bluuebunny/crossref_metadata_2025_split huggingface dataset:
Exacerbation of murine cutaneous leishmaniasis by adoptive transfer of parasite-specific helper T cell populations capable of mediating Leishmania major-specific delayed-type hypersensitivity.
Authors: Titus R G , Lima G C , Engers H D , Louis J A 
Published: December 2022

Abstract
The effect of adoptive transfer of in vitro-propagated Leishmania major-specific T cell populations on the course of experimentally induced cutaneous leishmaniasis was studied in mice. The L. major-specific T cells expressed the T helper/inducer phenotype and were able in vitro to a) mount a specific proliferative response, b) provide specific helper activity for antibody responses, c) activate parasitized macrophages resulting in L. major destruction, and d) secrete macrophage-activating factors as tested in a tumoricidal assay. These T cells were also found capable of transferring parasite-specific delayed-type hypersensitivity responses to normal syngeneic mice. Results indicated that the i.v. transfer of these L. major-specific T cell populations into normal syngeneic mice exacerbated cutaneous lesions induced by infection with L. major. This effect on the disease process appeared to be dependent upon recognition of parasite antigens by the injected T cells because no exacerbation of the disease process was seen after the transfer of similar T cell populations specific for an antigen unrelated to the parasite, namely ovalbumin. However, the inclusion of ovalbumin in the L. major infecting inoculum resulted in an exacerbating effect of ovalbumin-specific T cells on cutaneous leishmaniasis. These unexpected results were supported by observations showing that immunization of mice with L. major antigens in complete Freund's adjuvant 7 days before infection with L. major led to exacerbated lesions. A similar aggravation of L. major-induced cutaneous lesions was also observed in mice previously immunized with an unrelated antigen provided that this antigen was included in the L. major infecting inoculum.
Interaction of reovirus with cell surface receptors. IV. The reovirus type 3 receptor is expressed predominantly on murine Lyt-2,3+ and human T8+ cells.
Authors: Epstein R L , Finberg R , Powers M L , Weiner H L 
Published: December 2022

Abstract
Reovirus type 3 binds to approximately 20% of murine and human T cells via the viral hemagglutinin, a small outer capsid polypeptide. By using purified viral particles as a ligand in a standard plate separation technique, we have been able to enrich human peripheral blood and murine splenic T cells for reovirus receptor-positive cells (reovirus 3+) to levels of 88 to 92%. Analysis of reovirus 3+ T cells with monoclonal antibodies that identify inducer and suppressor/cytotoxic cells demonstrated that in the mouse, 68% of reovirus 3+ cells were Lyt-2+, and in the human, 60% were T8+. In reciprocal experiments, when subpopulations of murine and human T cells were prepared with the use of monoclonal anti-T cell reagents, 16% of Lyt-1+ and 81% of Lyt-2+ cells bound reovirus, whereas 30% of T4+ and 65% of T8+ cells bound reovirus. To determine whether reovirus type 3 identified a functional as well as a phenotypic category of cells, an antigen-specific cytotoxic T cell assay was employed. There was complete loss of cytotoxic activity in the reovirus 3+ cell population and slight enhancement of cytotoxic activity in the cell population from which reovirus 3+ cells were removed. This suggested that reovirus was binding to functionally active suppressor cells. Furthermore, adoptive transfer of antigen-specific T cells that were enriched for reovirus 3+ cells demonstrated suppression of cytoxic T cell activity. These results suggest that reovirus type 3 may identify a structure common to a subclass of murine and human T cells and that by using the virus as a natural biologic probe for cell surface receptors, one may be able to functionally segregate murine cytotoxic from suppressor T cells.
Molecular regulation of MHC class III (C4 and factor B) gene expression in mouse peritoneal macrophages.
Authors: Sackstein R , Colten H R 
Published: December 2022

