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H Braley-Mullen

Publications and source records attributed to H Braley-Mullen.

At least 73 records · Page 4Linked to original sources
PubMed1983

Characterization of a concanavalin A-induced amplifier T cell which augments in vitro antibody responses to DNP-Ficoll.

The addition of the T-cell mitogen concanavalin A (Con A) on Day 2 of a 4-day in vitro culture of murine spleen cells with the thymus-independent (TI) antigen DNP39-Ficoll resulted in significant enhancement of the direct antitrinitrophenyl (TNP) plaque-forming cell (PFC) response. This enhancement was mediated by a nylon wool- and antiimmunoglobulin-nonadherent amplifier T cell (TA). TA activity was not eliminated by in vitro treatment of T cells with anti-Thy 1.2 and complement (C). TA activity could be eliminated by pretreatment of mice with antilymphocyte serum (ALS) in vivo, followed by in vitro treatment of T cells with anti-Thy 1.2 + C. Thus, TA appear to bear a low surface density of Thy-1 antigen. These TA were relatively resistant to ALS used alone, to cyclophosphamide, and to low dose in vitro irradiation. TA were still present in the spleen 14 weeks after adult thymectomy (ATx). They were I-J positive and apparently belonged to the Lyt 1+2- T-cell subset.

Animals↗
PubMed1983

Characterization of the murine immune response to type 6 pneumococcal polysaccharide.

The antibody response to type 6 (Danish type 6A) pneumococcal capsular polysaccharide (S6) was determined in various strains of mice. S6 elicited a very low plaque-forming cell (PFC) response in most strains of mice. BALB/c mice responded better than most other strains, and the response to S6 was further characterized in BALB/c mice. Immunization with 1 to 5 micrograms of S6 induced a plaque-forming cell response of short duration which consisted totally of immunoglobulin M-producing PFC. Athymic nude mice produced three- to fivefold more PFC in response to S6 than their euthymic littermates, suggesting that thymus-derived (T) cells negatively influence the S6 response. Regulation of the response by T cells was further suggested by the ability of antilymphocyte serum to enhance the S6 PFC response and by the suppressed response induced by priming with a low dose of S6 3 days before immunization with an optimal dose of S6 (low dose paralysis). When concanavalin A was given 2 days after immunization with S6, the response was enhanced two- to sevenfold, suggesting that the response is also positively influenced by T amplifier cells. When the avidity of the antibody produced by S6-specific PFC was measured by a plaque inhibition test, the avidity of the anti-S6 antibody was found to be very low. These results suggest that S6 is a poor immunogen because the affinity of the S6-specific antibody and B cell surface receptors is low.

Animals↗
PubMed1983

Activation of type III pneumococcal polysaccharide-specific suppressor T cells in cyclophosphamide-treated mice requirement for recognition of antigen and I-J determinants on antigen coupled to syngeneic spleen cells.

Type III pneumococcal polysaccharide (S3) coupled to spleen cells (S3-SC) is a potent tolerogen in mice. Although tolerance induced by S3-SC has been shown to be T cell dependent, T cells from tolerant mice are unable to actively suppress the antibody response to S3 when transferred to normal mice. However, when mice are given cyclophosphamide (Cy) before injection of S3-SC, suppressor T cells (Ts) are induced and can be detected by their ability to suppress the response to S3 after transfer to normal mice. The Ts induced by S3-SC in Cy-treated mice are antigen specific and can bind to and be eluted from plates coated with a soluble membrane preparation of S3-SC (S3-SCSM) prepared from mice that are syngeneic with mice in which Ts are induced. Allogeneic S3-SCSM, free S3, or S3 coupled to non-membrane carriers do not bind the Ts. Moreover, under the same conditions, detectable Ts were not induced by free S3 in either normal or Cy-treated mice. These results suggest that these Ts are activated by, and have receptors for, S3 plus a self cell membrane determinant. The self cell membrane determinant required for Ts induction is apparently I-J since Ts are induced only when the antigen-coupled spleen cells share I-J with the Cy-treated mice in which Ts are activated. The necessity to treat mice with Cy to obtain detectable Ts is presumably due to the fact that S3-SC activates a contrasuppressor T cell in normal mice which interferes with Ts function, and this cell is eliminated by Cy.

