bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence for linkage of murine beta 2-microglobulin to H-3 and Ly-4.
Authors: Goding J W 
Published: December 2022

Abstract
Murine beta 2-microglobulin exists in 2 electrophoretically distinct forms; C57BL/6 mice possess the basic allele whereas BALB/c, CBA, AKR, and NZB possess the acidic allele. Mice heterozygous for beta 2-microglobulin express both alleles. Analysis of recombinant inbred mice suggests linkage of beta 2-microglobulin to H-2 or H-3. B10.C (28NX) mice (which possess the H-3c allele of BALB/c on a C57BL/10 background) possess the acid allele. Taken together, these results are consistent with the beta 2-microglobulin gene lying on chromosome 2, and being linked to H-3 and Ly-4.
Genetic control of experimental autoimmune myasthenia gravis in mice. II. Lymphocyte proliferative response to acetylcholine receptor is dependent on Lyt-1+23- cells.
Authors: Christadoss P , Krco C J , Lennon V A , David C S 
Published: December 2022

Abstract
The proliferative response of regional lymph node lymphocytes to Torpedo acetylcholine receptor (TAR) is under H-2 linked Ir gene control. In high responder B6 (H-2b) congenic mice, lymphocytes that proliferate in vitro in response to TAR are dependent on T cells of a subpopulation expressing the phenotype associated with helper functions, Lyt-1+23-.
Amphotericin B-induced resistance to Schistosoma mansoni.
Authors: Olds G R , Stewart S J , Ellner J J 
Published: December 2022

Abstract
Amphotericin B (AmB) increases host resistance against several infectious agents and tumors. We evaluated its effect on infections with the helminth Schistosoma mansoni. A single dose of 500 microgram i.p. or 25 microgram i.v. increased resistance in mice to a challenge with 500 or 100 S. mansoni cercariae. Schistosomula recovery from the lungs, 5 days after challenge, was reduced 33 to 40%. Adult worm recovery 8 wk after infection was reduced 36 to 43%, AmB was effective in protecting mice when given from 9 days before until the day of cercarial challenge but was ineffective 2 wk before or at all intervals after S. mansoni infection. To examine the mechanism of this resistance, we obtained peritoneal exudate cells (PEC) from animals treated with AmB and assessed their ability to kill schistosomula, the migrating larval stage of the parasite. Killing by adherent PEC 1 or 2 days after AmB treatment was the same as that of resident macrophages from untreated animals. Adherent PEC from animals 3 to 7 days after AmB treatment showed enhanced killing of schistosomula (38.0 plus or minus 3.0% at day 4, which exceeded control of 8.1 plus or minus 4.0%, p less than 0.01). These PEC also displayed increased killing of Staphylococcus aureus. When AmB was added to cultures of resident peritoneal adherent cells from untreated mice at 0.5 microgram/ml to 2.0 microgram/ml (concentrations not toxic to the organism), schistosomula killing was increased 1- to 6- fold. These findings demonstrate activation of murine macrophages by AmB in vitro and in vivo, which results in greater killing of this multicellular parasite and potentially contributes to enhanced resistance to infection.
Formation of IgE binding factors by human T lymphocytes.
Authors: Ishizaka K , Sandberg K 
Published: December 2022

Abstract
Peripheral blood mononuclear cells from ragweed-sensitive individuals formed soluble factors that inhibited rosette formation of Fc epsilon receptor (+) cells with IgE-coated ox erythrocytes when the cells were incubated with ragweed antigen E and human IgE. Either antigen E alone or IgE alone failed to induce the formation of the rosette inhibiting factors. Two-way mixed lymphocyte culture from 2 normal individuals followed by incubation of the activated lymphocytes with IgE induced the formation of the rosette-inhibiting factor. Normal human mononuclear cells cultured in the presence of T cell growth factor (TCGF) formed the soluble factor when they were incubated with IgE. The rosette-inhibiting factor in culture filtrates was specifically absorbed with IgE-coupled Sepharose and was recovered from the beads by elution at acid pH, indicating that the soluble factors have affinity for IgE. Because the lymphocytes cultured with TCGF were mostly T cells and contained neither B cells nor monocytes, it appears that the IgE-binding factors are derived from T cells.
In vitro induction of HLA-restricted cytotoxic T lymphocytes against autologous Epstein-Barr Virus transformed B lymphoblastoid cell line.
Authors: Fukukawa T , Hirano T , Sakaguchi N , Teranishi T , Tsuyuguchi I , Nagao N , Naito N , Yoshimura K , Okubo Y , Tohda H , Oikawa A 
Published: December 2022

