bluuebunny/crossref_metadata_2025_split huggingface dataset:
Restoration of in vitro immune responses of spleen cells from mice infected with Trypanosoma cruzi by supernatants containing interleukin 2.
Authors: Tarleton R L , Kuhn R E 
Published: December 2022

Abstract
During the course of Trypanosoma cruzi infection, mice become suppressed in the ability to produce IL 2. Addition of supernatants from concanavalin A-stimulated normal spleen cells or supernatants from EL 4 cells enhanced the suppressed in vitro response of infected spleen cells to sheep erythrocytes. This enhancement was demonstrable at various times after infection and was shown not to be the result of Con A stimulation alone. Spleen cells from infected mice respond to IL 2-rich supernatants in Mishell-Dutton cultures in a dose-dependent fashion. Absorption of IL 2 activity from EL-4 supernatants by CTLL-2 cells results in a decrease in the enhancing effect of the supernatants on the in vitro antibody responses of infected spleen cells. Also, the reversal of suppression occurs only if IL 2-rich supernatants are added within 24 hr of the initiation of cultures. These results indicate that defective IL 2 production may play a role in the inability of mice infected with T. cruzi to respond appropriately to neoantigens.
Intracellular processing of membrane and secreted immunoglobulin delta-chains.
Authors: Argon Y , Milstein C 
Published: December 2022

Abstract
Membrane-bound and secreted immunoglobulin delta-chains are synthesized by the mouse hybridoma B1-8 delta.1 as two primary translation products (45,000 and 42,000, respectively) and are converted into three N-glycosylated forms. In addition to N-glycosylation, another modification, reflected in a size increase of 2000 to 3000, occurs within 8 min of synthesis and may be O-glycosylation. After these initial modifications, the N-linked carbohydrates of all three forms are partially trimmed, apparently in the endoplasmic reticulum. The secreted delta-chains acquire galactose and sialic acids less than 10 min before they are secreted. Monensin and CCCP, which are potent inhibitors of IgD secretion, inhibit the terminal glycosylation but not the other modifications of delta-chains. CCCP blocks the intracellular transport of IgD at an earlier stage of trimming than monensin. Within 10 min of the removal of CCCP, some of the accumulated IgD is terminally glycosylated and secreted. Membrane IgD is processed similarly to secreted IgD up to the stage blocked by CCCP. These observations suggest that final trimming and terminal glycosylation of IgD occurs in the Golgi complex, and that the other modifications occur in pre-Golgi compartments, where secreted IgD spends most of its transit time. We suggest that the rate-limiting step in the intracellular transport of both types of IgD is the passage from the ER to the Golgi complex.
Functional activity in vivo of effector T cell populations. II. Anti-tumor activity exhibited by syngeneic anti-MoMULV-specific cytolytic T cell clones.
Authors: Engers H D , Lahaye T , Sorenson G D , Glasebrook A L , Horvath C , Brunner K T 
Published: December 2022

Abstract
The functional activity in vivo of murine tumor-specific cytolytic T lymphocyte populations and clones was studied. Tumor cell destruction induced after the i.v. injection of cytolytic effector cells was quantitated by monitoring the elimination of 131IUdR-labeled tumor cells in the peritoneal cavity by using whole-body counting techniques. Mixed leukocyte-tumor cell cultures were established by using spleen cells from C57BL/6 regressor mice that had rejected an intramuscular tumor induced by the injection of MSV-MoMuLV virus. This effector cell population was observed to eliminate syngeneic MoMuLV-induced tumor cells in a dose-dependent manner. Treatment of the effector cell population with monoclonal anti-Lyt-2 antibodies plus complement totally abrogated their ability to induce tumor cell destruction in the peritoneal cavity. MSV-MoMuLV-specific Lyt-2+ cytolytic T cell clones derived by micro-manipulation of T lymphocyte-tumor cell conjugates were also tested for functional activity in vivo. Several clones induced a rapid, specific elimination of 131I-labeled MBL-2 tumor cells from the peritoneal cavity after i.v. injection, whereas others were inactive. Both active and inactive clones were highly cytolytic and secreted MAF/IFN-gamma lymphokines. In contrast to previous results obtained in a tumor allograft model, the MSV-MoMuLV-specific cytolytic T cell clones that were active in vivo did not proliferate in vitro in response to stimulation with irradiated tumor cells plus filler spleen cells in the absence of an added source of interleukin 2.
The role of tumor-specific Lyt-1+2- T cells in eradicating tumor cells in vivo. I. Lyt-1+2- T cells do not necessarily require recruitment of host's cytotoxic T cell precursors for implementation of in vivo immunity.
Authors: Fujiwara H , Fukuzawa M , Yoshioka T , Nakajima H , Hamaoka T 
Published: December 2022

