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At least 559 records · Page 31Linked to original sources
PubMed1978

Normal erythropoietic helper T cells in congenital hypoplastic (Diamond-Blackfan) anemia.

To examine the erythropoietic function of T and null cells in congenital hypoplastic (Diamond-Blackfan) anemia, we fractionated the peripheral blood of three normal subjects and three affected patients into subclasses of null, T and B cells. Mixtures of these cells were co-cultured in plasma clots in the presence of erythropoietin. Erythroid colonies grew in cultures of normal null cells if either normal or patient T cells were co-cultured with them. Null cells of patients with hypoplastic anemia did not produce erythroid colonies under any culture conditions. We conclude that in this disorder, T cells function normally as helper cells in erythropoiesis and do not suppress colony formation, whereas the erythroid progenitor cells in the peripheral blood null-cell fractions are deficient in either number of function.

Adolescent↗
PubMedDate not supplied

Effect of screw placement on fixation in the humeral head.

The objectives of this study were (1) to determine the most advantageous screw locations within the humeral head when plate and screw fixation is to be used and (2) to determine the effect of positioning the screw tip abutting the subchondral bone. Ten paired humeral heads were harvested with a monoplanar cut through the anatomic neck. Through use of a standardized template, 7 holes were drilled and tapped in each specimen for insertion of 6.5-mm fully threaded cancellous screws perpendicular to the plane of the cut. Paired specimens were randomized into 2 groups, one with the screw purchase in central cancellous bone and the other with the screw purchase up to the subchondral bone. Each screw was pulled out axially at a displacement rate of 10 mm/min through use of a servohydraulic testing machine. The length of thread purchase, position within the head, and screw pullout load to failure were recorded. The normalized pullout force to failure was calculated by dividing absolute pullout force to failure by length of screw purchase. Data were analyzed by means of a 2-way repeated measures analysis of variance and post hoc Student-Newman-Keuls test. The central position had a significantly higher absolute pullout force to failure than all other sites (P < .05). By virtue of the humeral head shape, the central position also had a significantly greater length of screw purchase than all other positions (P < .05). The central position had a significantly higher relative pullout force to failure than all other positions (P < .05). Subchondral bone abutment positioning improved both the absolute and the relative pullout forces to failure (P < .05). When screws and plates are used in open reduction and internal fixation of a proximal humerus fracture, a major mode of failure is loss of fixation within the humeral head. On the basis of this study, optimal screw purchase with respect to bone fixation can be achieved by including screws located in the center of the humeral head in the subchondral abutment position. To minimize screw fixation failure, the anterosuperior position should be avoided. The pattern of distribution of the relative pullout force as measured in this study is consistent with previous observational studies of patterns of trabecular density within the humeral head.

Aged↗
PubMed2004

Selective pressures on the olfactory receptor repertoire since the human-chimpanzee divergence.

The availability of the sequence of the chimpanzee genome provides an opportunity to examine human genes and their chimpanzee orthologs and to analyze selective pressures that have been shaping the olfactory receptor repertoire since the human-chimpanzee divergence. We determined the ratio of nonsynonymous to synonymous changes for each of 186 orthologous pairs and then examined how the distribution of these ratios compares with the distribution expected under neutral drift. Consistent with the diminishing importance of olfaction for these species, we find no evidence for positive selection and we find evidence of weak purifying selection affecting over half of the repertoire.

Animals↗
PubMed2001

CD8+ T cells control the TH phenotype of MBP-reactive CD4+ T cells in EAE mice.

Trimolecular interactions between the T cell antigen receptor and MHC/peptide complexes, together with costimulatory molecules and cytokines, control the initial activation of naive T cells and determine whether the helper precursor cell differentiates into either T helper (TH)1 or TH2 effector cells. We now present evidence that regulatory CD8(+) T cells provide another level of control of TH phenotype during further evolution of immune responses. These regulatory CD8(+) T cells are induced by antigen-triggered CD4(+) TH1 cells during T cell vaccination and, in vitro, distinguish mature TH1 from TH2 cells in a T cell antigen receptor Vbeta-specific and Qa-1-restricted manner. In vivo, protection from experimental autoimmune encephalomyelitis (EAE) induced by T cell vaccination depends on CD8(+) T cells, and myelin basic protein-reactive TH1 Vbeta8(+) clones, but not TH2 Vbeta8(+) clones, used as vaccine T cells, protect animals from subsequent induction of EAE. Moreover, in vivo depletion of CD8(+) T cells during the first episode of EAE results in skewing of the TH phenotype toward TH1 upon secondary myelin basic protein stimulation. These data provide evidence that CD8(+) T cells control autoimmune responses, in part, by regulating the TH phenotype of self-reactive CD4(+) T cells.