Abstract
Cytotoxic T lymphocytes (CTL) against autologous EBV-transformed B lymphoblastoid cell line (LCL) were induced in vitro by culturing peripheral blood lymphocytes (PBL) of healthy donors together with mitomycin C-treated autologous LCL for 6 days. The cytotoxic cells developed only from the E-rosette-positive fraction but not from the negative fraction of PBL. These CTL killed autologous LCL but not PWM-stimulated autologous PBL. In addition, the CTL killed allogeneic LCL when at least 1 of the HLA-A antigens was identical with that of the LCL of CTL donor. However, identity of HLA-B and HLA-C antigens was not enough for a significant killing of allogeneic LCL. The specificity of the CTL was also confirmed by a cold target inhibition test. These results indicated that the CTL induced specifically recognized EBV-transformed cells with HLA restriction.
Spatially distinct allodeterminants of the H-2Kk molecule as detected by monoclonal anti-H-2 antibodies.
Authors: Ozato K , Henkart P , Jensen C , Sachs D H 
Published: December 2022

Abstract
In an attempt to delineate spatial relationships between various allodeterminants of cell surface MHC antigens, competitive binding studies were performed using 4 different monoclonal antibodies, each of which reacted with the H-2Kk antigen but with different serologic specificities. Competition was studied by examining the effect of unlabeled antibodies on the binding of each 125I-labeled antibody to spleen cells of the H-2a haplotype. Mutual inhibition was observed between 2 of the antibodies, and a 3rd antibody of lower affinity was inhibited by the first 2 antibodies but did not itself inhibit the binding of these antibodies. The 4th antibody did not block the binding of the other 3 labeled antibodies, and binding of this 4th labeled antibody was only partially inhibitable by the other 3 antibodies. These results indicate the presence of at least 2 spatially distinct allodeterminants on H-2Kk molecules expressed on the cell surface.
Induction of balanced immunoglobulin chain synthesis in free light chain-producing lymphocytes by mitogen stimulation.
Authors: Hannam-Harris A C , Smith J L 
Published: December 2022

Abstract
Neoplastic cells from 2 cases of CLL synthesized and secreted excess free Ig light chain in culture, confirmed by precipitation with anti-idiotypic antibody. Small and medium sized normal human spleen cell subpopulations, staining predominantly for surface IgM and D, also synthesized and secreted excess free light chain. PWM stimulation induced balanced synthesis of heavy and light chains in CLL and normal spleen subpopulations after 6 days in culture, accompanied in spleen but not CLL by the appearance of mature plasma cells. These data demonstrate that normal cell counterparts of neoplastic lymphoid synthesis patterns can be identified in spleen. Furthermore, the synthesis pattern alteration after PWM stimulation suggests a relationship between free light chain synthesis and B cell immaturity. The failure of CLL cells to develop into detectable plasma cells suggests a restricted maturation response to mitogen compared with normal spleen.
Activation of mouse macrophages for tumor cell killing. I. Quantitative analysis of interactions between lymphokine and lipopolysaccharide.
Authors: Pace J L , Russell S W 
Published: December 2022

Abstract
Lymphokine-rich supernatants from concanavalin A-stimulated spleen cell cultures failed to activate mouse peritoneal macrophages for tumor cell killing, providing that the assay system was free of detectable (less than 0.125 ng/ml) endotoxin. Instead, increasing amounts of lymphokine progressively increased the sensitivity of macrophages to activation by purified bacterial lipopolysaccharide (LPS). Conversely, the effect of minute amounts of lymphokine could be detected in the presence of relatively high (though nonactivating) concentrations of LPS. The latter observation was exploited to develop a highly sensitive, quantitative assay for lymphokine. In this assay, serially diluted supernatants were tested on macrophage monolayers in the presence of a constant concentration (3 ng/ml) of LPS. Under these conditions, the lymphokine dose-response curve was sigmoidal and therefore suitable for conversion to a linear plot using the logarithmic transformation of the von Krogh equation. Activity could be expressed quantitatively and reproducibly in terms of units of activity. By facilitating purification the assay should contribute to the development of a more precise biochemical understanding of the role of lymphokine in macrophage activation for tumor cell killing.
Relationship between epidermal Langerhans cell density ATPase activity and the induction of contact hypersensitivity.
Authors: Lynch D H , Gurish M F , Daynes R A 
Published: December 2022

