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Biomedical subjects

R H Gisler

Publications and source records attributed to R H Gisler.

At least 37 records · Page 2Linked to original sources
PubMed1980

Characterization of accessory cells required for helper T cell induction in vitro: evidence for a phagocytic, Fc-receptor, and Ia-bearing cell type.

The nature of the accessory cell type required for the in vitro induction of antigen-specific helper T (Th) cells to soluble antigen was determined. Two different sources of adherent accessory cells were investigated: peritoneal exudate cells (PEC) and macrophages derived from bone-marrow cells (BMM phi), which were cultured for 8 days in vitro with colony-stimulating factor. PEC and BMM phi were rosetted with EA-SRBC and separated by sedimentation into Fc gamma receptor-positive and negative fractions. Only the Fc gamma receptor-positive fraction was active in Th-cell induction. By means of the fluorescence-activated-cell sorter (FACS-II), PEC or BMM phi were separated either into phagocytic and nonphagocytic, or Ia-positive and Ia-negative cell populations. Only phagocytic and Ia-positive accessory cells induced antigen specific Th cells. In conclusion, the accessory cell is adherent, phagocytic, carries Fc gamma-receptors and Ia products, and thus expresses the most important characteristics of the macrophage lineage.

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PubMed1979

Ia-bearing bone marrow-cultured macrophages induce antigen-specific helper T cells for antibody synthesis.

In bone marrow cell (BMC) cultures supplemented with colony-stimulating factor (CSF), accessory cells develop that are capable of inducing specific helper T cells. These accessory cells become effective after 4 days in culture and can be found not only in the adherent but also in the nonadherent cell population. On the other hand, very few accessory cells with helper cell-inducing capacity are obtained in BMC cultures without CSF. The active BMC-derived cell type has been shown to carry Ia surface antigen, since pretreatment with anti-Ia serum and complement abolished the capacity of these cells to function like macrophages in helper T cell induction. Moreover, the appearance of functional accessory cells in these cultures coincided with the presence of Ia-bearing cells.

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PubMed1977

Characterization of suppressive immunoglobulin-binding factor (IBF). I. Production of IBF by a theta-positive lymphoma (L-5178-Y).

L-5178-Y, a theta-positive, Fc receptor-bearing mouse thymoma cell line spontaneously releases immunoglobulin-binding factor (IBF) upon short-term incubation in vitro. IBF produced by L-5178-Y cells is identical in its biologic activity with IBF produced by Fc receptor positive alloantigen-activated T cells. It suppresses the in vitro plaque response of mouse spleen cells to sheep erythrocytes by interfering mainly with the late phase of the generation of antibody-forming cells. Therefore, L-5178-Y thymoma affords a homogeneous source of IBF in sufficient quantities for the study of its biochemical nature and the mechanism by which it interferes with cells participating in antibody synthesis.

Animals↗
PubMed1976

Reversible binding of a T cell factor on IgG-coated sepharose beads.

Supernatants of alloantigen-activated T cells contain a number of factors, including an immunoglobulin-binding factor (IBF) which inhibits complement-induced hemolysis of sheep erythrocytes coated with anti-Forssman IgG antibodies and a factor which suppresses IgM antibody synthesis in vitro. These two factors may be identical, since they are simultaneously retained on Sepharose beads to which IgG has been coupled and can be recovered by elution at pH 2.8. They do not bind to Sepharose beads to which IgM of F(ab')2 fragment of IgG has been coupled, demonstrating that they have a selective affinity for the Fc region of IgG. In addition, the fixation of IBF on the Fc portion of IgG reversibly inhibits subsequent binding of the first component of complement (C1), thus indicating that IBF does not irreversibly alter the C1 binding site(s) of IgG.

Animals↗
PubMed1976

Trypsin increases in vitro antibody synthesis and substitutes for helper T cells.

Trypsin, a neutral protease, enhanced the direct plaque response of T cell-suffiecient mouse spleen cell cultures to sheep erythrocytes (SRBC) and significantly increased the number of spontaneous PFC against SRBC in cultures without antigen. Moreover, trypsin proved to be able to substitute for T cells in nu/nu spleen cell cultures stimulated with SRBC. Its restorative capacity in this type of response was comparable to the one of lipopolysaccharide. Restoration of antibody synthesis in T cell-deprived cultures could not be explained by enzymatic alteration of SRBC. The data are discussed in terms of a possible role of hydrolytic enzymes released by accessory cells during the induction of an antibody response.

Animals↗
PubMed1975

Suppression of in vitro antibody synthesis by immunoglobulin-binding factor.

Alloantigen-activated mouse T cells secrete a factor which binds to the Fc fragment of IgG and blocks complement (C) activation by IgG (immunoglobulin-binding factor, IBF). IBF was found to suppress the direct plaque-forming cell (PFC) response of mouse spleen cell cultures to sheep erythrocytes and to dinitrophenylated aminoethyldextran (T-independent antigen). Purification of IBF by affinity chromatography on IgG-coated Sepharose columns led to an increase of the suppressive capacity with IgG, IgM, or Fab2 from IgG) the factor responsible for inhibiting the PFC response could not be dissociated from that responsible for the inhibitory activity of IBF on C-dependent hemolysis. No effect was seen when cultures were pretreated for 6 h, or when IBF was added at 72 h. These data are compatible with the view that IBF is a soluable mediator of suppressor T cells which may interfere with terminal differentiation of antibody-forming cell precursors.

Animals↗
PubMed1974

Complement-dependent B-cell activation by cobra venom factor and other mitogens?

It has been proposed that two distinct signals are required for the triggering of the precursors of antibody-forming bone marrow-derived cells (B cells): (a) the binding of antigen or of a mitogen to the corresponding receptor sites on B-cell membranes and (b) the interaction of activated C3 with the C3 receptor of B lymphocytes. There is growing evidence that B-cell mitogens and T (thymus-derived cell)-independent antigens are capable of activating the alternate pathway of the complement system (bypass). Therefore, the effect of another potent bypass inducer was investigated with regard to B-cell activation and the role of C3. Purified, pyrogen-free cobra venom factor was mitogenic for both T and B lymphocytes (cortisone-resistant mouse thymus cells and lymph node lymphocytes from congenitally athymic mice). Venom factor could substitute for T cells by restoring the potential of antibody formation to sheep red blood cells in mouse B-cell cultures supplemented with macrophages or 2-mercaptoethanol. Venom factor may be capable of conferring activated C3 to the C3 receptor of B lymphocytes: preincubation of lymphoid cells with homologous serum or plasma, 10 mM EDTA, and sepharose-coupled venom factor converted with serum to an enzyme active against C3, inhibited their capacity to subsequently form rosettes with sheep erythrocytes sensitized with amboceptor and C5-deficient mouse complement. In the absence of EDTA, preincubation of freshly prepared B-cell suspensions with C3-sufficient homologous serum also blocked their subsequent interaction with complement-sensitized erythrocytes and at the same time rendered them reactive to an otherwise T-cell-specific mitogen. Moreover, mitogen induced B-cell proliferation in lymph node (but not in spleen) cell cultures, appeared to depend on the availability of exogenous C3: zymosan-absorbed fetal bovine serum (only 8.3% site-forming units remaining) supported T-cell activation by phytohemagglutinin, concanavalin A, and venom factor, but failed to sustain B-cell stimulation by pokeweed mitogen, lipopolysaccharide, and venom factor. T-cell-dependent antibody formation in composite cultures containing T cells or T-cell-substituting B-cell mitogens, B cells, and macrophages, always required the presence of C3-sufficient serum.

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