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A Pierres

Publications and source records attributed to A Pierres.

43 records · Page 3Linked to original sources
PubMed1982

Characterization of an Lyt-1+ cytolytic T-cell clone specific for a polymorphic domain of the I-Ak molecule.

We have characterized a cytolytic T-cell clone, isolated from a A.TH anti-A.TL mixed lymphocyte culture, which recognized a private determinant of the I-Ak molecule. This specificity has been confirmed by inhibition of effector-target cell interaction by anti-I-Ak monoclonal antibody (mAb). Comparison of the inhibitory capacity of various mAb and the spatial arrangement of their epitopes (defined in previous studies by antibody-binding competition) indicated that the antigenic site recognized by this cytolytic T-cell clone was topologically related to one of the major polymorphic domains of the Ak molecule. This clone expressed the Thy-1.2+, Lyt-1.+, Lyt-1.2+low and I-As- cell surface phenotype. Testing of several rat mAb, screened for their ability to inhibit H-2K/D-specific cytolysis at the level of the effector cells, revealed that two anti-p94, 180 mAb but not various anti-Lyt-2 mAb inhibited the lytic function of this anti-I-Ak T-cell clone.

Animals↗
PubMed1982

Lymphoid cell surface interaction structures detected using cytolysis-inhibiting monoclonal antibodies.

We screened monoclonal antibodies obtained by xenogeneic immunization for their capacity to inhibit T cell-mediated cytolysis. These antibodies fell into two classes according to the cell structures they recognized, of 30-35 K and 94-180 K apparent molecular weight, respectively. The main features of these structures and of their interaction with the corresponding antibodies were reviewed. The inhibition of cytolysis by these antibodies was shown to occur mainly at the effector cell level, at the recognition stage of cytolysis, and to depend on the nature of target cells, effector cells, and link between these cells. T cell functions other than cytolysis were also inhibited by some of these antibodies. We considered various possible mechanisms to account for the inhibition of cytolysis by these mAb. We favor an hypothesis based on inhibition by these mAb of lymphoid cell surface interaction structures. This hypothesis was discussed within the general framework of cell interaction structures in immunological and non-immunological experimental systems.

Animals↗
PubMed1980

Mechanisms of regulation of cell-mediated immunity. VI. Antigen density dependence of the induction of genetically restricted suppressor cells.

We have investigated the relationship of antigen density on cell surfaces to the induction of genetically restricted suppressor T cells (Ts). It was found that Ts able to suppress the development of hapten-specific contact sensitivity were induced by the i.v. inoculation of trinitrobenzene sulfonate (TNBS) hapten-coupled cells. The Ts induced by this technique were found to be gentically unrestricted in terms of generation or expression when 10 mM TNBS were used to prepare the hapten-coupled cells. Transferable suppression could be obtained by 10 mM coupled allogeneic cells or, alternatively, TNP-coupled Ia- syngeneic erythrocytes or even H-2-negative syngeneic tumor cells. However, 1 mM TNBS-derivatized hapten-coupled cells induced Ts that were able to suppress only recipients syngeneic with the tolerogen. The significance of these findings to our understanding of the induction and expression of Ts and the triggering signals that are necessary for their activation are discussed.

Animals↗
PubMed1978

The specific suppression of contact sensitivity.

The ability of 2,4,6 trinitrobenzenesulfonic acid (TNBS)-induced regulatory cells to modulate the generation of contact sensitivity (CS) to picryl chloride has been studied. We have confirmed that such suppressor cells can modulate CS and have extended these observations to demonstrate that suppressor factors, liberated by suppressor cells in supernatants, can limit the generation of CS. We have also confirmed that hapten-coupled membrane products can induce tolerance to PCl. The investigation of the properties of the suppressor factors has revealed that they are hapten-specific and bear H2 coded specificities.

Animals↗
PubMed1977

The I-J subregion codes for determinats on suppressor factor(s) which limit the contact sensitivity response to picryl chloride.

The cell-mediated immune reactivity (CMI) of mice to contact chemicals such as picryl chloride (PCI) is influenced by thymus-derived suppressor T lymphocytes (1,2). The development of these suppressor T lymphocytes is stimulated by the intravenous administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS). Zembala and Asherson have further demonstrated that a specific suppressor factor(s) can be detected in the supernates of cultured suppressor T cells. This factor suppresses the transfer of contact sensitivity (CS) to PCl (1,2). In experiments reported elsewhere (3), we have shown that the PCl suppressor supernates of Zembala and Asherson can also suppress the development of contact sensitivity to PCl. The immunochemical analysis of suppressor factor (SF) operative in the CS response to PCl has revealed many similar properties (3) to other suppressive moieties functioning to limit the plaque-forming cell (PFC) response to dinitrophenylated-keyhole limpet hemocyanin (DNP-KLH) as well as the strict antigen specificity of each respective suppressive factor, suggested that there might be a common origin of these substances. Indeed, in each case these respective factors were found to bear determinants controlled by the H-2 gene complex (4,5). Recently, in selected systems, the I-J subregion has been found to code for the Ia determinants present on suppressor cells (6) and suppressor factors (4,5). In accord with these findings, we report that antigen-specific SF which limit the CS response to PCl bear I-J determinants, implying that analogous suppressive regulatory mechanisms in CMI as well as antibody responses may be determined by genes of one subregion of the H-2 complex.

Animals↗
PubMedDate not supplied

Influence of surface charges on cell adhesion: difference between static and dynamic conditions.

We tested the hypothesis that nonspecific repulsion, as a result of electrostatic forces and (or) steric stabilization effects, impaired adhesion more efficiently under dynamic than under static conditions. Cells from the human monocytic line THP1 were plated on a glass surface. Spherical particles bearing monoclonal antibodies specific for antigens expressed by THP1 cells (CD11b, CD18, CD35, CD64) were then added and adhesion was quantified. The effect of neuraminidase treatment of THP1 cells was also studied. Adhesion was then measured in a flow chamber under low shear flow (wall shear rate was 11 or 22 s-1), allowing a quantitative determination of cell adhesion frequency. The following conclusions were obtained: (i) under static conditions, neuraminidase treatment had little effect on adhesion (only CD18-mediated interaction was significantly increased at 4 degrees C after enzyme treatment); (ii) under dynamic conditions, neuraminidase treatment significantly increased binding; (iii) surprisingly, there was no clear relationship between the length of adhesion molecules involved in the interaction and binding efficiency; and (iv) such parameters as cell shape and topographical distribution of adhesion molecules may strongly influence adhesion under flow. It is concluded that a dynamic reorganization of the pericellular matrix following intercellular contact may play an important role in regulating adhesion.

Cell Adhesion↗