybridomas. II. Antibody-independent tumor cytotoxicity and its dissociation from IL-1 production and Ia expression.

Cloned macrophage hybridoma cells derived from fusions between splenic adherent cells of CKB mice and the drug-marked P388D1 cell line were studied to further understand macrophage-mediated tumoricidal activity at the clonal level. Most of the macrophage hybridomas were specifically activated by a combination of lymphokine and lipopolysaccharide (LPS), but were not activated by either agent alone. There is no apparent correlation between macrophage-mediated tumor cytotoxicity and the ability of LPS to induce interleukin 1 (IL-1) secretion or of concanavalin A (Con A) supernatants containing interferon-gamma to increase H-2 and Ia expression. Thus, one hybridoma clone which was unable to kill tumor cells was still sensitive to LPS and lymphokine activation by the latter criterion.

Animals↗