bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human B lymphoblastoid cell lines provide an interleukin 1-like signal for mitogen-treated T lymphocytes via direct cell contact.
Authors: Arnold A , Lipkowitz S , Suthanthiran M , Novogrodsky A , Stenzel K H 
Published: December 2022

Abstract
The B lymphoblastoid cell lines (B-LCL) 8392, SB, 1788, and Daudi provide accessory cell activity for mitogen-treated T cells, whereas the T lines MOLT-4, 8402, CEM, and HSB do not provide this function. Direct cell contact is required for the accessory cell activity, and active lymphocyte growth factors could not be detected in the supernatants of the B-LCL. The B-LCL also present alloantigens to responding T cells, and this response is independent of additional accessory cells. The target for the B-LCL is the responding T cell itself, rather than a minor contaminating population of endogenous accessory cells. This conclusion is based on the finding that, under culture conditions in which T cells do not proliferate in response to PHA, accessory cell activity of the B-LCL is maintained. Paraformaldehyde- or glutaraldehyde-treated B-LCL retain their accessory cell activity at levels of these agents that completely eliminate metabolic activity of the B-LCL, as determined by incorporation of leucine, thymidine, and uridine into macromolecules. This treatment eliminates alloantigen presentation by the B-LCL. T cells treated with IO-4 or with monoclonal anti-T3 antibodies fail to respond to highly purified IL 1, and respond minimally to supra-optimal concentrations of IL 2. Nevertheless, these cells respond maximally to the accessory cell activity of the B-LCL. The IO-4 treated cells or cells exposed to anti-T3 also proliferate in response to TPA. Together, our data suggest that the B-LCL provide an IL 1-like signal for mitogen-treated T cells via direct cell contact, in the absence of detectable soluble IL 1.
Lymphokine-induced cytotoxicity: requirement of two lymphokines for the induction of optimal cytotoxic response.
Authors: Yang S S , Malek T R , Hargrove M E , Ting C C 
Published: December 2022

Abstract
Lymphokines induce the generation of cytotoxic cells (LICC) in the absence of antigenic or mitogenic stimulation. In the present study, we have demonstrated that at least two lymphokines are involved. They are interleukin 2-conditioned medium (CM-IL 2), which was produced by W/Fu rat spleen cells cultured with concanavalin A-conjugated Sepharose beads, and cytotoxic cell differentiation factor-conditioned medium (CM-CCDF), which was produced primarily by the unstimulated mouse peritoneal macrophages. It was first established that CCDF synergized with IL 2 to induce the generation of LICC in normal spleen cells, and that this process was specifically blocked by the rat anti-IL 2 receptor monoclonal antibody. The maximal synergistic effect was obtained by using 10% CM-CCDF (v/v) and 0.1 to 0.3 U/ml of CM-IL 2. Higher doses of IL 2 (3 to 10 U/ml) reduced the cytotoxic response. The effectors of LICC were Thy-1+, Lyt-2- and AGM1-; therefore, they were neither classic CTL nor NK cells. The precursors were AGM1+, Lyt-2- cells that were consistent of being NK-like cells. When examining the temporal relationship between CCDF and IL 2, we found that 4 hr preincubation of the responders with IL 2 was sufficient to activate the cytotoxic precursor cells. CCDF was needed later for the differentiation of the activated precursors into cytotoxic effectors. In contrast, preincubation of the responders with CCDF, followed by additional incubation with IL 2, failed to induce any cytotoxic response. These results established that lymphokine-induced cytotoxicity can be separated into two phases. In the activation phase, IL 2 provides the first signal to activate the cytotoxic precursors, with the process being completed in 4 hr. In the differentiation phase, CCDF provides the second signal to induce the differentiation of the IL 2-activated precursors into cytotoxic effectors, with this process requiring 48 hr to complete. The sequential presence of these lymphokines at an appropriate time during the activation and differentiation phases is critical for the generation of LICC response.
Characterization of a murine monoclonal antibody specific for an allotypic determinant on T cell antigen receptor.
Authors: Staerz U D , Rammensee H G , Benedetto J D , Bevan M J 
Published: December 2022