Abstract
To study the molecular regulation of C4 and factor B synthesis in mouse peritoneal macrophages, mouse C4 cDNA clones isolated from an H-2d haplotype liver cDNA library, and a previously described mouse factor B cDNA clone, pBmB2 (9), were used to assess quantitative and qualitative differences in C4 and factor B mRNA in resident and elicited cells. The C4 clones that were isolated, pBmS2 (1 Kb) and pBmS10 (0.9 Kb), overlap and together span a 1.5 Kb coding region of mouse pro-C4, extending from the alpha-chain through the gamma-chain; four nucleotide substitutions are evident in comparing 316 bp of the sequence of clone pBmS10 to that of a previously described mouse C4 clone, pMLC4/w7-2 (23). By using these probes, Northern blot analysis of total cellular RNA revealed similar C4 mRNA levels in resident peritoneal macrophages from high-C4 (B10.A) and low-C4 (C3HeB) strains. Pulse and pulse-chase studies of C4 and factor B synthesis were performed on resident, starch-elicited, and thioglycollate-elicited peritoneal macrophages at two culture time periods, 0 to 9 and 24 to 33 hr, and total cellular RNA was isolated from each population at 4.5 and 28.5 hr of culture for Northern blot analysis of C4 and factor B mRNA content. The data demonstrate that as previously reported, C4 production decreases in elicited compared with resident macrophages and decreases with time in culture; however, factor B synthesis does not differ among resident and elicited cells and it increases with time in culture. The variations in C4 and factor B production by mouse peritoneal macrophages are not associated with alterations in C4 and factor B protein processing, catabolism, or secretion; rather, they are a function of differences in net amounts of C4 and factor B mRNA. These data provide direct evidence that the regulation of expression of these class III MHC genes in mouse peritoneal macrophages is a pretranslational event.
A glycopeptide extract can inhibit cytotoxic T lymphocyte-target cell conjugation in an H-2-restricted manner.
Authors: Pimlott N J , Miller R G 
Published: December 2022

Abstract
Glycopeptides extracted from P815, a DBA/2 (H-2d) mastocytoma, were able to inhibit conjugate formation between anti-H-2d CTL and an H-2d target, but were not able to inhibit conjugate formation between anti-H-2k or anti-H-2b CTL and an appropriate target. This genetically specific effect was seen for CTL generated in primary bulk cultures and for long-term CTL lines, and was observed regardless of the strain combinations used to generate CTL. The phenomenon was quantitatively reproducible between independent experiments and between three separate preparations of P815 glycopeptide. These results suggest that recognition by CTL involves cell surface carbohydrate groups, and that the structure of these groups is influenced by H-2.
Cloned cytolytic T cells can suppress primary cytotoxic responses directed against them.
Authors: Fink P J , Rammensee H G , Bevan M J 
Published: December 2022

Abstract
In vivo and in vitro, murine peripheral T cells can suppress or "veto" the activation of cytotoxic T lymphocytes directed against antigens presented by those T cells. This suppression is antigen-specific and H-2-restricted. The recognition event initiating this suppression appears to be unidirectional; precursors of cytotoxic T lymphocytes recognize the antigen-bearing veto cell and are thereby inactivated--the veto cell need not recognize the CTL precursor. We show here that 3/3 cytolytic T cell clones can exert veto activity in vitro on normal spleen cells which do not bear antigens the T cell clones can recognize. This suppression results in greatly diminished cytotoxic activity generated during a primary 5-day mixed lymphocyte culture against antigens which the veto cell expresses, but not against third-party antigens present in the same culture. In this same system, a noncytolytic T cell clone will not serve as a source of veto cells. Secondary cytotoxic responses are relatively resistant to the veto cell activity of cloned cytolytic T cells. The cloned veto cells do not suppress the generation of cytotoxic activity directed against antigens they recognize (and presumably carry over via antigen-specific receptors). Cold target competition during the cytotoxic assay has been eliminated as a possible mechanism for T cell clone-induced suppression, and suppression cannot be reversed by the addition to the mixed lymphocyte cultures of supernatants from concanavalin A-activated spleen cells. It is suggested that this mechanism of inactivating primary cytotoxic T lymphocyte responses could play an important role in the maintenance of self-tolerance and in the induction and maintenance of tolerance to allografts.
Sequential substages of natural killer cell-derived cytolytic factor (NKCF)-mediated cytolysis as defined by glutaraldehyde modulation of the target cell.
Authors: Deem R L , Targan S R 
Published: December 2022