Animals↗
PubMed2003

Regulatory CD8+ T cells fine-tune the myelin basic protein-reactive T cell receptor V beta repertoire during experimental autoimmune encephalomyelitis.

A significant number of self-reactive T cell clones escape thymic negative selection and are released into the periphery, where some are potentially pathogenic. The clonal expansion of self-reactive T cells is known to be limited during initial antigen encounter by apoptotic or anergic mechanisms, regulatory CD4+ T cells, and cytokines. Here we report that superimposed on these mechanisms, during the evolution of autoimmunity in experimental autoimmune encephalomyelitis (EAE), CD8+ T cells are induced, which fine-tune the peripheral self-reactive T cell receptor (TCR) repertoire. We assayed the myelin basic protein-reactive TCR repertoire in naive, EAE-recovered mice as well as EAE-recovered mice depleted of CD8+ T cells by TCRV beta surface expression, complementarity-determining region 3 length distribution, and complementarity-determining region 3 sequencing analysis. In EAE-recovered mice, certain myelin basic protein-reactive CD4+V beta 8.2+ clones are significantly decreased and this decrease is not observed if CD8+ T cells were depleted from these mice. The clones that persist in CD8+ T cell-intact mice are highly diverse in contrast to the clones expanded in CD8+ T cell-depleted mice, which are dominated by the significant outgrowth of a few clones. Importantly, the T cell clones that expand in the absence of CD8+ T cell control are enriched in potentially pathogenic self-reactive T cell clones capable of inducing EAE in vivo.

Adoptive Transfer↗
PubMed1976

Distribution of Ia-like molecules on the surface of normal and leukemic human cells.

Antiserum to a glycoprotein antigen complex of 23,000 and 30,000 dalton subunits (p23,30), isolated and purified from a human lymphoblastoid B cell line, was shown to be highly specific for human bursal-equivalent-processed (B) cells, reactive with 15-20% of human Null cells, but completely unreactive with human thymus-processed (T) cells. The p23,30 antigen is widely distributed on chronic lymphatic leukemic cells, 85% of acute lymphatic leukemic cells, all acute myelogenous leukemic cells, but not on chronic myelogenous leukemic cells. A rabbit antiserum specific for normal human thymocytes has also been prepared; it is reactive only with precisely that subset of acute lymphatic leukemic cells (15%) whose members do not have p23,30 on their surfaces.

B-Lymphocytes↗
PubMed1977

Inhibition of proliferative and plaque-forming cell responses by human bone-marrow-derived lymphocytes from peripheral blood by antisera to the p23, 30 antigen.

A recently described technique for the polyclonal induction of plaque-forming cells from human bone-marrow derived (B) lymphocytes of peripheral blood has been used to assess the role of a human Ia-like antigen (p23,30) in differentiation of human B cells. In particular, the effects of antisera to p23,30 on the plaque-forming cells and proliferative responses of human B cells stimulated by pokeweed mitogen or soluble products of activated human thymus-derived lymphocytes (T cells) have been examined. Antisera to p23,30 eliminated the development of plaque-forming cells induced by both T cell products and pokeweed mitogen. While these antisera also abrogated B cell proliferation induced by T cell supernatants, the proliferative response generated by pokeweed mitogen was only partially reduced. It was also determined that while the p23,30 antigen continues to be expressed on fully differentiated plaque-forming cells, antisera to this determinant exert inhibitory effects on B cell differentiation only when present during the early stages of B cell cultures. These results lend further support to the analogy between p23,30 and murine Ia antigens. Moreover, they demonstrate a major role for this antigen in the early events involved in human B cell differentiation into antibody-forming cells.

Antigen-Antibody Reactions↗
PubMed1980

High molecular weight antigens present on human T cells.