Abstract
The present study determines the Ly phenotype of T cells mediating tumor cell rejection in vivo and investigates some of cellular mechanisms involved in the in vivo protective immunity. C3H/HeN mice were immunized to syngeneic X5563 plasmacytoma by intradermal (i.d.) inoculation of viable X5563 tumor cells, followed by the surgical resection of the tumor. Spleen cells from these immune mice were fractionated by treatment with anti-Lyt antibodies plus complement, and each Lyt subpopulation was tested for the reconstituting potential of in vivo protective immunity in syngeneic T cell-depleted mice (B cell mice). When C3H/HeN B cell mice were adoptively transferred with Lyt-1-2+ T cells from the above tumor-immunized mice, these B cell mice exhibited an appreciable cytotoxic T lymphocyte (CTL) response to the X5563 tumor, whereas they failed to resist the i.d. challenge of X5563 tumor cells. In contrast, the adoptive transfer of Lyt-1+2- anti-X5563 immune T cells into B cell mice produced complete protection against the subsequent tumor cell challenge. Although no CTL or antibody response against X5563 tumors was detected in the above tumor-resistant B cell mice, these mice were able to retain Lyt-1+2- T cell-mediated delayed-type hypersensitivity (DTH) responses to the X5563 tumor. These results indicate that Lyt-1+2- T cells depleted of the Lyt-2+ T cell subpopulation containing CTL or CTL precursors are effective in in vivo protective immunity, and that these Lyt-1+2- T cells implement their in vivo anti-tumor activity without inducing CTL or antibody responses. The mechanism(s) by which Lyt-1+2- T cells function in vivo for the implementation of tumor-specific immunity is discussed in the context of DTH responses to the tumor-associated antigens and its related Lyt-1+2- T cell-mediated lymphokine production.
1,25-Dihydroxyvitamin D3 inhibits antigen-induced T cell activation.
Authors: Bhalla A K , Amento E P , Serog B , Glimcher L H 
Published: December 2022

Abstract
The proliferative response of murine spleen and thymus cells to antigen but not to lectin was inhibited by the active metabolite of vitamin D3, 1,25-(OH)2D3. To directly examine the effect of 1,25-(OH)2D3 on T cell activation in the absence of other complicating interactions, we utilized a panel of cloned Ia-restricted T cell hybridomas that secrete IL 2 on activation by cloned Ia-bearing stimulator cells (TA3) or when stimulated by mitogen. Physiologic concentrations of 1,25-(OH)2D3 (0.01 to 0.1 nm) inhibited the antigen-induced secretion of IL 2 by several of these T cell hybridomas. This inhibition was dependent on the concentration of the free hormone and could be overcome by increasing the number of Ia-bearing stimulator cells used. Pretreatment of the T hybridoma but not the TA3 stimulator cell with 1,25-(OH)2D3 resulted in inhibition of activation. These results are consistent with the finding that specific 1,25-(OH)2D3 receptors are present on the T cell hybridomas but are lacking in TA3 cells. 1,25-(OH)2D3 failed, however, to inhibit the activation of the T cell hybridomas by lectin or by an anti-Thy-1 antibody. These findings suggest that 1,25-(OH)2D3 may be interfering with early events of antigen-induced T cell activation, perhaps by hindering T cell recognition of the relevant antigen on stimulator cell surfaces. This system should prove useful in studying the molecular mechanisms by which 1,25-(OH)2D3 acts to inhibit T cell activation and subsequent IL 2 production.
Phorbol esters inhibit the functional activation of cytotoxic precursors in mixed lymphocyte cultures.
Authors: Masucci M G , Torsteinsdottir S , Pear W , Carstensen A , Klein E 
Published: December 2022