Animals↗
PubMed1982

Differential effect of activated T amplifier cells on B cells responding to thymus-independent type 1 and type 2 antigens.

Concanavalin A (Con A), antilymphocyte serum (ALS), and the allogeneic effect have all been shown to enhance antibody responses to thymus-independent (TI) antigens by a T cell-dependent mechanism. Enhancement presumably involves an effect on the responding B cells by amplifier T cells (TA) that are activated by the particular agent used, i.e., Con A, ALS, or allogeneic cells. In the present study the ability of these agents to augment antibody responses to TI-1 and TI-2 antigens was compared. It was found that antibody responses to TI-2 antigens were markedly enhanced by allogeneic cells or ALS given with antigen. Antibody responses to TI-1 antigens were in all cases unaffected. Because TI-1 and TI-2 antigens primarily stimulate separate subpopulations of B cells, these results suggest the B cell subset that responds to TI-1 antigens, i.e., Lyb-5-negative B cells, may not be responsive to signals from nonspecifically activated TA. This conclusion was further supported by experiments demonstrating that responses to TI-2 antigens could not be enhanced in mice that have only Lyb-5-negative B cells, i.e., CBA/N x BALB/c F1 males, and that responses to a T-dependent antigen (HRBC) could be augmented by the allogeneic effect in normal mice but not in mice lacking Lyb-5-positive B cells.

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PubMed1981

Adoptive transfer of experimental autoimmune thyroiditis (EAT) with in vitro activated lymph node cells from thyroglobulin-sensitized guinea pigs: characterization of the cell that transfers EAT.

Relatively low numbers of lymph node cells (LNC) from Strain 2 or Strain 13 guinea pigs sensitized with guinea pig thyroglobulin (GPTG) could transfer experimental autoimmune thyroiditis (EAT) to normal syngeneic recipients after in vitro culture with GPTG. The EAT induced in recipients of cultured LNC was similar in incidence and severity to EAT induced by active immunization with GPTG in complete Freund's adjuvant. The cells that were effective in transferring EAT were shown to be immunoglobulin-negative, nylon wool nonadherent, and Ia-negative. The effector cells were sensitive to irradiation after in vitro activation, indicating that cell proliferation in the recipient is required for development of EAT. Recipient animals often developed moderate to severe lesions of EAT yet none had detectable delayed hypersensitivity to GPTG and the majority also had no detectable anti-GPTG antibody.

Animals↗
PubMed1981

Induction of IgG memory responses with polyvinylpyrrolidone (PVP) is antigen dose dependent.

Irradiated recipients of spleen cells from mice primed with a very low dose (0.0025 microgram) of the thymus-independent (TI) antigen polyvinylpyrrolidone (PVP) produced PVP-specific IgG memory responses after secondary challenge with a T-dependent (TD) form of PVP, PVP-HRBC. The IgG memory responses induced by low doses of PVP were similar in magnitude to those induced by the TD antigen PVP-HRBC. The induction of IgG memory by the TI form of antigen was markedly dependent on the dose of PVP used to prime donor mice. Spleen cells from mice primed with an amount of PVP (0.25 microgram) that induces an optimal primary IgM response did not produce significant IgG antibody after challenge with PVP-HRBC. The inability of higher doses of PVP to induce IgG memory may be due, at least in part, to the fact that such doses of PVP were found to induce tolerance in PVP-specific B cells and could suppress the induction of memory induced by PVP-HRBC. Low doses of PVP did not interfere with the induction of memory by PVP-HRBC. Expression of IgG memory responses in recipients of PVP-HRBC or low-dose PVP-primed cells was found to be T cell dependent. Moreover, only primed T cells could reconstitute the response of recipients of primed B cells, suggesting that the ability of PVP to induce IgG memory may be related to its ability to prime T helper cells. Expression of the IgG memory response in recipient mice also required the use of a TD antigen for secondary challenge, i.e., mice challenged with PVP did not develop IgG. The inability of PVP to elicit IgG antibody was due in part to the fact that 0.25 microgram PVP was tolerogenic, i.e., it could interfere with the expression of memory in mice simultaneously challenged with both PVP and PVP-HRBC.