A series of eight high molecular weight (140,000-220,000) glycoproteins on human peripheral T cells were recognized by radioimmunoprecipitation with a rabbit antiserum. The pattern of antigens present on each of eight human T cell lines studied was unique, and no line displayed the range of antigens present on peripheral T cells. The pattern of bands on peripheral T cells changed after allogeneic or lectin stimulation. Adsorption/elution experiments with antiserum showed that some of these proteins were antigenically related, and at least three different groups of proteins were present. Two of these groups could be partially distinguished by their ability to bind to ricin or lentil lectin and by their reactivity with two additional rabbit antisera. On some cell lines, it was found that proteins bound by lentil lectin but not ricin were precursors of higher molecular weight material recognized by ricin. Taken together, the data suggest that these proteins may be the products of a multigenic or multiallelic system, probably equivalent to the murine Ly 5 antigens.

Antigens, Surface↗
PubMed1981

Plasma cell dyscrasia and peripheral neuropathy: identification of the myelin antigens that react with human paraproteins.

In some cases of polyneuropathy and plasma cell dyscrasia, the monclonal antibodies react with human peripheral nerve myelin. To identify the myelin antigens involved, we separated the proteins of human central and peripheral nerve myelin by polyacrylamide gel electrophoresis, transferred the proteins onto nitrocellulose sheets, and used an immunoenzymatic technique to detect the reactive antigens. Serum IgM but not IgG from three patients with neuropathy and complement-fixing anti-human myelin IgM paraproteins immunostained a protein of approximately 100,000 daltons in human peripheral nerve myelin and a protein or closely migrating proteins of similar size in human central nervous system myelin. In a fourth patient, both IgM and IgG immunostained the antigen. Immunostaining was specific for the paraprotein light chain type, and absorption of the patients' sera with human peripheral nerve myelin eliminated the reaction with the central nervous system proteins. No reaction was seen with rabbit peripheral nerve myelin or with membranes prepared from human myotubes, human T cells, or human fibroblasts. Control sera from six patients with neuropathy and IgM paraproteins that did not react with myelin, from four patients with IgM paraproteins but no neuropathy, and from three normal subjects did not immunostain myelin.

Antibodies, Monoclonal↗
PubMed1981

Dissection of distinct human immunoregulatory T-cell subsets by a monoclonal antibody recognizing a cell surface antigen with wide tissue distribution.

A monoclonal antibody, PVR-11, was obtained after hybridization of X63Ag8.653 murine myeloma cells with spleen cells from a mouse immunized with human lymphocytes. It recognizes a 175,000- to 185,000-dalton surface antigen present on approximately 80% of normal human peripheral T lymphocytes, 50% of non-T non-B cells, and less than 10% of B cells as determined by complement-dependent microcytotoxicity. It is also present on various leukemia T cells, on some but not all T lymphoblastoid cell lines, and on a small fraction of some B lymphoblastoid cell lines. Some B-cell chronic lymphocytic leukemia cells also express the PVR-11 antigen. Functional analysis of normal human T lymphocytes demonstrated that the PVR-11-depleted T-cell subset contains the precursors of both cytotoxic and suppressor cells but lacks helper cells. On the other hand, cytotoxic effector T cells express the PVR-11 antigen. These results demonstrate that antigenic determinants with relatively wide tissue distribution can dissect functionally distinct human immunoregulatory T-cell subsets.

Antibodies↗
PubMed1987

Structure and expression of the human and mouse T4 genes.

The T4 molecule may serve as a T-cell receptor recognizing molecules on the surface of specific target cells and also serves as the receptor for the human immunodeficiency virus. To define the mechanisms of interaction of T4 with the surface of antigen-presenting cells as well as with human immunodeficiency virus, we have further analyzed the sequence, structure, and expression of the human and mouse T4 genes. T4 consists of an extracellular segment comprised of a leader sequence followed by four tandem variable-joining (VJ)-like domains, a transmembrane domain, and a cytoplasmic segment. The structural domains of the T4 protein deduced from amino acid sequence are precisely reflected in the intron-exon organization of the gene. Analysis of the expression of the T4 gene indicates that T4 RNA is expressed not only in T lymphocytes, but in B cells, macrophages, and granulocytes. T4 is also expressed in a developmentally regulated manner in specific regions of the brain. It is, therefore, possible that T4 plays a more general role in mediating cell recognition events that are not restricted to the cellular immune response.