Abstract
We have investigated the effect of phorbol esters on T cell activation and generation of suppressor and cytotoxic activity in mixed lymphocyte cultures (MLC). The presence of 30 nM P(Bu)2 during the sensitization phase inhibited the generation of allospecific cytotoxicity and also decreased the killing potential against NK-sensitive targets. The inhibition was not mediated by direct blocking of the lytic capacity nor by suppression of clonal expansion of cytotoxic cells through modulation of lymphokine production. The presence of P(Bu)2 enhanced cell proliferation, but inhibited the functional activation of lymphocytes and consequent generation of Dr antigen-positive T cells. Because the presence of the compound did not affect the MLC-induced generation of suppressor activity, it is likely that P(Bu)2 selectively blocks the maturation of cytotoxic precursors. Surface-marker analysis with OKT monoclonal antibodies revealed that the effects on lymphocyte activation were associated with a decrease in OKT3 and OKT4 reactivity and an increase in the percentage of OKT8-positive cells. The decrease in OKT4 reactivity was not due to selective loss of this lymphocyte subpopulation, because P(Bu)2 was equally mitogenic for the purified OKT4- and OKT8-positive subsets. The results suggest that the effect of P(Bu)2 on cell differentiation and its ability to modulate the expression of functional markers in lymphocyte subsets may interfere with T-T cell cooperation that controls the functional maturation of cytotoxic precursors.
Lymphocyte activation antigens. I. A monoclonal antibody, anti-Act I, defines a new late lymphocyte activation antigen.
Authors: Lazarovits A I , Moscicki R A , Kurnick J T , Camerini D , Bhan A K , Baird L G , Erikson M , Colvin R B 
Published: December 2022

Abstract
Lymphocyte activation entails a sequence of events identified by analyzing the time course of expression of various distinctive cell surface molecules on lymphocytes that appear early (before initiation of DNA synthesis), parallel with DNA synthesis and cellular proliferation, or late (after peak proliferation). In this study we present identification of a novel late lymphocyte activation antigen, Act I, utilizing a murine monoclonal antibody. Anti-Act I was identified in a fusion of NS1 with BALB/c spleen cells immunized with a human tetanus toxoid-reactive T lymphoblast line. Flow cytometry analysis shows that Act I antigen is present in markedly greater amounts on activated T and B lymphocytes than on resting, small peripheral blood lymphocytes. Act I expression by these lymphocytes is promoted by PHA, tetanus toxoid, or alloantigens and lags behind maximal thymidine incorporation by 1 to 2 days. Thymocytes can be triggered to express Act I antigen during maturation induced by PHA/T cell growth factor stimulation. In vitro, anti-Act I does not affect antigen- or lectin-stimulated T cell proliferation, T cell-mediated lymphocytotoxicity, or T cell growth factor-induced proliferation of T lymphoblasts. By immunoperoxidase analysis, Act I antigen is restricted to lymphoid tissue, staining many lymphocytes in the paracortex, germinal centers, and mantle zones of lymph nodes, tonsil, and spleen. By immunoprecipitation, the Act I antigen is a single band of 63,000 m.w. on reduced or nonreduced SDS gels. The distribution, size, time course, and functional correlates indicate that Act I is different from other known T cell activation markers detected with anti-Tac, OKT9, B3/25, OKT10, 4F2, CBL1, and anti-Ia-like antibodies. Although the function of Act I is still undetermined, it may serve as a useful marker of a late stage of activation in vitro and in vivo.
Human tonsil B lymphocyte function. II. Pokeweed mitogen-induced plasma cell differentiation of B cell subpopulations expressing multiple heavy chain isotypes on their surface.
Authors: Mudde G C , Verberne C J , de Gast G C 
Published: December 2022

Abstract
Human tonsil non-T cells were successfully separated into surface IgM+G-ve (sIgM+G-), sIgM+G+, sIgM-G-, and sIgM-G+ B cell fractions. The two-step separation technique used did not affect the pokeweed mitogen- (PWM) induced plasma cell differentiation of the B cells. The highest percentages of plasma cells after PWM stimulation were found in the sIgM- fractions, and the lowest percentage was in the sIgM+G- fraction (20.8 +/- 2.3%), the latter predominantly cytoplasmic mu-chain-positive (c mu +) (84.1 +/- 3.5%) plasma cells. In this fraction, almost no c gamma + plasma cells were found. The sIgM+G+ produced c mu + (47.5 +/- 7.5%), c gamma + (35.7 +/- 5.8%), and c alpha + (16.8 +/- 4.0%) plasma cells. All three isotypes were found on the surface of the B cells in this fraction before PWM stimulation. The sIgM-G- fraction contained about 10% plasma cells before stimulation, which were predominantly c gamma +. After PWM stimulation, primarily c alpha + (64.2 +/- 4.3%) plasma cells were found. The sIgM-G+ fraction produced both c gamma + (75.0 +/- 2.3%) and c alpha + (24.1 +/- 2.5) plasma cells. A mu to gamma class switch did not occur in vitro in the sIgM+G- fraction on PWM stimulation, and the sIgM+G+ fraction did not complete in vitro the mu to gamma switch it had started in vivo.
Biologic properties of interleukin 3. II. Serologic comparison of 20-alpha-SDH-inducing activity, colony-stimulating activity, and WEHI-3 growth factor activity by using an antiserum against IL 3.
Authors: Bowlin T L , Scott A N , Ihle J N 
Published: December 2022

