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C Heusser

Publications and source records attributed to C Heusser.

67 records · Page 4Linked to original sources
PubMed1985

Factors influencing human IgE synthesis in vitro and in vivo.

Several pitfalls may affect studies on human IgE synthesis in vitro. In this paper, the requirement for stringent specificity of the anti-IgE antibodies used and for assessment not only of IgE detectable in culture supernatants but also as cell-associated IgE is emphasized. The use of cycloheximide-treated cultures as controls also leaves wishes open. Activated, human T cells and T cell hybridomas produce IgE-binding factors, which may be detected by a sensitive in vitro test and which may apparently also become the endeavour of synthesis by molecular biological techniques. Although the evidence available in rodents for the role of IgE-binding factors in modulating IgE synthesis has not yet been fully reproduced by us in man, the fact that classical IgE-enhancing procedures in rodents (e.g. radiotherapy, T cell suppression) also affect IgE production in man leads to believe that similar immunoregulation mechanisms apply to various mammalian species studied so far.

Antibody Formation↗
PubMed1984

Monoclonal antibodies specific for murine IgM I. Characterization of antigenic determinants on the four constant domains of the mu heavy chain.

Seventeen monoclonal rat antibodies with specificities for mouse mu heavy chain recognize seven distinguishable determinants that are located on the four constant region domains. All determinants are present on secreted, intracellular and membrane bound IgM, and all but two are expressed on isolated mu heavy chain. One antibody, specific for a site in the first constant region domain, recognizes a determinant that is present on IgM of AKR, C3H/HeJ, C57BL/6J, SJL, DBA/2, BALB/c, NZB and CBA/J mouse strains, but not on IgM of A.TH, A/J and A.CA strains of mice.

Animals↗
PubMed1984

A multirange ELISA for the measurement of plasma renin in humans and primates.

A sensitive solid phase enzyme-linked immunosorbent assay (ELISA) has been developed using two anti-human renin monoclonal antibodies, which were shown to bind both human as well as primate renin at two different epitopic sites. One monoclonal antibody (3-36-16) was used to coat each well of a 96 well microtitre plate in which renin, contained in 5 to 20 ul of plasma, was allowed to react. Plates were then incubated with the gamma globulin (gamma G) fraction of a rabbit anti-human renin serum followed by development with sheetp anti-rabbit gamma G conjugated to alkaline phosphatase. Quantification was carried out by the addition of the alkaline phosphatase substrate, p-nitrophenylphosphate, which produced a colorimetric reaction. The sensitivity of the assay is 25 pg ml-1. The method recognises both active and inactive renin from plasma, kidney, amniotic fluid and chorionic cells. Plasma renin can be measured within 6 hours when values are greater then 150 pg ml-1 or within 24 hours when plasma values are less than 150 pg ml-1. The ELISA has already been used to measure total immunoreactive renin in plasma obtained from patients with several forms of hypertension. The values ranged from 25 pg ml-1 in patients with primary aldosteronism to as large as 60 ng ml-1 in a patient with a renin-secreting tumour.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Immunoglobulin idiotopes expressed by T cells. I. Expression of distinct idiotopes detected by monoclonal antibodies on antigen-specific suppressor T cells.

The idiotopic repertoire expressed by antigen-specific suppressor T cells (Ts) generated by Streptococcus pneumoniae strain R36a (Pn) in BALB/c strain mice was investigated using a panel of five monoclonal anti-idiotopic antibodies against TEPC-15/HOPC-8 myeloma proteins. Previous studies suggested that the anti-idiotopic antibodies recognize distinct idiotopic determinants within the T15 idiotype, and that Pn-reactive B cells express all of those idiotopes as shown by a specific inhibitory effect of the anti-idiotopic antibodies on induction of anti-Pn response in vitro as well as on the mature antibody plaque-forming cells. In this study we asked the question of whether anti-idiotopic (Id) can block the inductive and/or effector phases of generation of Ts which act on the Pn-reactive B cells. The presence of anti-Id during the activation of T cells with Pn did not prevent the generation of Ts. However, suppression mediated by Ts on responder lymphocytes (cultures of spleen cells or B cels) was inhibited (reversed) by four out of five anti-Id. Some of the antibodies recognize hapten (phosphorylcholine)-inhibitable Id in the paratope of Ig whereas others are directed against nonparatopic Id. These data indicate that the antigen receptor on Ts includes VH sequences both within and without the immunoglobulin in paratope, and that the Id repertoir of Ts overlaps with that of B cells.

Animals↗
PubMed1982

Mutations affecting the structure and function of immunoglobulin M.