Abstract
Repeated immunization of normal C57L/J (H-2b) mice with peripheral T cells from BALB.B (H-2b) mice results in the production of antibodies which react with the T cell receptor. A monoclonal antibody-producing hybridoma, F23.1, was isolated from immunized C57L/J mice showing this property. This monoclonal antibody recognizes approximately 25% of peripheral T cells in BALB mice. It stains approximately the same fraction of T cells and precipitates the same heterodimer as the rat monoclonal antibody described previously that was made against isolated receptor material. The allotypic determinant recognized by this monoclonal antibody is present in most common laboratory strains (BALB, C57BL, CBA, A, DBA, C3H) and is absent in C57L, C57BR, and SJL mice. Sorting peripheral T cells from BALB.B or (SJL X BALB/c)F1 mice for the F23.1+ and F23.1- subsets revealed that both populations contain approximately the same CTL precursor frequency for alloantigen. Thus, the T cell receptor allotype defined by F23.1 is present on CTL. Furthermore, cytotoxicity mediated by an F23.1+ CTL line could be blocked specifically by the F23.1 monoclonal antibody. Under appropriate conditions, the monoclonal antibody F23.1 bound to Sepharose 4B beads can induce resting peripheral T lymphocytes of allotype-positive strains to proliferate.
Preferential expression of VK21E light chains on IdX Ia.7 positive monoclonal anti-I-E antibodies.
Authors: Devaux C , Moinier D , Mazza G , Guo X J , Marchetto S , Fougereau M , Pierres M 
Published: December 2022

Abstract
We previously characterized major (IdX Ia.7) and minor (IdI) idiotopes in a collection of monoclonal alloantibodies reactive with monomorphic (i.e., Ia.7-like) determinants in the structural domain I of the murine class II I-E molecules. In this report, preliminary structural characterization of this antibody family is presented. First, the contribution of isolated H and L chains of the anti-Ia.7 cluster I mAb 41.A to IdX Ia.7 and IdI 41.A idiotope expression was evaluated by testing the capacity of these chains, either isolated or reassociated in homologous or heterologous hybrid Ig, to inhibit the binding of rat or mouse anti-idiotope mAb to IdX Ia.7+ mAb coated plates. It was found that the IdI 41.A idiotope defined by the mouse anti-idiotopic mAb H90-21.1 required the presence of both 41.A H and L chains for complete expression, while the rat mAb-defined IdX Ia.7 idiotope could be detected on isolated and on reassociated 41.A L chain. To evaluate further the structural correlates of the IdX Ia.7 idiotope, H, L, or both H and L chains of 5 A.BY, 4 A.TH and 1 C3H.SW IdX+ anti-Ia.7 mAb, as well as that of 3 A.TH IdX- anti-I-E or anti-I-A and -I-E mAb were subjected to NH2-terminal amino acid sequencing. These analyses demonstrated a) that different H chains corresponding to different subgroups (at least to the VHII and VHIII) could be expressed without apparent modification of IdX Ia.7 idiotope expression and b) that 9 of 11 IdX+ anti-Ia.7 mAb utilized highly homologous L chains of the VK21E subgroup. The relevance of these findings to the genetic control of the idiotypic markers identified in the Ia.7 system is discussed.
Characterization of three monoclonal antibodies which induce and modulate superoxide anion generation in guinea pig macrophages.
Authors: Yagawa K , Kaku M , Ichinose Y , Aida Y , Tomoda A 
Published: December 2022

Abstract
Three monoclonal antibodies (Ab), termed KY 12, KY 22, and KY 25 and raised against guinea pig macrophages, induced superoxide anion (O2-) generation in the cells. Although each monoclonal Ab bound to macrophages, each had a different pattern of binding to other cell types. In response to each of the Ab, the amount of O2- generated by 5 X 10(5) macrophages was between 0.5 and 0.7 nmol/min and was augmented threefold to fivefold by the addition of F(ab')2 fragments of rabbit Abs to mouse Ig. When macrophages were pretreated with soluble immune complexes (I.C.) prior to stimulation by the monoclonal Ab, the O2- generation stimulated by KY 12 or KY 22 was reduced by more than 70%. In contrast, pretreatment of macrophages with I.C. did not reduce O2- generation in response to KY 25. KY 12 and KY 22 stimulated adenyl cyclase activity in macrophages, but KY 25 did not. Pretreatment of the cells with soluble I.C. did not interfere with the enhancing effect of the monoclonal Ab on adenyl cyclase activity. Pretreatment of macrophages with KY 12 reduced by over 60% of subsequent generation of O2- in response to wheat germ agglutinin, I.C., formyl-methionyl-leucyl-phenylalanine, phorbol myristate acetate, KY 22, or KY 25. KY 22 or KY 25 did not suppress the generation of O2- in response to other stimuli. These results suggest that KY 22 and KY 25 activate O2- generation in a manner that differs from that of KY 12. These monoclonal Ab should prove useful in examining the regulation of O2- production.
Leishmania amastigotes: resistance to complement-mediated lysis is not due to a failure to fix C3.
Authors: Mosser D M , Wedgwood J F , Edelson P J 
Published: December 2022

