bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of physical stress on sensitivity of lymphocytes to inhibition by prostaglandin E2.
Authors: Goodwin J S , Bromberg S , Staszak C , Kaszubowski P A , Messner R P , Neal J F 
Published: December 2022

Abstract
Physical stress is associated with depressed cellular immune function. We have found that lymphocytes from subjects undergoing either of 2 stressful events, cardiac surgery or childbirth, are more sensitive to inhibition by PGE2. For example, the concentration of PGE2 required for 50% inhibition of 3H-thymidine incorporation (ID50) into phytohemagglutinin-stimulated lymphocytes from patients undergoing cardiac surgery went from 1.5 X 10(-8) M on the day before surgery to 3 X 10(-9) M on the day after surgery. This increase in sensitivity to PGE2 was accompanied by a significantly decreased lymphocyte proliferative response (27 to 68% of control, depending on mitogen dose) and a 50% increase in the percentage of E rosette-positive cells with receptors for the Fc portion of IgG. The increased sensitivity to PGE and the depressed mitogen responses returned to preoperative values by day 10. The depressed mitogen responses of the postoperative patients were completely restored to normal by removal of glass-adherent cells before culture. In addition, the responses of the postoperative patients and the women in labor were partially restored by the addition of indomethacin, a prostaglandin synthetase inhibitor, to the cultures. Thus it would appear that physical stress causes lymphocytes to become more sensitive to prostaglandin E2, and the increased sensitivity to inhibition by this immunomodulator is responsible in part for the depressed cellular immune function after physical stress.
Cell-mediated lympholytic responses against autologous cells modified with haptenic sulfhydryl reagents. I. Effector cells can recognize two distinct classes of hapten-reactive self sites on cell surface proteins.
Authors: Levy R B , Shearer G M , Richardson J C , Henkart P A 
Published: December 2022

Abstract
Mouse spleen cells were modified with a sulfhydryl-reactive reagent, N-iodoacetyl-N'-(5-sulfonic-1-naphthyl) ethylene diamine (I-AED) and used as stimulator cells in primary in vitro cultures with unmodified spleen cells of the same strain. CTL could be readily demonstrated when tested on hapten-modified syngeneic target cells. These CML responses were hapten specific and H-2 restricted. In the H-2b strain, effector cell populations were identified that recognized AED in association with K-end and D-end coded self MHC products. Functional modification of the target cells by I-AED can be effectively blocked by prereacting the cells with other SH-reagents, which is consistent with CTL recognition of the hapten on cysteine residues. Since these premodifications of the cell surface do not block the functional modification by trinitrobenzene sulfonate (TNBS), the sulfhydryl-reactive compounds and TNBS modify distinct classes of cell surface groups as determined by CTL function. The results of antibody inhibition experiments are also consistent with this interpretation. Using fluorescent labeled anti-hapten antibodies, FACS II analysis showed that there are approximately 20-fold fewer AED than TNP groups on the approximately 20-fold fewer AED than TNP groups on the cell surface when equivalent concentrations of I-AED and TNBS are compared. The possibility is discussed that these sulfhydryl-reactive compounds can be used together with the H-2Kb mutants for the localization of H-2 coded self determinants recognized in association with foreign antigens.
Cell-mediated lympholysis responses against autologous cells modified with haptenic sulfhydryl reagents. II. Analysis of the genetic control and H-2-restricted pattern of cytotoxic responses to sulfhydryl and amino reactive reagents.
Authors: Levy R B , Henkart P A , Shearer G M 
Published: December 2022

Abstract
N-iodoacetyl-N'-(5-sulfonic-1-naphthyl)ethylene-diamine modified autologous cells are shown to induce respective high and low AED-self CTL responses by spleen cells from H-2b and H-2k mice. The lysis mediated by effector populations from both haplotypes was highly H-2 restricted. Cytotoxic responses induced by a 2nd sulfhydryl- (SH) specific reagent, dithionitrobenzoic acid (DTNB), were shown not to be cross-reactive at the effector cell level with AED-self but exhibited the same high and low CTL response patterns as those induced against AED-self. These Ir-effects reported for the 2 SH reactive compounds are discussed in relation to the opposite Ir-patterns demonstrated against a number of amino (NH2) reactive compounds. The difference of self-recognition sites is suggested to account for the contrasting results observed in the response patterns induced by SH- and NH2-reactive compounds. The AED-self CTL response was found to exhibit Kk-self over Db-self Ir regulation. Thus, this latter type of genetic control appears to function independently of whether the hapten is an SH- or NH2-reactive compound.
In vivo release of eosinophil chemoattractant activity in human allergic skin reactions.
Authors: Ting S , Zweiman B , Lavker R M , Dunsky E H 
Published: December 2022

