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Biomedical subjects

L Shen

Publications and source records attributed to L Shen.

At least 325 records · Page 18Linked to original sources
PubMed1981

Synergy between IgG and monoclonal IgM antibodies in antibody-dependent cell cytotoxicity.

Hybridoma-derived mouse monoclonal IgM anti-ox erythrocyte (ORBC) antibodies, which differed in their ability to exhibit complement-mediated cytotoxicity, direct agglutination and sensitization of indicator cells for detection of receptors for IgM on erythrocytes, failed to mediate antibody-dependent cell cytotoxicity (ADCC) by human K cells. Polyclonal rabbit IgM anti-ORBC antibodies were also incapable of mediating ADCC. However, one of the IgM monoclonal antibodies studied (clone 100) was highly efficient in synergizing with IgG in ADCC, especially when the E rosette-forming enriched fraction was used as a source of effector cells. This synergy was greater after overnight incubation of the lymphocytes and was partially blocked by human IgM. Since all the monoclonal antibodies studied bound efficiently to target ORBC as determined by the additional binding of 125I-labeled anti-k antibodies, the synergy did not appear to be due to a quantitative difference in the binding capacity of the antibodies. That the synergistic effect of purified clone 100 IgM was not due to heterophile IgG antibody was indicated by its sensitivity to reduction and lack of binding to a protein A column. The data are discussed in terms of the possible in vivo relevance of IgG-IgM synergy to immune protection, especially during the development of a primary antibody response when limiting amounts of specific IgG antibodies could be made more effective with the more abundant IgM antibodies.

Animals↗
PubMed1980

Cloning and sequence analysis of cDNAs encoding two distinct somatostatin precursors found in the endocrine pancreas of anglerfish.

Complementary DNAs for two distinct anglerfish somatostatin peptides (termed I and II) have been cloned in bacterial plasmids and sequenced. The nucleotide sequence for somatostatin I encodes a large percursor peptide (molecular weight 13,300) in which the somatostatin hormones is at the carboxyl terminus. The predicted 14-amino acid sequence for anglerfish somatostatin I is the same as mammalian somatostatin. Somatostatin II is also synthesized as part of a larger precursor (molecular weight 14,100) with the presumptive somatostatin hormone also at the carboxyl terminus. The 14-amino acid sequence of somatostatin II differs from somatostatin I at two internal residues (Tyr in place of Phe 7 and Gly in place of Thr 10). The two different somatostatins may have distinct biological activities. Homologies in the amino acid sequences of the two peptides outside the somatostatin moiety suggest other regions of the molecules have biological functions.

Amino Acid Sequence↗
PubMed1980

Chemotactic factor-induced membrane potential changes in rabbit neutrophils monitored by the fluorescent dye 3,3'-dipropylthiadicarbocyanine iodide.

Rabbit neutrophil leucocytes take up the cationic, fluorescent dye 3,3'-dipropylthiadicarbocyanine iodide (DiS-C3-(5)). Treatment with valinomycin and K+ then produces characteristic changes in suspension fluorescence that indicate that the dye enters the cells in a potential-dependent fashion and that the resting membrane potential lies between -66 and -86 mV. The peptide, N-fMet-Leu-Phe, a potent chemoattractant for neutrophils, added to stained cell suspensions, induces fluorescence intensity changes. These occur over an 8-10 min period. The time course of this response is profoundly affected by the omission of Ca2+ from the medium. When this ion is present (1.26 mM) a small, transient increase in intensity is observed, superimposed on a sustained decrease. On the other hand, in the absence of added Ca2+ a large, transient increase is observed. The ED50 for this is 1.1 x 10(-10) M. These changes are not elicited by N-fMet-Phe (10(-9) M) and are inhibited by the antagonist Boc-Leu-Phe-Leu-Phe. However, a component of zymosan-activated rabbit plasma, which is complement-derived, induces identical fluorescence changes that are not inhibited by the antagonist, confirming that neutrophil activation by complement operates through an independent receptor. The fluorescence responses to the chemotactic peptide and the activated-plasma component may be interpreted in terms of changes in neutrophil membrane potential brought about by alterations in cell ionic permeability at an early stage during activation. The transient increase corresponds to a depolarisation that may be associated with a change in Na+ permeability, while the sustained decrease corresponds to a membrane hyperpolarisation.