Abstract
Langerhans cells have been implicated as playing a crucial role as antigen-processing cells in the induction of positive immune responses to antigens presented through the skin. We have investigated the effects of carcinogenic doses of UVB-irradiation, psoralen plus UVA light (PUVA), PABA containing sunscreen preparations, and topically applied corticosteroids on both Langerhans cell densities and immunologic responsiveness to contact sensitizers applied to the treated site. The data presented demonstrate that UV-irradiation of skin or topical application of corticosteroids can create a local milieu in which DNFB cannot function as an effective stimulator of contact hypersensitivity. Further, we have shown that the effect induced by UV light is reversible, does not appear to be related to the numerous tissue destructive effects of UVB-irradiation, and that the correlation with the density of ATPase-positive cells is not absolute.
Use of a synthetic hapten in the demonstration of the Thomsen-Friedenreich (T) antigen on neuraminidase-treated human red blood cells and lymphocytes.
Authors: Bray J , Lemieux R U , McPherson T A 
Published: December 2022

Abstract
Using an artificial T hapten, we have confirmed that human sera contain agglutinins for neuraminidase-treated red blood cells (N'RBC), specific for the disaccharide beta DGal(1 leads to 3)alpha DGalNAc. Further, we have shown that these agglutinins are antibodies largely of the IgM subclass that bind equally to neuraminidase-treated lymphocytes (N'lymphocytes). The anti-T antibody in human serum is cytotoxic for N'RBC in complement fixation assays. The synthetic hapten has biologic activity as shown in inhibition experiments and by the specificity of a rabbit antibody raised to the hapten for the naturally occurring antigen on N'RBC and N'lymphocytes. An immunoadsorbent prepared from the hapten was used to obtain biologically active antibodies from human serum with specificity for the naturally occurring antigen.
Mitogenic response of human peripheral blood lymphocytes to a purified C. albicans polysaccharide fraction: lack of helper activities is responsible for the in vitro unresponsiveness to a second antigenic challenge.
Authors: Piccolella E , Lombardi G , Morelli R 
Published: December 2022

Abstract
Human peripheral blood lymphocytes primed with MPPS (a polysaccharide fraction extracted from C. albicans) were unable to respond to a second challenge of the same antigen. The proliferative response of these lymphocytes was restored by both mitomycin C-treated fresh autologous lymphocytes and by helper factors. Removal of Ia+ cells from fresh lymphocytes abolished the helper effect. On the other hand, when primed lymphocytes were depleted of Ia+ cells, the helper factor-responding cells were eliminated, whereas Ia- cells maintained the capacity to respond to fresh autologous lymphocytes. A model for cell-cell cooperation involved in the regulation of the immune response to this antigen is proposed.
Regulation of T cell differentiation: in vitro induction of 20 alpha-hydroxysteroid dehydrogenase in splenic lymphocytes from athymic mice by a unique lymphokine.
Authors: Ihle J N , Pepersack L , Rebar L 
Published: December 2022

Abstract
The enzyme 20 alpha-hydroxysteroid dehydrogenase (20 alpha SDH) has previously been shown to be a specific enzyme marker of mature T cells. In vivo, the expression of 20 alpha SDH is thymus dependent, in that splenic lymphocytes from athymic mice have only low levels of activity, although the levels of enzyme activity increase gradually with age. In vitro, 20 alpha SDH can be induced in splenic lymphocytes from nu/nu mice by conditioned media from mitogen- or alloantigen-stimulated normal lymphocytes. Induction is rapid in vitro. Beginning after a lag period of approximately 6 hr, enzyme activity increases linearly for approximately 20 to 30 hr resulting in a 5- to 10-fold increase in activity. Induction is blocked by mitomycin C, suggesting a requirement for cell proliferation. The phenotype of both the precursor and the induced lymphocyte populations is Thy 1.2-, Lyt 1-, 2-, suggesting that induction of 20 alpha SDH expression is an early step in T cell differentiation. The factor responsible for 20 alpha SDH induction has been partially purified and is distinct from other known lymphokines in both its biochemical and functional properties. The term interleukin 3 is proposed for this factor.
H-2 negative teratocarcinoma cells become H-2 positive when passaged in genetically resistant host mice.
Authors: Ostrand-Rosenberg S , Cohan V L 
Published: December 2022