Abstract
Amastigote forms of Leishmania major are sensitive to lysis by fresh serum, whereas those of L. donovani are resistant. To understand the basis for this resistance we have examined the interaction of complement with amastigotes of seven strains of leishmania. Complement activation was determined by measuring the ability of amastigotes to consume complement from normal serum and by identifying parasite surface-bound C3. All of the strains that were tested activated complement, including both those that are resistant and those that are susceptible to inactivation by fresh serum. Complement consumption by amastigotes was measured as a decrease in the ACH 50 titers of serum exposed to parasites. L. major, L. donovani, and L. mexicana mexicana (strain 1VLM) amastigotes decrease titers by 35.7, 33.5, and 40.3%, respectively. The binding of C3 to amastigotes was judged qualitatively by immunofluorescence and quantitatively by a C3 radiobinding assay. L. major amastigotes bind an average of 6.6 X 10(4) molecules of C3 per parasite. L. mexicana amazonensis, L. mexicana mexicana, and L. donovani bind an average of 3.9 X 10(4), 5.9 X 10(4), and 3.7 X 10(4) molecules, respectively. In all cases, C3 binding is the result of alternative pathway activation requiring Mg++ but not Ca++. Amastigotes of the disseminating strains of leishmania represent the first example of a group of protozoa that activate early complement components leading to fixation of C3, but that are resistant to inactivation by complement.
Characterization of Schistosoma mansoni antigen-reactive T cell clones that form granulomas in vitro.
Authors: Lammie P J , Linette G P , Phillips S M 
Published: December 2022

Abstract
Granuloma formation and modulation in schistosomiasis are a consequence of discrete subpopulations of T lymphocytes and the mediators they produce. In the present study, T cell clones reactive to soluble egg antigen (SEA) were developed to analyze the roles of T cells in Schistosoma mansoni egg-induced granuloma formation. In an in vitro granuloma assay, 1 X 10(5) T cells specifically augmented the response of 2 X 10(6) normal spleen cells to SEA-coupled but not purified protein derivative-coupled polyacrylamide beads. In vitro granulomatous responses by individual clones were correlated with their capacity to mediate local delayed-type hypersensitivity reactions in footpad swelling assays. Phenotypic analysis of the seven clones characterized in the present study demonstrated that they were L3T4+, Ly-2.2-. An analysis of supernatants of T cells pulsed with concanavalin A or SEA + antigen-presenting cells was also undertaken in an attempt to correlate in vitro granuloma formation with lymphokine production. Stimulated T cells (but not unstimulated T cells) produced interleukin 2, macrophage activating factor, migration inhibitory factor, and eosinophil stimulation promoter in response to both mitogenic and antigenic stimuli. The results suggest that individual clones of T cells are capable of producing a variety of mediators that influence their ability to activate and to recruit cells into granuloma formation. The model may be useful in the analysis of specific antigens and regulatory interactions and their contribution to granuloma formation.
Recombinant gamma-interferon induces changes in expression and shedding of antigens associated with normal human melanocytes, nevus cells, and primary and metastatic melanoma cells.
Authors: Herlyn M , Guerry D , Koprowski H 
Published: December 2022

Abstract
Recombinant gamma-interferon (rIFN-gamma) induced or augmented the expression of HLA-DR class II antigens on melanocytes isolated from newborn foreskin, from congenital, common acquired, and dysplastic nevi, and from primary and metastatic melanoma. The stimulatory effect of rIFN-gamma on HLA-DR antigen expression was suppressed by the addition of the phorbol ester TPA or its analog PDBu to the culture medium. Whereas rIFN-gamma did not significantly alter the expression of melanoma-associated, non-class II antigens on melanoma cells, there was a marked decrease in the expression of antigens associated with nevus cells. In addition, rIFN-gamma stimulated shedding of antigens. Increased antigen shedding was most apparent for an intracytoplasmic melanoma-associated protein of 80kd, followed by the ganglioside GD2 and by an alkali labile ganglioside. The simultaneous stimulation of class II antigen expression and shedding of melanoma-associated antigens as well as suppression of nevus-associated antigen expression could play an important role in the host immune response to premalignant and malignant melanocytic lesions.
Human T cell leukemia/lymphoma virus-infected antigen-specific T cell clones: indiscriminant helper function and lymphokine production.
Authors: Volkman D J , Popovic M , Gallo R C , Fauci A S 
Published: December 2022