Anaphylatoxins↗
PubMed1980

Subpopulations of human peripheral granulocyes and monocytes express receptors for IgA.

Receptors for the Fc portion of immunoglobin on human peripheral blood cells were enumerated by rosette formation with ox erythrocytes sensitized with rabbit IgG, IgA, and IgM. A large percentage of purified polymorphonuclear leukocytes and monocytes were found to express receptors for IgA. These receptors were also found to exist on a significantly greater percentage of lymphocytes than was previously observed. The receptors for IgA were specific, as verified by blocking studies using purified human immunogloblins. In addition, some polymorphonuclear leukocytes and monocytes were observed concomitantly to posses independent receptors for both IgG and IgA. These studies may indicate that IgA can cooperate with monocytes or polymorphonuclear leukocytes through receptors for IgA on these cells and perhaps mediate immune defense on mucosal surfaces. Initial studies on antibody-dependent cellular cytotoxicity suggested that IgA alone is ineffectual in supporting cytolysis by nonactivated human peripheral blood cells.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1979

Parathyroid hormone release is not associated with acute sympathetic arousal in goats.

Physiological activation of the sympathetic adrenomedullary (SAM) axis following both thermal and non thermal stress was assessed by changes in serum norepinephrine, glucose and/or protein as well as indices of peripheral blood flow. The occurrence of elevated serum parathyroid hormone (PTH) did not reliably reflect SAM activation as might be predicted from pharmacological studies that document a beta adrenergic receptor mechanism in the parathyroid gland that mediates catecholamine stimulated release of PTH into the circulation. The beta agonist isoproterenol at 1 microgram/min for 60 min did produce a transient increase in serum PTH at 20 min. Overall, the data raise doubts about the physiological significance of the adrenergic receptor in the parathyroid gland. Significant increases in serum PTH of 67% and 109% above basal respectively were seen following ruminal loading with cold and thermoneutral water. Associated with the PTH change were increased serum phosphorus and elevated or constant serum protein and serum total calcium.

Animals↗
PubMed1979

Evidence for antibody-dependent cell-mediated cytotoxicity by T cells bearing receptors for IgG.

Human lymphocyte populations comprising T cells, T depleted lymphocytes, and T cells enriched for, or depleted of, IgG Fc receptor-bearing (TG) cells, were separated using rosette techniques. All lymphocytes were assessed for the ability to lyse antibody-coated chicken erythrocytes and SL2 mouse lymphoma cells. Their activity was compared with that of monocytes and neutrophil-enriched preparations. IgG Fc receptor positive cells within the T population were highly active in both cytotoxicity assays; the activity could not be ascribed to contamination by monocytes or neutrophils. The TG cells forming junctions with the target cells possessed a characteristic ultrastructure.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1977

Inhibition of dopamine-induced release of growth hormone by thyrotropin-releasing hormone.

The effects of thyrotropin-releasing hormone (TRH) and dopamine (DA) on serum growth hormone (GH) levels were examined in the adolescent male baboon. Intravenously administered DA (40 microgram/kg-min-1 for 20 min) raised serum GH and glucose and lowered serum insulin concentrations but caused no increase in blood pressure. Concomitant intravenous infusion of TRH at 2 doses (96 ng/kg-min-1 and 40 microgram/kg-min-1 for 20 min) blocked the DA-induced increase in serum GH. The relatively low effective doses of TRH used to suppress the DA-induced GH increase suggest an interaction with catecholamines at the hypothalamic and/or pituitary to influence GH release.

Animals↗
PubMed1976

Characteristics of the effector cells mediating cytotoxicity against antibody-coated target cells. II. The mouse nonadherent K cell.