Abstract
The substages of natural killer cell-derived cytolytic factor (NKCF)-mediated cytolysis have been examined by using the bifunctional protein cross-linking reagent glutaraldehyde. Glutaraldehyde (2 X 10(-4%)) enhanced both the level and rate of lysis mediated by NKCF when the factor was prebound to the L929 target cell. However, glutaraldehyde enhanced lysis only when added at specific time points (2 to 4 hr after addition of NKCF, which was 6 to 8 hr before any lysis occurred), indicating that NKCF-mediated lysis is a dynamic process. When 10(-3%) glutaraldehyde was added at the same time as NKCF, inhibition of lysis was observed. Pretreatment of L929 target cells, but not of NKCF, with glutaraldehyde resulted in inhibition of NKCF-mediated cytolysis. In addition, it was shown that glutaraldehyde-pretreated L929 and K562 cold target cells were not as effective in competing for binding of NKCF in a cold target competition assay, or as effective in absorbing NKCF at 4 degrees C, indicating that glutaraldehyde modified the NKCF receptor to block binding of NKCF to the target cell. Thus, NKCF-mediated cytolysis can be divided into at least four substages based upon sequential modulation by glutaraldehyde: 1) NKCF binding stage (inhibited by glutaraldehyde), 2) glutaraldehyde-enhanceable nonlytic stage, 3) glutaraldehyde-nonenhanceable nonlytic stage, and 4) glutaraldehyde-nonenhanceable lytic stage.
Response of human B cells to Staphylococcus aureus Cowan I: T-independent proliferation and T-dependent differentiation to immunoglobulin secretion involve subsets separable by rosetting with mouse erythrocytes.
Authors: Ito S , Lawton A R 
Published: December 2022

Abstract
We separated T-depleted mononuclear cells into subsets by rosetting with mouse erythrocytes and studied proliferation and differentiation responses to Staphylococcus aureus Cowan I (SAC), pokeweed mitogen (PWM), and a combination of the two polyclonal activators. All of the T cell-independent proliferation of unfractionated B cells in response to SAC was attributable to mouse erythrocyte rosette-forming cells (BMR+). BMR- cells were not stimulated to proliferate by SAC in the presence or absence of T cells, but did proliferate to PWM plus irradiated T cells. Co-stimulation of BMR+ cells with SAC and PWM in the presence of autologous T cells did not lead to immunoglobulin secretion. The B cells stimulated to divide by SAC apparently do not become responsive to B cell differentiation factors and are distinct from those that undergo T cell-dependent differentiation.
Human IgE synthesis in vitro by pokeweed mitogen-stimulated human lymphoid cells: verification with a reconfirmed epsilon-specific radioimmunoassay.
Authors: Chen P P , Nonaka M , O'Hair C H , Cohen P A , Zuraw B L , Katz D H 
Published: December 2022

Abstract
This study was performed to address the controversy concerning human IgE biosynthesis in vitro induced by stimulation with pokeweed mitogen (PWM) or other agents. The controversy has focused on the specificity of reagents employed for quantitatively determining human IgE in culture supernatant fluids. Specifically, questions have been raised as to whether certain anti-human IgE antibody reagents possess anti-idiotypic reactivities, thereby resulting in reactions with Fab determinants of polyclonal immunoglobulins which would yield false-positive readings of IgE protein levels. We present a detailed analysis confirming that the goat anti-human IgE antibody designated GAHE(PS), which was initially isolated by affinity chromatography with the same IgE(PS) myeloma protein used for immunization, binds poorly, if at all, with IgG, IgA, or IgM immunoglobulins, even at excessive concentrations (100 micrograms/ml). Moreover, GAHE(PS) displayed no reactivity with Fab fragments of IgG or free L-chains prepared from pooled polyclonal IgG isolated from Cohn fraction II. A second GAHE reagent was prepared by purification by affinity chromatography on a second, completely unrelated IgE myeloma protein (DZA), which differed from IgE(PS) in light chain class, thereby resulting in a reagent, designated GAHE(DZA), which was completely devoid of any possible reactivity with L-chain or idiotypic determinants affiliated with IgE(PS). By utilizing both reagents, the studies presented here confirmed that PWM-stimulated human lymphoid cell cultures synthesize increased quantities of IgE, which can be detected in comparable amounts by both GAHE(DZA) and GAHE(PS) in supernatant fluids from such cultures. Because incorporation of the reversible protein synthesis inhibitor, cycloheximide, totally abolished the PWM-induced increases in IgE levels in such cultures, these results verify that such increases reflect de novo synthesis of human IgE as a result of PWM stimulation in vitro.
Dissociation in the production of B cell-stimulating factors (BCGF and BCDF) and interleukin 2 by T cells from a common variable immunodeficient patient.
Authors: Saiki O , Shimizu M , Saeki Y , Kishimoto S , Kishimoto T 
Published: December 2022