Abstract
The ability of human T cell leukemia/lymphoma virus (HTLV)-I to alter the function of infected T lymphocytes was examined directly by investigating the properties of an antigen-specific T cell clone before and after transformation with HTLV-I. Following infection, the T4 antigen-specific clone manifested a tenfold increase in its surface interleukin 2 (IL 2) receptor (Tac) density and acquired the viral determinants p19, p24, and 4D12 not present in the uninfected clone. Prior to infection, the T cell clone responded to antigen stimulation in the presence of histocompatible antigen-presenting cells with proliferation and secretion of multiple lymphokines, including IL 2, B cell growth factor (BCGF), B cell differentiation factor (BCDF), and interferon-gamma (IFN-gamma). Following infection, the T cell clone both proliferated and produced constitutively three of these lymphokines (BCGF, BCDF, and IFN-gamma) in the absence of accessory cells or antigen. Co-cultivation with any accessory cells regardless of histocompatibility resulted in increased proliferation and lymphokine production. IL 2 production by the HTLV-I-transformed cell, however, could not be detected. Similarly, the uninfected clone was able to provide B cell help for Ig production only when stimulated with both histocompatible cells and antigen. In contrast, the infected cell provided T cell help to B cells in an unregulated manner, independent of antigen or histocompatibility. Thus, functions such as the induction of proliferation, B cell help, and lymphokine production, which are finely regulated in uninfected antigen-specific T cell clones, became indiscriminant after HTLV-I infection.
Murine monoclonal anti-DNA autoantibodies bind to endogenous bacteria.
Authors: Carroll P , Stafford D , Schwartz R S , Stollar B D 
Published: December 2022

Abstract
Several bacterial species (including Streptococcus faecalis, Bacillus cereus, Staphylococcus aureus, and Escherichia coli) were tested for their ability to react with monoclonal anti-DNA antibodies that were derived from MRL-lpr/lpr mice. S. faecalis reacted with 8/15 of such antibodies. The binding was unaffected by DNase, but it was competitively inhibited by DNA. F(ab')2 fragments of the monoclonal antibodies reacted with the bacteria, but Fc fragments did not. Phospholipids extracted from the bacterial cells were able to bind to three representative anti-DNA antibodies that also bound to whole bacteria. The results suggest that bacterial phospholipids might provide an immunogenic stimulus for the production of antibodies that cross-react with DNA. We propose that some anti-DNA auto-antibodies and anti-bacterial antibodies evolve from a restricted group of antibodies with high avidity for the phosphodiester groups that occur in DNA and bacterial cells walls.
Activation of mouse lymphocytes inhibits induction of rapid cell death by x-irradiation.
Authors: Lowenthal J W , Harris A W 
Published: December 2022

Abstract
A distinctive property of the resting lymphocyte is its ability to die rapidly in interphase after x-irradiation. Suspensions of thymocytes and peripheral lymphocytes from BALB/c mice were irradiated with doses ranging from 10 to 10,000 rad (0.1 to 100 Grays), and their viability was measured by eosin dye exclusion at intervals through 3 days of culture. After an initial latent period of a few hours, viability declined exponentially in a dose-dependent fashion. Doses as low as 20 rad caused some lymphocytes to die rapidly. After 1000 rad, 90% of the cells became nonviable in 15 to 20 hr and 99% in 25 to 35 hr. Peripheral lymphocytes showed a somewhat earlier loss of viability than did thymocytes, and were killed especially rapidly by 10,000 rad. Enriched T cells and B cells were killed by irradiation at equal rates, and medullary thymocytes were killed at the same rate as the whole thymocyte population. In contrast with resting cells, T and B lymphocytes activated by mitogens were not subject to such rapid induction of cell death. Irradiation with 1000 rad reduced the viability of activated cells by only 50% at a time when less than 1% of nonstimulated lymphocytes remained alive. Similarly, cloned lines of antigen-specific helper and cytotoxic T cells showed only a delayed and slow loss of viability after receiving 1000 rad. The state of activation can therefore be a significant determinant of the immunologic consequences of irradiation.
Cross-reactive idiotype family observed in the phthalate-specific B cell repertoire of adult BALB/c mice: diversity of IgM compared with IgG monoclonal anti-phthalate antibodies.
Authors: Luo S C , Bankert R B 
Published: December 2022

