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PubMed1978

Role of membrane receptors in the induction of an in vitro secondary anti-hapten response. II. Antigen-immunoglobulin receptor interaction is not required for B memory cell proliferation.

In this study it has been investigated whether the interaction of antigen and B cell surface immunoglobulin (sIg) is required for full clonal expansion of memory B cells specific for the hapten, p-azophenyl-lactoside (lac). Cultures of lac-primed B cells and keyhole limpet hemocyanin (KLH)-specific T cells were activated in three ways: (a) by the antigen lac-KLH, (b) in the absence of lac epitopes by attaching KLH to the H-2 antigens of the B cells, and (c) in similar conditions where lac epitopes were supplied on carriers unrecognized by helper T cells. Dilution analyses showed that the yield of IgG anti-lac plaques per activated precursor was identical in all situations, and that the increased responses observed in the presence of lac epitopes were due to an increase in the frequency of activated precursors. Our results thus indicate that specific interacting T cells convey both the differentiative and proliferative signals to B memory cells, and are at variance with proposals advocating that an antigen-induced proliferative phase is succeeded by a T-cell-dependent differentiative event. We suggest that the effect of sIg-antigen interaction may be to cycle some precursors into a more easily activated state.

Animals↗
PubMed1992

T cell memory: a role for MHC class II molecules on T cells?

A proportion of human T cells express MHC class II molecules. In this paper, the hypothesis is advanced that these MHC class II molecules present antigenic peptides acquired from interaction with other antigen-presenting cells (e.g. during the primary response) and can therefore interact in a cognitive manner with T cells with the same specificity. Memory is maintained in the physical form as clusters of T cells expressing T cell receptors and the cognate peptide-MHC class II complex; by virtue of their cognate interaction with each other these cells turn over gradually and return to the cluster when they recirculate. When fresh antigen is introduced, it is presented to some of these T cells by non-T antigen-presenting cells that provide a second signal leading to vigorous activation of the T cell. The proximity and cognate interaction of other T cells of the same specificity allows a chain reaction to occur, leading to rapid development of the secondary response. The hypothesis, which is testable, is proposed because of doubts concerning the current concept of memory as applied to T cells, and a need to understand the consequences of the expression of MHC class II molecules by a subset of T cells.

Animals↗
PubMed1976

Generation of T memory cells in one-way mixed lymphocyte culture. IV. Primary and secondary responses to soluble and insoluble membrane preparations and to ultraviolet-light-inactivated stimulator cells.

Neither normal CBA (H-2k) nor purified spleen T cells respond in vitro to soluble or insoluble membrane preparations or to ultraviolet-light-inactivated stimulator cells of the allogeneic DBA/2 (H-2d) strain. However, CBA spleen cells deprived of phagocytic cells show a slight proliferative response under these conditions. After being primed against mitomycin-blocked DBA/2 cells in one-way mixed lymphocyte culture, the secondary blast-derived T 'memory' cells display a good secondary blast (proliferative) response to both membrane antigens and to ultraviolet-light-inactivated stimulator cells. In addition to this, the secondary T lymphocytes--in contrast to nonprimed T cells--respond by cytotoxicity when ultraviolet-light-inactivated cells are used as the second stimulant.

Animals↗
PubMed1978

Differential sensitivity of memory cell subpopulations to anti-immunoglobulin and complement.

Evidence is presented for the unique sensitivity of memory cells bearing surface immunoglobulin G1 (IgG1) to functional elimination with anti-immunoglobulin (anti-Ig) sera and complement (C). Treatment of cells for adoptive transfer with C and anti-gamma1, anti-kappa, or anti-Ig significantly reduces the number of plaque-forming cells (PFC) of only the IgG1 isotype found in adoptive recipients. An increase in PFC of other isotypes accompanies the decrease in IgG1 PFC; there is no net change in the total PFC response. The depletion of IgG1 PFC requires treatment of transferred cells with both specific antisera and C; antisera directed against other isotypes show no significant effects. The maintenance of the magnitude of PFC response, compensation, is discussed.

Animals↗
PubMed1976

Mechanisms by which hapten conjugates of pneumococcal polysaccharide interfere with the challenge of anti-hapten memory cells.