A cell of lymphoid morphology capable of killing antibody-coated chicken erythrocytes was isolated from nonimmune mouse spleen using a combination of carbonyl iron treatment and glass bead column passage. This non-phagocytic effector cell, which is referred to as the nonadherent K (killer) cell, is distinguished from the non-phagocytic myeloid K cell described earlier (Greenberg, A.H., Shen, L. and Roitt, I.M., Clin. Exp. Immunol. 1973. 15:251) by its relatively weak surface adherence properties and low concentration within the mouse spleen. The cell is further characterized by its relatively large size, lack of theta or immunoglobulin determinants, the presence of Mg++-independent complement receptors, affinity for aggregated IgG2 myeloma proteins, inhibition by cytochalasin B and good survival in cell culture. The possible lineage of the cell is discussed.

Animals↗
PubMed1975

Serum immunoreactive parathyroid hormone and 25-hydroxyvitamin D in patients with uremic bone diseases.

Bone histologic parameters and serum iPTH and 25-OHD were measured in 20 patients with end-stage renal failure treated with hemodialysis. By bone histologic criteria, the patients were divided into three groups: mild, osteomalacic, and fibrotic. The increase in serum iPTH was much greater in the fibrotic group than in the mild or osteomalacic groups. In the uremic patients as a group, there were significant correlations between serum iPTH and both percent marrow fibrosis and percent resorbing surface. In the mild and fibrotic groups together, serum iPTH was also correlated with percent forming surface. This and other findings suggested that most of the bone changes in the mild and fibrotic groups could be explained by excess PTH. The difference in bone changes and in serum iPTH between the mild and fibrotic groups could be related to our eariler findings that duration of renal disease was much greater in the fibrotic than in the mild group. The lowest increment in serum iPTH was found in the osteomalacic group. In this group, percent resorbing surface was not increased and there was only a slight increase in marrow fibrosis. Thus in all three groups, serum iPTH appeared to reflect parathyroid status. The cause of the elevated serum iPTH and for the intergroup differences was not apparent inasmuch as serum calcium was normal in all three groups. Serum 25-OHD was significantly elevated in the osteomalacic and fibrotic groups. Because none of our patients had received preparations containing vitamin D, the elevated serum 25-OHD in the osteomalacic and fibrotic groups is consistent with altered vitamin D metabolism in these two groups. There was a direct relationship between percent osteroid area and serum 25-OHD. However, whether or not altered vitamin D metabolism contributed to the mineralization defect in uremic bone disease could not be established.

Adult↗
PubMed1975

Characteristics of the effector cells mediating cytotoxicity against antibody-coated target cells. I. Phagocytic and non-phagocytic effector cell activity against erythrocyte and tumour target cells in a 51Cr release cytotoxicity assay and [125I]IUdR growth inhibition assay.

Both phagocytic and non-phagocytic effector cells were able to kill rabbit antibody-coated chicken erythrocytes (CRBC) while only non-phagocytic effector cells were active against alloantibody-coated SL2 lymphoma. In addition to the variation in susceptibility of erythrocyte and tumour target cells to various effector cell populations, it was found that different tumour cells can vary markedly in their ability to be killed by non-immune spleen cells in the presence of antibody. It is postulated that both the type of antibody and certain characteristics of the cell membrane are important in determining whether target cells are susceptible to antibody-dependent cell-mediated cytotoxicity detected by the 51Cr release assay. It was also demonstrated that alloantibody-coated P-815-Y mastocytoma, which showed very little evidence of cytotoxicity in the 51Cr release assay, was markedly inhibited in its ability to incorporate [125I]IUdR after incubation with antiserum and non-immune spleen cells. This growth inhibition in the absence of cytotoxicity, or cytostasis, is discussed in relation to the potential mechanisms of target cell damage, and in the light of recent observations (Plata, Gomard, LeClerc and Levy, 1974; Newlands and Roitt, 1975) that cytotoxicity and growth inhibition assays detect different effector cell populations in tumour-bearing animals.

Animals↗