Abstract
A highly conserved clonotype has been identified within the repertoire of B cells specific for the negatively charged hapten phthalate. The prototype of this phthalate-specific clonotype is a primary-response hybridoma (2E9) that produces a mu,kappa anti-phthalate antibody. The 2E9 monoclonal antibody was found to share idiotypic determinants with several other independently-derived mu,kappa and gamma 1,kappa anti-phthalate monoclonal antibodies and with a significant proportion of conventional anti-phthalate antibodies derived from all of the BALB/c mice immunized with phthalate-keyhole limpet hemocyanin. Competitive RIA analysis of the 2E9 idiotypic relatedness between primary and secondary response antibodies was consistent with the hypothesis that the primary response mu,kappa antibodies represent a conserved germ-line product, whereas the secondary response to gamma 1,kappa antibodies reflect somatic variants of the 2E9 clonotype. Further analysis with a site-specific anti-idiotype reagent suggests that the idiotypic differences between mu,kappa and gamma 1,kappa monoclonal antibodies occur at positions outside of the combining site. Fine specificity analysis of the monoclonal antibodies expressing the 2E9 cross-reactive idiotype (CRI) also supports this hypothesis. Seven to 35% of the anti-phthalate antibodies after a single immunization with phthalate-KLH and 1 to 10% of the antibodies after a second immunization express the 2E9 CRI. The 2E9 CRI was also found in several other strains of mice, and its expression was associated exclusively with anti-phthalate antibodies.
Adenosine; a physiologic modulator of superoxide anion generation by human neutrophils. Adenosine acts via an A2 receptor on human neutrophils.
Authors: Cronstein B N , Rosenstein E D , Kramer S B , Weissmann G , Hirschhorn R 
Published: December 2022

Abstract
Adenosine specifically inhibits superoxide anion generation by N-formyl-methionyl-leucyl-phenylalanine-stimulated neutrophils without affecting either degranulation or "aggregation." We present data that also supports the hypothesis that adenosine engages a specific cell surface receptor to mediate inhibition of stimulated neutrophils. Theophylline (10 and 100 mu M), a competitive antagonist at adenosine receptors, reversed the effects of adenosine (0.1 mu M) on superoxide anion generation by stimulated neutrophils. The adenosine analogue 5'N-ethylcarboxamidoadenosine (NECA) was a more potent inhibitor of superoxide anion generation than either N6-phenylisopropyladenosine (PIA) or adenosine, an order of potency consistent with that previously demonstrated for adenosine A2 receptors. 2-Chloroadenosine inhibited superoxide anion generation at concentrations similar to NECA. [3H]-NECA and [3H]-2-chloroadenosine bound to a single receptor on intact neutrophils. The characteristics of the receptors for [3H]-NECA and [3H]-2-chloroadenosine were similar (Kd = 0.22 and 0.23 mu M, respectively; number of binding sites = 9.31 and 11.1 X 10(3) sites/cell, respectively). NECA, 2-chloroadenosine, adenosine, and PIA inhibited binding of [3H]-NECA with a rank order similar to that for inhibition of superoxide anion generation (NECA = 2-chloroadenosine greater than adenosine greater than PIA). There was 50% inhibition of superoxide anion generation by NECA at approximately 20% receptor occupancy. Adenosine, derived from damaged tissues, may serve as a specific, endogenous modulator of superoxide anion generation by activated neutrophils through interaction at this newly described receptor on human neutrophils.
Distribution and fate of free and liposome-encapsulated [3H]nor-muramyl dipeptide and [3H]muramyl tripeptide phosphatidylethanolamine in mice.
Authors: Fogler W E , Wade R , Brundish D E , Fidler I J 
Published: December 2022

Abstract
The pharmacokinetics and metabolism of i.v. administered free (unencapsulated) or liposome-encapsulated hydrophilic [3H]-labeled nor-muramyl dipeptide (nor-MDP) and lipophilic [3H]-labeled muramyl tripeptide phosphatidylethanolamine (MTP-PE) were evaluated. In addition we also examined the distribution and fate of these immunomodulators subsequent to intranasal (i.n.) administration. Unique patterns of circulatory clearance, organ distribution, metabolism, and excretion were observed for each of the four preparations. Nor-MDP in saline was rapidly cleared from the circulation and excreted in the urine as intact molecules. MTP-PE dissolved in saline was cleared from the circulation at a slow rate and found within various organs as intact MTP-PE, lyso-MTP-PE, and MDP. Following the i.v. administration of nor-MDP or MTP-PE in liposomes, patterns of clearance and organ distribution corresponded to that of liposome distribution, i.e., the reticuloendothelial system. Extensive dissociation of hydrophilic nor-MDP from the carrier liposomes occurred, and the immunomodulator was recovered in the urine. In contrast, MTP-PE entrapped in liposomes was retained in target organs for the duration of the study. The i.n. instillation of radiolabeled nor-MDP or MTP-PE was associated with the accumulation of these immunomodulators in the brain. Our results demonstrate the feasibility of targeting hydrophilic and lipophilic immunomodulators to cells of the macrophage-histiocyte series.