Incubation of trinitrophenylated hemocyanin (TNP-KLH)-primed spleen cells with microgram amounts of 2,4-dinitrophenyl (DNP) or 2,4,6-trinitrophenyl (TNP) conjugates of pneumococcal polysaccharide type 3 (SIII) for as little as 5 min at 4 degrees C results in a specific "block" of the 19 S and 7 S adoptive memory response to TNP-KLH. This hapten-SIII-induced block of anti-hapten memory B cell responsiveness seems to be an example of specific receptor blockade. The block is specific and can be prevented by simultaneous incubation of the primed cells with hapten-protein conjugates which presumably compete with the hapten-polysaccharide for attachment to the B cell surface via anti-hapten Ig receptors. Removal via capping of these Ig receptors by exposure of TNP-KLH-primed memory cells to rabbit anti-mouse Fab serum for 45 min at 37 degrees C renders these cells refractory to the blocking effect of hapten-SIII. Once the hapten-SIII has attached to the memory cells, these blocked cells can be "rescued" (i.e. returned to a state of responsiveness) by incubating these cells with either mouse anti-SIII at 37 degrees C or rabbit anti-DNP serum at 4 degrees C. Since a papain digest of the IgG fraction of rabbit anti-DNP did not rescue the cells while the intact IgG did, a capping off of the TNP-SIII was proposed as the mechanims for this return to responsiveness of the hitherto blocked cells. A rescue was not seen by treatment of recipient mice with such B cell mitogens as dextran sulfate, endotoxin or purified protein derivative of tuberculin.

Animals↗
PubMed1978

Specific inhibition of cytotoxic memory cells produced against UV-induced tumors in UV-irradiated mice.

Cytotoxic responses of UV-irradiated mice against syngeneic UV-induced tumors were measured by using a 51Cr-release assay to determine if UV treatment induced a specific reduction of cytotoxic activity. The in vivo and in vitro primary responses against syngeneic tumors and allogeneic cells were unaffected, as was the "memory" response (in vivo stimulation, in vitro restimulation) against alloantigens. In contrast, the memory response of UV-treated mice against syngeneic, UV-induced tumors was consistently and significantly depressed. The cytotoxicity generated by tumor cell stimulation in vivo or in vitro was tumor-specific and T cell-dependent. Since the primary response against syngeneic UV-induced tumors produces apparently normal amounts of tumor-specific cytotoxic activity, UV-treated mice may not reject transplanted syngeneic tumors because of too few T effector memory cells. These results imply that, at least in this system, tumor rejection depends mostly on the secondary responses against tumor antigens and that at least one carcinogen can, indirectly, specifically regulate immune responses.

Animals↗
PubMed1975

Enrichment of memory cells carrying receptors for a protein antigen (HSA). II. Improved enrichment technique, using BSA density gradient separation.

Mice primed to human serum albumin (HSA) by means of an HSA--sheep red cell conjugate, developed a high level of memory to HSA, with little concomitant antibody production ('pure priming'). The proportion of HSA-specific antigen-binding cells was determined in the spleens of the primed mice by means of a rosette technique, using an HSA-donkey red cell conjugate. The specificity of the rosette-forming cells (RFC) was confirmed by the ability of soluble HSA to inhibit rosette formation. Highly enriched rosette suspensions (up to 40-fold enrichment) were prepared by bovine serum albumin density gradient centrifugation. The enriched suspensions could transfer adoptively memory to HSA, whereas the rosette-depleted fractions were totally inactive. It was thus confirmed that memory cells are included in the antigen-binding cells. A detectable level of memory could be transferred with 3000 rosettes. RFC similarly isolated from spleens of non-primed mice could also transfer a low level of responsiveness to HSA, but only when large numbers (70,000) were injected, together with primed, RFC-depleted spleen cells.

Animals↗
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.

Animals↗
PubMed1992

Cell subsets responding to purified hepatocytes and evidence of indirect recognition of hepatocyte major histocompatibility complex class I antigen. II. In vitro-generated "memory" cells to class I+ class II- hepatocytes.

Purified hepatocytes stimulate the development of L3T4-, Ly2+ allospecific cytolytic T cells from naive splenocytes after 5 days in primary mixed lymphocyte-hepatocyte culture (MLHC). Previous studies indicate that the immunogenicity of purified hepatocytes relates to the expression of MHC class I antigen. The purpose of the following experiments was to identify the cell subsets that specifically recognize hepatocyte MHC class I antigen. We employed primed lymphocyte testing (PLT) in order to test for a "second set" response. Cells from primary MLHC reverted to a functionally quiescent state when they were grown in culture for an additional 7-9 days. The cells were then tested for cytotoxicity or rechallenged with allogeneic, syngeneic, or "third party" hepatocytes and tested for proliferation. Allocytotoxicity was low on day 12 in MLHC, but the sensitized cell population demonstrated peak proliferation in response to allogeneic hepatocytes 48 hr after restimulation. When bulk PLT cells were immunodepleted, both L3T4+, Ly2- and L3T4-, Ly2+ T cell subsets demonstrated a "second set" response to allogeneic hepatocytes consistent with specific recognition of and retention of "memory" for hepatocyte MHC class I alloantigen.

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