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PubMed1980

Direct demonstration of specific suppressor T cells in the mice tolerant to type III pneumococcal polysaccharide: two-step requirement for development of detectable suppressor cells.

Spleen cells from CAF1 mice made tolerant to type III pneumococcal polysaccharide (S3) with S3 coupled to syngeneic spleen cells (S3-SC) develop S3-specific suppressor T cells (Ts). These Ts could be demonstrated consistently only when spleen cells from tolerant mice were cultured in vitro with the specific antigen and the specific tolerogen. Spleen cells from normal mice cultured under the same conditions did not suppress the antibody response to S3. When different numbers of Ts were transferred to normal CAF1 mice, an unusual dose-effect pattern was observed. Maximal suppression of the S3 response occurred when relatively low numbers of Ts, 3 to 30 x 10(5) per recipient, were transferred, whereas larger numbers of cells, 150 x 10(5) per recipient, were not suppressive. These results indicate that a presumably T-independent antigen, S3, can activate antigen-specific Ts. These Ts exhibit unusual dose effects upon transfer and require both an in vivo induction period and in vitro activation for development of maximal activity. These latter observations suggest that S3 may activate a different population of T cells with suppressor function than do conventional T-dependent antigens. The loss of suppression observed when greater than optimal numbers of cells were transferred suggests that a second type of T cell, which has the ability to 'neutralize' the activity of S3-specific Ts, is also induced in the same spleen cell population.

Animals↗
PubMed1980

Antigen requirements for priming of IgG producing B memory cells specific for Type III pneumococcal polysaccharide.

B cells from mice primed with various amounts of the T-independent (TI) antigen Type III pneumococcal polysaccharide (S3) or with the T-dependent (TD) form of S3, i.e. S3-HRBC, were transferred to irradiated recipients with T cells from S3-HRBC primed mice. After immunization with S3-HRBC, significant S3-specific IgG memory responses were produced only by those mice which received B cells from mice primed with the TD antigen. Activation of amplifier T cells (TA) at the time of priming with S3 resulted in increased IgG production by transferred B cells although the amount of IgG produced was still substantially less than that produced by B cells from S3-HRBC primed mice. An amount of S3 (0.6 microgram) which induces optimal primary IgM responses was found to suppress the induction of B memory cells by S3-HRBC. Lower amounts of S3 were not suppressive yet they were still unable to induce IgG memory in B cells. Taken together the results suggest that the TI antigen S3 does not induce differentiation of B cells to IgG producing memory cells because S3 is unable to activate a cell type (presumably T helper cells) which is required for this inductive process to occur.

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PubMed1978

Antigen requirements for induction of B-memory cells: studies with dinitrophenyl coupled to T-dependent and T-independent carriers.

Mice were primed with dinitrophenyl (DNP) (trinitrophenyl, TNP) coupled to thymus-independent (TI) or thymus-dependent (TD) carriers. B cells from these mice were transferred to irradiated recipients with T cells from keyhole limpet hemocyanin (KLH)-primed mice. After secondary immunization with DNP-KLH a significant DNP-specific IgG memory response was produced only by mice which received B cells which had been primed with TD antigens. TI antigens were unable to induce differentiation of B-cell precursors to IgG producing memory B cells but they did not suppress the induction of B-memory cells by TD antigens. The results indicate that TI antigens fail to activate a cell type which is required for the induction of memory B cells.

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