Abstract
The murine 402AX teratocarcinoma is an H-2 negative, nullipotent stem cell tumor of testicular origin. Previous studies have demonstrated that host strain resistance and susceptibility to this tumor are under the control of 2 genes, one of which is closely linked to the mouse major histocompatibility complex. Earlier studies determined the lack of antigenic modulation and the absence of H-2 antigens on 402AX cells passaged in vitro or in genetically susceptible hosts. The present studies demonstrate that when passaged in genetically resistant host mice [C57BL/10, B10.SM, and B10.129(6M)], the H-2 negative 402AX cells modulate to become positive for H-2b antigens, as detected by indirect immunofluorescence, microcytotoxicity, and quantitative absorption. Two to 4 days of in vivo growth in resistant hosts is necessary for H-2b antigens to be expressed. H-2 positive tumor cells removed from resistant hosts and placed in culture become H-2 antigen negative within 1 to 4 hr in vitro. H-2 antigen turn-on on the teratocarcinoma cells is specific for the H-2 haplotype of the tumor cell origin (129, H-2b); alien H-2 antigens are not expressed. The observation that only teratocarcinoma cells growing in genetically resistant hosts turn-on for H-2 antigens suggests that major histocompatibility antigens on target cells are required for an efficient host cell-mediated immune response against tumor cells.
Antigenic characterization of a T-CLL with heteroantisera and monoclonal antibodies: evidence for the T cell lineage of an Ia-positive, Fc-IgG--positive, suppressor-cell subpopulation.
Authors: Strong D M , Pandolfi F , Slease R B , Budd J E , Woody J N 
Published: December 2022

Abstract
In a previous report, peripheral blood mononuclear T cells from a patient with T-chronic lymphocytic leukemia (T-CLL) were shown to bear receptors for the Fc portion of IgG (T gamma). Moreover, the ability of these cells to rosette with sheep erythrocytes was strongly inhibited by a preincubation of the cells with theophylline. These data indicated that they represent a highly purified subpopulation of Fc-IgG receptor-positive, low-affinity rosetting cells with in vitro suppressor activity on lectin-induced proliferation of normal lymphocytes. They also were reactive in antibody-dependent cell-mediated cytotoxicity but had no reactivity in natural killer cell assays. These cells were studied in this report with several heteroantisera and monoclonal antibodies. Results indicate that these T-CLL cells express a T cell antigenic pattern (OKT-3+) and the majority are Ia positive. They also react with the OKT-8 reagent (a reagent detecting the subset of T cells that contains the cytotoxic/suppressor cells), whereas they are negative with OKT-4 (which reacts with the subset of T cells that contains helper cells) and OKT-6 (thymocyte) antibodies. Heteroantisera also support the results obtained with monoclonal reagents. Despite some recent evidence showing that a high percentage of T gamma cells may belong to the monocyte-myeloid lineage, these T-CLL cells were negative with OKM-1, a monoclonal antibody reported to detect a monomyeloid antigen. These results suggest that a distinct subpopulation of suppressor T cells can be identified by membrane-marker phenotyping.
Gluten-sensitive enteropathy. I. The T-dependent anti-A-gliadin antibody response maps to the murine major histocompatibility locus.
Authors: Trefts P E , Kagnoff M F 
Published: December 2022

Abstract
We examined the genetic control of the murine humoral immune response to purified A-gliadin, a protein derived from wheat gluten, which is known to cause small intestinal disease in susceptible individuals. Studies with congenic and noncongenic inbred strains of mice revealed that the T-dependent humoral immune response to A-gliadin is under the control of genes mapping to the mouse major histocompatibility complex (MHC). These findings in mice establish a clear linkage between the MHC and the regulation of the immune response to a protein capable of causing human disease.
The cell-mediated lympholysis-inducing capacity of highly purified human monocytes and T lymphocytes in primary and secondary mixed leukocyte cultures.
Authors: Spits H , de Vries J E , Terhorst C 
Published: December 2022