Abstract
In the course of an analysis of lymphocyte functions of common variable immunodeficiency patients, we found one patient whose T lymphocytes released B cell differentiation factor (BCDF) and B cell growth factor (BCGF) without IL 2 production upon stimulation with Con A. The patient was a 68-yr-old woman with hypo-gamma-globulinemia (IgM: 31 mg/dl, IgG: 223 mg/dl, IgA: 23 mg/dl); she suffered from cryptococcal meningitis and pulmonary tuberculosis with a negative result of skin tests to PPD and cryptococcal antigen. The number of T cells and the ratio of T cell subsets (Leu-2a and Leu-3a) was normal. T cells showed no proliferative response to Con A and a low response to PHA (one-tenth of normal response). The addition of patient T cells to normal T cells did not inhibit the proliferation of normal T cells when stimulated by Con A. The culture supernatant of Con A-stimulated T cells contained no IL 2 activity when assayed by an IL 2-dependent T cell line. Expression of Tac antigen was not impaired by Con A stimulation and the addition of partially purified IL 2 from the supernatant of Jurkat T cell line-induced proliferation of Con A-stimulated T cells, indicating that the defect observed was not in IL 2-responding cells but in IL 2-producing cells. In contrast, the culture supernatant of the T cells stimulated by Con A or PHA contained BCDF activity as much as that of normal T cells when assayed by Cowan I-stimulated normal B cells or the B lymphoblastoid cell line SKW6-CL4. The supernatant also contained BCGF activity. These results suggest that B cell-stimulating factor (BCGF, BCDF) and IL 2 may be synthesized by different subsets of T cells or that the synthesis of those lymphokines are independently regulated in the same cells.
Response to and production of interleukin 2 by peripheral blood and cerebrospinal fluid lymphocytes of patients with multiple sclerosis.
Authors: Merrill J E , Mohlstrom C , Uittenbogaart C , Kermaniarab V , Ellison G W , Myers L W 
Published: December 2022

Abstract
In an effort to further characterize the defective proliferative response of T lymphocytes to mitogens in multiple sclerosis (MS) patients, we examined the response to and production of interleukin 2 (IL 2) by both peripheral blood lymphocytes (PBL) and cerebrospinal fluid mononuclear cells. We also examined the proportion of cells bearing receptors for IL 2 and transferrin. Chronic progressive MS patients have an abnormally low response to exogenous IL 2 as compared to controls. Whereas acute relapse patients' PBL demonstrated a normal IL 2 response during an exacerbation, they showed reduced responsiveness during remission. These abnormalities could not be explained by different dose or kinetic response optima to PHA or IL 2, nor could they be explained by depressed numbers of IL 2 or transferrin receptor-bearing lymphocytes. Production of IL 2 by PBL was also abnormal in MS patients. Chronic progressive patients produced elevated levels of IL 2, whereas acute relapse patients undergoing an exacerbation produced diminished levels of IL 2. During remission, these levels returned to that of controls'. The effect of 1200 rad x-irradiation or nylon wool removal of adherent cells was a significantly greater augmentation of IL 2 production in MS patients than in other neurologic disease or normal controls. Cerebrospinal fluid lymphocytes from MS patients had normal proportions of IL 2 receptor-bearing cells, but were deficient in their IL 2 response and production as compared to autochthonous or control PBL. The inability of some MS patients' lymphocytes to clonally expand in response to IL 2 might contribute to the pathogenicity of the disease.
Experimental allergic encephalomyelitis: successful treatment in vivo with a monoclonal antibody that recognizes T helper cells.
Authors: Brostoff S W , Mason D W 
Published: December 2022

Abstract
Monoclonal antibody W3/25, which recognizes rat T helper cells, was injected i.p. or i.v. into Lewis rats with clinical signs of experimental allergic encephalomyelitis (EAE). This treatment, which was given 12 or 13 days after inducing EAE by the injection of purified myelin basic protein, significantly affected the course of the disease in that treated animals recovered, on the average, in 2 days, whereas control animals exhibited signs of EAE for a minimum of 4 days. Two pan-T cell monoclonal antibodies given in similar dosage failed to affect the course of the disease.
A permanent rat T cell line that mediates experimental allergic neuritis in the Lewis rat in vivo.
Authors: Linington C , Izumo S , Suzuki M , Uyemura K , Meyermann R , Wekerle H 
Published: December 2022