Abstract
An antiserum was prepared against IL 3 and was characterized. Purified Ig from the serum precipitated iodinated IL 3. By using conditioned media from 35S-labeled WEHI-3 cells, a 28,000 dalton protein and a 14/16,000 dalton doublet were specifically immune-precipitated, indicating that the immune Ig reacted with a limited number of WEHI-3-derived proteins. The immune Ig comparably inhibited the ability of purified IL 3 to induce the expression of 20-alpha-SDH, to induce proliferation of the FDC-P1 factor-dependent cell line, or to induce colony formation by bone marrow cells in soft agar. These results support the concept that IL 3 mediates these diverse biologic activities. By using conditioned media from WEHI-3 cells or from an MLR, the immune Ig completely inhibited induction of 20-alpha-SDH or proliferation of FDC-P1 cells, demonstrating that all of the activity is associated with a factor serologically identical to IL 3 purified from WEHI-3-conditioned media. In contrast, the immune Ig did not inhibit bone marrow colony formation by partially purified CSF-2, demonstrating that serologically as well as biochemically, CSF-2 is distinguishable from IL 3. Similarly, the immune Ig did not inhibit IL 2-induced proliferation of a cloned cytotoxic T cell line.
Difference in requirement of macrophage products for concanavalin A-induced production of eosinophil chemotactic factor and macrophage chemotactic factor from guinea pig lymphocytes in vitro.
Authors: Hirashima M , Tashiro K , Sakata K , Yoshimura T , Hayashi H 
Published: December 2022

Abstract
Differences between the conditions for an eosinophil chemotactic factor (ECF) and macrophage chemotactic factor (MCF) production by lymphoid cells of mesenteric lymph nodes and spleen were studied in guinea pigs. If lymphoid cells were washed less than 4 hr after concanavalin A (Con A) stimulation and were cultured for an additional 24 hr, they failed to produce ECF, whereas Con A stimulation for 1 hr before washing was sufficient to stimulate them to produce MCF. Subsequently, it was shown that heat-labile soluble factors (termed ECF-PF) with potentiating activity for ECF production are produced from macrophages by 5 micrograms/ml Con A activation. When ECF-PF were added to the cell culture with 5 micrograms/ml Con A, the lymphoid cells could produce ECF even when they were washed 2 hr after Con A stimulation and were cultured for an additional 24 hr, suggesting that ECF-PF plays a critical role in the early stage of ECF production. The lymphoid cells were also able to produce ECF even when they were cultured with ECF-PF and a suboptimal dose of Con A (1 microgram/ml) for ECF production. Protein synthesis seemed to be essential for ECF-PF production. The ECF-PF activity was associated with two separated molecular fractions with m.w. of about 50,000 to 70,000 and of 10,000 to 20,000. It is thus suggested that ECF is produced from T cells by Con A stimulation under conditions which differ, at least, from those for MCF in the requirement of ECF-PF.
Reconstitution of an inactive antigen-specific T cell suppressor factor by incubation of the factor with prostaglandins.
Authors: Kato K , Askenase P W 
Published: December 2022

Abstract
Experiments were performed to test the hypothesis that prostaglandins are crucial to the ability of an antigen-specific T cell suppressor factor to deliver a suppressive signal. In the system employed, T suppressor cells release an antigen-specific factor (TsF) that suppresses the ability of effector cells to transfer contact sensitivity (CS) skin swelling responsiveness to adoptive recipients. Culture of TsF-producing cells in the presence of indomethacin caused production of an inactive TsF that could be reconstituted by incubation of this inactive factor with low concentrations of certain prostaglandins such as PGE2 or PGE1. Subsequently, nearly all the prostaglandins were removed by dialysis, and the reconstituted TsF then acted as an antigen-specific suppressor of CS effector cells. Neither the inactive factor nor prostaglandins were suppressive alone. Furthermore, the prostaglandins are crucial to the constitution of TNBSA-F, the non-antigen-binding subunit of the TsF that probably delivers the ultimate suppressive signal. These results provide a new type of antigen-specific role for prostaglandins in immunoregulation and indicate that simple, local, hormonal molecules in physiologic concentrations can have a crucial and long-lasting role in constituting the suppressive activity of antigen-specific regulatory macromolecules released by suppressor T cells.
Antigen recognition by H-2-restricted T cells. II. A tryptic ovalbumin peptide that substitutes for processed antigen.
Authors: Shimonkevitz R , Colon S , Kappler J W , Marrack P , Grey H M 
Published: December 2022

