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Biomedical subjects

B Landen

Publications and source records attributed to B Landen.

8 recordsLinked to original sources
PubMed1979

Protease activity on the surface of HSV-infected cells.

Monolayers of primary rabbit kidney cells infected with HSV type I bound lymphoblastoid (Raji) cells, to which the third component (C3) of the complement system had been attached (Raji-C3). This induction of cell contact did not occur on non-infected monolayers and was dependent on C3. The interaction could be suppressed by the presence of protease inhibitors (1 mM-TLCK or-PMSF). The results are interpreted as indicating de novo expression of protease activity on the surface of HSV-infected cells. This protease is characterized by its potential to activate C3 and its inhibition by TLCK.

Animals↗
PubMed1979

Complement receptor analogous factors in human serum: I. Isolation of a molecule inhibitory for complement dependent rosette formation, its identification as alpha 1-antitrypsin and its functional characterization.

A glycoprotein was isolated from human plasma which partially inhibited C3 carrying erythrocytes from binding to complement receptor cells (CR+C). Based on its physicochemical characteristics and its antigenicity this glycoprotein was identified as alpha 1-antitrypsin (alpha 1-AT). The activity of alpha 1-AT towards C3 and its fragments was unaffected by heating but it was destroyed by periodic acid. The isolated carbohydrate moiety of alpha 1-AT showed the same effect as the intact molecule. Using F(ab)2 of IgG-anti-alpha 1-AT could be demonstrated on Raji cells and human erythrocytes. Treatment of these CR+C with IgG-anti-alpha 1-AT resulted in a blockade of their C3 receptor activity. The results suggest, that alpha 1-AT interacts through its carbohydrate portion with C3 and its fragments and functions as a complement receptor molecule.

B-Lymphocytes↗
PubMed1979

Identity of C3- and C5-receptors on lymphoid cells.

Tannic acid-treated SRBC, incubated with increasing concentrations of C5 (Etan-C5) can be attached to C3 receptor-carrying (Raji) cells. This binding is dependent on the amount of C5 on Etan-C5 and can be inhibited by pretreatment on the Raji cells with either C5 or C3. Similar inhibition by soluble C3 and C5, respectively, is obtained for the interaction between Raji cells and Etan-C3. In addition, the immune adherence reaction between Ehum and EAC1423b could be blocked by previous treatment of Ehum with C5 or C3. These results suggest the presence of binding sites for C5 on lymphoid cells and their identity with C3 receptors.

Binding Sites↗
PubMed1978

C3-mediated cytoadherence. II. Dependence of cell attachment on similar topographic distribution of the receptors (for C3) and the ligands (C3/C3b).

Particles carrying C3 in a random distribution (Etan-C3) bound to C3 receptor (Raji+) cells independent of temperature and irrespective of whether the Raji cells were fixed with glutardialdehyde. In contrast, the reactivity of EAC43b, having grouped C3b in clusters, was dependent on temperature. The interaction with Raji cells was inhibited if the latter were treated with a fixative. The reaction of both Etan-C3 and EAC43b was a function of the concentration of C3 and C3b, respectively. The conclusion is drawn that for the interaction between C3/C3b-carrying particles and C receptor cells the receptors and the ligands have to be grouped in a similar typographic distribution, irrespective if this arrangement is provided already from the beginning or if it is obtained only by lateral movement of one or both reaction partners.

Animals↗
PubMed1977

Complement bridges between cells analysis of a possible cell-cell interaction mechanism.

Different leukocytes (Raji, Daudi, Rael lymphoid cells; human peripheral blood lymphocytes, and guinea pig granulocytes), which had been coated with C3 by incubation of 37 degrees C for 20 min in a C3 solution, were demonstrated to form rosettes with erythrocytes coated with complement components (EAC142). The percentage of rosettes was dependent of the amount of C3 present on the cells. Loading of the lymphoid cells with C3 was a time- and temperature-dependent process. C3b was unable to serve the same purposes, although C3 and C3b occupied the C3 receptors on the lymphoid cells to a comparable degree. C3 functions in a similar manner. The C42 enzyme can be replaced by trypsin, so that bridging units may consist of C3 + C42, C5 + C42 OR C3 + trypsin, and C5 + trypsin. Bridging units can be constructed also from C4 + C1. It is suggested that enzymes on one cell liberate labile binding groups of complement components on adjacent cells, thus inducing coupling of the two cells. The possibility is raised that this type of cell interlinkage may play a role in vivo, since there is accumulating evidence that complement components are expressed in the plasma membrane of different cells.

Cell Communication↗