Amino Acid Sequence↗
PubMed1998

T cell vaccination induces T cell receptor Vbeta-specific Qa-1-restricted regulatory CD8(+) T cells.

Vaccination of mice with activated autoantigen-reactive CD4(+) T cells (T cell vaccination, TCV) has been shown to induce protection from the subsequent induction of a variety of experimental autoimmune diseases, including experimental allergic encephalomyelitis (EAE). Although the mechanisms involved in TCV-mediated protection are not completely known, there is some evidence that TCV induces CD8(+) regulatory T cells that are specific for pathogenic CD4(+) T cells. Previously, we demonstrated that, after superantigen administration in vivo, CD8(+) T cells emerge that preferentially lyse and regulate activated autologous CD4(+) T cells in a T cell receptor (TCR) Vbeta-specific manner. This TCR Vbeta-specific regulation is not observed in beta2-microglobulin-deficient mice and is inhibited, in vitro, by antibody to Qa-1. We now show that similar Vbeta8-specific Qa-1-restricted CD8(+) T cells are also induced by TCV with activated CD4(+) Vbeta8(+) T cells. These CD8(+) T cells specifically lyse murine or human transfectants coexpressing Qa-1 and murine TCR Vbeta8. Further, CD8(+) T cell hybridoma clones generated from B10.PL mice vaccinated with a myelin basic protein-specific CD4(+)Vbeta8(+) T cell clone specifically recognize other CD4(+) T cells and T cell tumors that express Vbeta8 and the syngeneic Qa-1(a) but not the allogeneic Qa-1(b) molecule. Thus, Vbeta-specific Qa-1-restricted CD8(+) T cells are induced by activated CD4(+) T cells. We suggest that these CD8(+) T cells may function to specifically regulate activated CD4(+) T cells during immune responses.

Animals↗
PubMed2004

Monoallelic expression and asynchronous replication of p120 catenin in mouse and human cells.

The number of autosomal mammalian genes subject to random monoallelic expression has been limited to genes highly specific to the function of chemosensory neurons or lymphocytes, making this phenomenon difficult to address systematically. Here we demonstrate that asynchronous DNA replication can be used as a marker for the identification of novel genes with monoallelic expression and identify p120 catenin, a gene involved in cell adhesion, as belonging to this class. p120 is widely expressed; its presence in available cell lines allowed us to address quantitative aspects of monoallelic expression. We show that the epigenetic choice of active allele is clonally stable and that biallelic clones express p120 at twice the level of monoallelic clones. Unlike previous reports about genes of this type, we found that expression of p120 can be monoallelic in one cell type and strictly biallelic in another. We show that in human lymphoblasts, the silencing of one allele is incomplete. These unexpected properties are likely to be wide-spread, as we show that the Tlr4 gene shares them. Identification of monoallelic expression of a nearly ubiquitous gene indicates that this type of gene regulation is more common than previously thought. This has important implications for carcinogenesis and definition of cell identity.

Alleles↗
PubMed1999

The relationship between in vivo emptying of the gallbladder, biliary pain, and in vitro contractility of the gallbladder in patients with gallstones: is biliary colic muscular in origin?

BACKGROUND: This study sought to determine whether there is a positive correlation between gallbladder emptying, biliary pain, and in vitro contractility. METHODS: Ultrasound measurements were carried out on 25 gallstone patients. The response of gallbladder strips to 1.75*10(-11) to 5.25*10(-7) M cholecystokinin-8 was recorded. In a second study 23 patients filled in pain questionnaires, and in vitro studies were again carried out. RESULTS: Of five patients with no gallbladder emptying, four had in vitro contraction. Overall, a significant, positive linear correlation was found (P < 0.0001). In the second study in vitro contractility showed a positive linear correlation with pain. CONCLUSION: Gallbladder emptying correlates with contractility. However, since most 'non-contractors' can contract, we suggest the term 'non-emptying' or 'emptying' to describe gallbladder dynamics. The positive correlation between pain and contractility suggests that biliary pain has a muscular component.

Cholelithiasis↗