Abstract
A rat T cell line of the "helper" phenotype (W3/25-positive, OX 8-negative) has been derived from Lewis rats inoculated with P2 protein isolated from bovine PNS myelin. The line LiP2/A is exquisitely specific for P2 protein, exhibiting no reactivity to bovine basic protein or to PPD. In addition to responding strongly to the intact P2 protein, the line cells show some response to a synthetic peptide containing the neuritogenic amino acid sequence of P2 protein (SP-B, residues 66-78). Intravenous inoculation of naive rats with as few as 10(4) activated LiP2/A cells leads to the onset of mild clinical signs of experimental allergic neuritis. Higher doses of cells lead to more severe clinical disease. Histologic examination of clinically ill animals confirmed the disease as EAN. The pathologic lesions were confined to the PNS and spared the central nervous system. The lesions consisted of marked perivascular cuffs and infiltrates of inflammatory cells associated with marked degenerative changes--demyelination and some axonal degeneration.
The murine IL 2 receptor. I. Monoclonal antibodies that define distinct functional epitopes on activated T cells and react with activated B cells.
Authors: Ortega G , Robb R J , Shevach E M , Malek T R 
Published: December 2022

Abstract
The properties of three distinct rat monoclonal antibodies, designated 3C7, 7D4, and 2E4, to the murine IL 2 receptor have been compared in binding, biochemical, and functional assays. 3C7 appears to define an epitope near or identical to the IL 2-binding site of the receptor, because 3C7 inhibited the binding of radiolabeled IL 2 to CTL-L cells and because unlabeled IL 2 inhibited the binding of FITC-3C7 to CTL-L cells. 7D4 and 2E4 had no effect on IL 2 binding. Competitive antibody-binding studies confirmed that the epitope seen by 3C7 was distinct from the epitope(s) seen by 7D4 and 2E4. Sequential immunoprecipitation studies demonstrated that all three antibodies were reactive with the same molecular species, and that each precipitated identical components of 20,000 to 25,000 daltons, 50,000 to 60,000 daltons, and 100,000 to 120,000 daltons from the surface of CTL-L. FACS studies demonstrated a quantitatively and qualitatively identical cell distribution for the antigen defined by each antibody. They failed to stain more than 95% of resting lymphocytes, but were strongly reactive with Con A T blasts and substantially less reactive with LPS B blasts. Unlabeled IL 2 was also able to inhibit the binding of FITC-3C7 to LPS B cell blasts, suggesting the presence of IL 2-binding sites on activated B cells. Each antibody inhibited IL 2-driven proliferation of HT2 or CTL-L cells. 3C7 and 7D4 were more potent inhibitors of proliferation than was 2E4, and the combined use of 3C7 and 7D4 resulted in greater levels of inhibition of proliferation than that shown from the use of either antibody alone. Collectively, the results support the hypothesis that these antibodies detect two distinct functional regions of the IL 2 receptor.
High-level secretion of interleukin 2 by a subset of proliferating thymic lymphoblasts.
Authors: Caplan B , Rothenberg E 
Published: December 2022

Abstract
We have characterized the thymocytes that can be induced to secrete interleukin 2 (IL 2) after polyclonal stimulation with Con A. For maximal activation, an important adjunct to the Con A is the phorbol ester TPA. In the presence of TPA, IL 2 production by thymocytes is relatively independent of adherent accessory cells; this allows us to compare the abilities of different thymic subpopulations to make IL 2. The most numerous class that includes IL 2 producers is made up of cells with a typical "medullary" population, the phenotype: moderately small, postmitotic cells that fail to bind peanut agglutinin. In addition, however, a population of large, proliferating lymphoblasts is competent in IL 2 production directly as isolated. Relative to the total "medullary" population, the lymphoblasts are enriched for the ability to make IL 2. They account for a significant proportion of the total IL 2 produced by thymocytes, and demonstrate that this aspect of immunocompetence is not restricted to cells that have finished their intrathymic proliferation. The IL 2-producing lymphoblasts do not bind peanut agglutinin or express thymus-leukemia antigen, but they do express high levels of Lyt-1. Although distinct from most medullary thymocytes, therefore, they are also distinct from the majority of cortical blast cells for which a direct precursor role has been established. They may be a subset of the rare proliferating blast cells in the medulla. Further heterogeneity in the thymic IL 2 producers is demonstrated by their expression of the Lyt-2 glycoprotein. The majority of IL 2 producers are Lyt-2- as are the majority of peripheral T "helper" cells. However, a distinct minority of the thymic IL 2 producers express Lyt-2. Therefore, the ability of some peripheral Lyt-2+ cells to secrete IL 2 may be determined at the time of their initial programming in the thymus.