Using a hybridoma cell line which secretes hapten-specific immunoglobulin M (IgM), we have isolated a variety of mutants which produce abnormal immunoglobulin. Immunoglobulin was tested for the size and composition of the component heavy and light chains and for variable and constant region related functional and serological activities. Some mutants secrete IgM which seems to be defective in hapten binding; others make IgM which appears not to activate complement. Many of the mutants secrete monomeric as opposed to pentameric IgM. In some cases, the defect apparently correlates with structural alterations in the mu heavy chain: partial deletion, polypeptide addition, and abnormal glycosylation have been observed. These mutant cell lines provide a means of identifying the structural basis of IgM function and of studying the biochemistry of IgM synthesis and processing.

Animals↗
PubMedDate not supplied

Natural lymphocyte activation in postnatal development of germ-free and conventional mice.

The degree of activation of B and T cells in the developing spleen during postnatal life was studied in germ-free (GF) and specific-pathogen-free (SPF) BALB/c mice of the same breeding stock. We found that the progeny of GF mothers up to 3 weeks of age contain higher numbers of activated splenic cells than baby SPF mice, thus suggesting qualitative differences in maternally-derived antibodies. This "advantage" of GF mice is also indicated by an anticipated maturation of the splenic lymphoid compartment and is reflected in higher frequencies of B and T lymphocytes in adult life. In both kinds of mice, the frequency of activated cells is very high at birth and then declines, reaching minimal values by 4 weeks of age. Later, activated B cells increase sharply in SPF mice, suggesting polyclonal activation mediated by bacterial products. Results are discussed on the basis of the mutual influences between B and T cells in the establishment of a functional network.

Animals↗
PubMedDate not supplied

IgE synthesis.

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Animals↗
PubMedDate not supplied

Increased plasma renin during renin inhibition. Studies with a novel immunoassay.

The response of renin release to the administration of renin inhibitors cannot be studied with conventional enzymatic methods used to measure plasma renin. In the present experiments, a novel multirange enzyme-linked immunosorbent assay for human and primate renin was used to investigate the changes in plasma immunoreactive renin after renin inhibition. A potent and long-acting statine-containing renin inhibitor, CGP 29 287, was injected in conscious marmosets after mild or severe sodium depletion. In mildly sodium-depleted marmosets, CGP 29 287 (0.1 mg/kg i.v.) reduced mean arterial blood pressure and completely inhibited plasma renin activity for up to 30 minutes. This response was associated with a transient increase in plasma immunoreactive renin concentration. After a dose of 1.0 mg/kg i.v., the reduction of mean arterial pressure and the complete inhibition of plasma renin activity persisted for up to 120 minutes. These effects were accompanied by a sustained increase in plasma immunoreactive renin concentration. In severely sodium-depleted marmosets, CGP 29 287 (1.0 mg/kg i.v.) induced a marked fall in systolic blood pressure and complete inhibition of plasma renin activity within 30 minutes of injection. Plasma immunoreactive renin levels increased to 257% of pretreatment values. The converting-enzyme inhibitor enalaprilat (2 mg/kg i.v.) induced a fall in systolic blood pressure of similar magnitude, which was accompanied by an increase in plasma renin activity. Levels of plasma immunoreactive renin increased to 210% of pretreatment values. Hydralazine (0.2 mg/kg i.v.) did not increase plasma renin activity or plasma immunoreactive renin levels despite a comparable hypotensive effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Peyer's patches and mesenteric lymph nodes are the sites of first appearance of IgE bearing B lymphocytes and hapten specific IgE antibody forming cells in BPO-KLH sensitized mice.

Antigen specific IgE responses originate in gut associated lymphoid tissue (GALT) of mice sensitized with benzylpenicilloyl-keyhole limpet hemocyanin (BPO-KLH) in alum, regardless of the route (intraperitoneal [i.p.], oral [gavage], subcutaneous [s.c.], intramuscular [i.m.] or intravenous [i.v.]) used for immunization. When BALB/c mice were injected i.p. with BPO-KLH (10 micrograms) in alum, B lymphocytes bearing membrane bound IgE (sIgE+B cells) first appeared simultaneously in Peyer's patches (PP) and mesenteric lymph node (MLN) on day 8. BPO specific IgE antibody forming cells (AFC) also appeared in PP on day 8, but were not found in MLN until day 10. On day 8, no sIgE+B cells or IgE AFC were found in bone marrow (BM) or other lymphoid organs. The appearance of sIgE+B cells and IgE AFC in PP and MLN was transient; these cells were no longer detected in PP on days 14 and 24, respectively, or in MLN on days 14 and 36, respectively. sIgE+B cells and IgE AFC did not appear in spleen until day 12, where they were detected through day 70. Although sIgE+B cells were never found in BM, IgE AFC appeared in BM on day 18, where they were detected through day 70. No sIgE+B cells or IgE AFC were found in other lymph nodes (OLN) on days 0-70. Boosting did not induce the reappearance of sIgE+B cells or IgE AFC in PP, the reappearance of sIgE+B cells in MLN, the appearance of sIgE+B cells in BM, or the appearance of sIgE+B cells or IgE AFC in OLN.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