Abstract
A 17-amino acid tryptic peptide of chicken ovalbumin, designated P323-339, that substituted for processed antigen when presented by glutaraldehyde prefixed accessory cells to specific I-restricted T hybridomas was characterized. The peptide antigen could not be demonstrated to have any specific or stable interactions with accessory cell Ia antigens by either direct binding or functional assays for inhibition of specific T cell activation. In addition, the T cell receptor for I-restricted antigen had no affinity for free antigen alone. A rabbit antibody specific for the antigenic peptide inhibited presentation when introduced before but not after binding of the peptide to accessory cells. These results extend our earlier finding that accessory cell-mediated processing of chicken ovalbumin can be completely explained by the fragmentation of the native molecule into smaller m.w. peptides, and suggests that if an antigen/Ia complex is important in T cell activation, it forms significantly only in the presence of the T cell receptor for I-restricted antigen.
Idiotypic analysis of a monoclonal anti-Sm antibody. II. Strain distribution of a common idiotypic determinant and its relationship to anti-Sm expression.
Authors: Pisetsky D S , Semper K F , Eisenberg R A 
Published: December 2022

Abstract
The idiotypes borne by Y2, a monoclonal anti-Sm antibody of MRL-lpr/lpr mouse strain origin, were investigated to elucidate genetic mechanisms in this autoantibody response. An anti-Y2 anti-idiotypic antiserum was raised in a rabbit and was rendered specific for idiotype by extensive absorption with globulins of the B6 and BALB/c strains as well as the BALB/c myeloma UPC 10. By using a sensitive assay for idiotype by inhibition ELISA, the Y2 determinant was found to be commonly expressed in sera of MRL-lpr/lpr and MRL-+/+ mice. Moreover, sera of several normal strain mice also bore the idiotype and, in mice bearing the lpr gene, idiotype levels were increased 1.5 to fivefold, even in the absence of a serum anti-Sm response. The relationship of this idiotype to anti-Sm expression was further assessed by determining the idiotype content of affinity-purified anti-Sm antibodies from MRL-lpr/lpr mice. Anti-Sm from serum pools or individual animals showed no significant enrichment of the Y2 idiotype in comparison to unselected MRL-lpr/lpr IgG. These results suggest that the Y2 idiotype defines only a minor component of the anti-Sm autoantibody response, and that most antibodies with this determinant express other antigenic specificities.
The role of I-A/E molecules in B lymphocyte activation. I. Inhibition of lipopolysaccharide-induced responses by monoclonal antibodies.
Authors: Forsgren S , Pobor G , Coutinho A , Pierres M 
Published: December 2022

Abstract
A panel of 22 different monoclonal antibodies, including specificities against various antigenic clusters of I-A and I-E molecules, were probed over a wide range of concentrations for their ability to inhibit lipopolysaccharide-induced B lymphocyte proliferation and maturation to immunoglobulin-secreting plaque-forming cells (PFC). Most antibodies were competent to inhibit up to 80 to 100% of the response of appropriate target cells, although having little or no effect on irrelevant spleen cell cultures. Mixtures of either anti-I-A or anti-I-E specificities were more efficient inhibitors than individual antibodies, as shown by the average concentrations required for 50% inhibition (30 and 300 ng/ml, respectively). The selective role of I-A/E molecules in B cell activation was demonstrated by the failure of anti-K antibodies of the same isotype, bound in comparable amounts to target cells, to modulate B cell responses in parallel cultures. Fc receptor-mediated inhibitory effects were further excluded by equivalent inhibition obtained with anti-I-A antibodies of the IgM class. Anti-I-A/E antibodies appear to inhibit the inductive phase of B cell responses, as suggested by limiting dilution experiments performed in the presence of 50% inhibitory concentrations of antibodies: 50% of the control number of reactive clones were found to respond, but those that escaped inhibition developed to control sizes of progenies producing PFC.