Abstract
In this study the capacity of T cells and monocytes to induce cell-mediated lympholysis (CML) in primary and secondary MLC was investigated. The T lymphocytes were enriched by rosetting with sheep red blood cells (E) and further purified by sedimentation at unit gravity, which completely removed the contaminating monocytes. In addition, a highly purified monocyte population was obtained by 1 X G sedimentation of the non-E rosette-forming cells. These purified T cells have a poor CML-inducing capacity in primary and secondary MLC. In contrast, monocytes were very effective in inducing CML in both primary and secondary MLC. Induction of CML by monocytes in primary MLC was inhibited by heterologous anti-Ia-like antisera, indicating that the induction of CML by monocytes was related to the presence of HLA-DR (Ia-like) antigens on these cells.
Immunologic control of the ascites form of murine adenocarcinoma 755. V. Antibody-directed macrophages mediate tumor cell destruction.
Authors: Langlois A J , Matthews T , Roloson G J , Thiel H J , Collins J J , Bolognesi D P 
Published: December 2022

Abstract
An in vitro assay has been developed that mimics the potent in vivo protective capacity of B6 anti-AD755a serum in a passive therapy protocol. In the presence of small volumes of hyperimmune serum or IgG2a antibody, thioglycollate-elicited B6 mouse peritoneal cells (PEC) inhibit the growth of AD755 Cl.10 target cells and other cells provided that they express FLV-related antigens. When hyperimmune serum is replaced by normal serum, or elicited PEC from BALB/c mice are used, growth inhibition of the AD755 Cl.10 target cells is not seen. The latter is in accord with the inability to protect BALB/c mice with the anti-AD755a serum. Tumor cells to which antibody has been pre-bound are not inhibited by thioglycollate-elicited B6 PEC, analogous to the undiminished tumorigenicity of antibody-bound AD755a cells in vivo. These results, along with those presented in the accompanying papers, have led to the construction of a model to explain the specificity and mechanism of the potent in vivo passive protection characteristic of this system. The major features of this model are that the protective IgG2a antibody must first interact with an appropriate host effector cell, presumably of the monocyte/macrophage lineage, and that such an antibody-directed cell then binds to the tumor cell and effects its elimination, possibly by a phagocytic mechanism.
The failure of nonresponder mice to develop IgG memory assessed by in vitro culture with an antigen-LPS conjugate.
Authors: Furman A , Sercarz E E 
Published: December 2022

Abstract
A hen egg-white lysozyme-lipopolysaccharide complex (HEL-LPS) can stimulate an in vitro IgG response, but only from HEL-primed B lymphocytes; unprimed cells only produce an IgM response. These conditions were used to determine whether IgG memory B cells are cryptically induced in B10 nonresponder (H-2b) mice after an HEL injection protocol. The usual i.p. immunization that triggers IgG memory production in congenic responder strain mice fails to yield IgG in vitro from HEL-primed B10 spleen cells after stimulation with HEL-LPS. However, injection protocols immunogenic for B10 mice do engender IgG-memory cells. These results imply that the T helper cell population necessary for triggering B cells to the IgG memory stage cannot develop in the nonresponder mouse, presumably due to HEL-specific T suppressor cells.
Macrophage receptors for IgE: binding of IgE to specific IgE Fc receptors on a human macrophage cell line, U937.
Authors: Anderson C L , Spiegelberg H L 
Published: December 2022

Abstract
Human IgE was found to bind to the human macrophage line U937. Binding was specific for IgE in that it was inhibited by 3 different human IgE myeloma proteins and by Fc fragments prepared from IgE, but not by IgE Fab fragments or by myeloma proteins representative of the 4 IgG subclasses or by a rat IgE myeloma protein. Dissociation and association rates were rapid, with estimated t1/2 of less than 1 min. The Ka was 4.15 X 10(7) liter/mol. Between 53,000 and 93,000 sites per cell were calculated. The U937 receptor for IgE was trypsin sensitive, whereas the receptor for IgG on the same cell was relatively trypsin resistant.
Early dominance of irradiated host cells in the responder profiles of thymocytes from P leads to F1 radiation chimeras.
Authors: Korngold R , Bennink J R , Doherty P C 
Published: December 2022

Abstract
The number of cells in the thymus of [k leads to (b X k)F1] radiation (100 rad) chimeras increases approximately 10-fold between 7 and 14 days after reconstitution with bone marrow. At least 50% of the cells in thymus on day 14 are of host origin and respond to virus presented in the context of both H-2k and H-2b when primed in irradiated, virus-infected (b X k)F1 recipients. Strong CTL responses can be generated from thymocytes of donor origin on day 21. All evidence of a significant host thymocyte component has disappeared by day 28. The responsiveness of 14-day thymocytes is not abrogated by pretreatment of the mice used to make the chimeras with anti-thymocyte serum or by using doses of irradiation as high as 1200 rads to eliminate host components.