Abstract
A search was made for in vivo release of factor(s) that may be responsible for prominent eosinophil accumulations in human allergic skin reactions. Using a specially designed skin chamber appended to the base of unroofed skin blisters, we have found at ragweed-challenged sites in sensitive subjects the release of significantly greater histamine (15 +/- 3 ng/ml) than at control sites (3 +/- 0.5 ng/ml). Eosinophil accumulation after 2 hr was also significantly greater on membrane filters appended to ragweed-challenged sites than control sites (55 +/- 15 vs 4 +/- 0.5). Intradermal injection of ultrafiltrates of the chamber fluids from antigen-challenged sites, but not of fluids from control sites, induced prominent eosinophil accumulation (mean = 25/mm2) when injected intradermally in autologous uninvolved skin. Neither ultrafiltered antigen solution nor histamine (employed in concentrations similar to those released in the chambers) evoked such in vivo responses when injected intradermally in the same subjects (mean = less than 1/mm2). The eosinophil responses to injected ultrafiltered chamber fluid from antigen-challenged sites peaked at 30 min, whereas even greater eosinophil responses to unaltered antigen started after 60 min. These findings suggest that in vivo release of a low m.w. factor or factors other than histamine is very likely responsible for at least part of the in vivo eosinophil accumulation in human allergic reaction sites. Additional findings suggest that a significant portion of the time lag between intradermal antigen and dermal eosinophil accumulation is encompassed by local mediator release.
mu Polypeptide phenotypes of lymphoid and myeloid cell lines containing RNA transcripts of the immunoglobulin C mu gene.
Authors: Walker I D , Harris A W 
Published: December 2022

Abstract
We have examined whether polyadenylated-RNA molecules encoded by the immunoglobulin C mu gene (C mu RNA) that have recently been shown to occur in mouse T lymphoma, myeloid tumor, and pre-B lymphoma cell lines are translated. Three T lymphoma, 1 myeloid tumor, and 4 Abelson lymphoma cell lines, all known to contain C mu RNA molecules, were examined for evidence of synthesis of mu polypeptides using radioimmunoassay, biosynthetic peptides were detected in any of the T lymphoma or myeloid cell lines, although mu-chains were readily detected in 2 B lymphoma lines known to contain small amounts of mu mRNA. Detection failure is unlikely to be the result of assay insensitivity and was not caused by lack of an appropriate antiserum reactivity or a requirement for mu-chains to be associated with immunoglobulin light chains. Proteolytic activity that might degrade newly synthesized mu polypeptides in these cell lines was not detected. In 3 of the 4 Abelson lymphoma cell lines containing C mu RNA, corresponding polypeptides were absent, although in the 4th they were easily detected, indicating that transcription of the C mu gene is not the sole determinant of whether a cell will synthesize the corresponding polypeptide. The parallel between the C mu RNA+, mu polypeptide- Abelson cell lines and the T lymphoma cell lines suggests that the onset of C mu transcription may occur in both T and B lineages before translational competence is acquired.
In vitro growth of murine T cells. VI. Accelerated skin graft rejection caused by adoptively transferred cells expanded in T cell growth factor.
Authors: Rosenstein M , Eberlein T , Kemeny M M , Sugarbaker P H , Rosenberg S A 
Published: December 2022

Abstract
The ability of adoptively transferred cytotoxic T cells expanded in T cell growth factor (TCGF) to induce accelerated graft rejection of B10.BR skin grafts from normal B6AF1 recipient mice was tested. In vitro sensitized cells expanded in regular TCGF were capable of accelerating graft rejection when adoptively transferred i.v. 1 day after grafting. Cells expanded in LF-TCGF (lectin-free) were more effective in accelerating graft rejection than cells expanded in lectin containing TCGF. Nonsensitized cells or cells sensitized to irrelevant B10.D2 antigenic determinants in vitro and subsequently expanded in LF-TCGF were unable to induce accelerated rejection of the B10.BR grafts. Expanded cytotoxic effector cells known to be immunologically active in vivo were also unable to accelerate graft rejection if irradiated with 2000 R before adoptive transfer. The ability of cells to lyse the appropriate targets in 4-hr 51Cr release assays correlated poorly with the effectiveness of these cells after in vivo injection. These studies are the first to demonstrate that cytotoxic cells expanded in TCGF are capable of mediating a cytotoxic function in vivo.
Discordant expression of 2 Epstein-Barr virus-associated antigens, EBNA and RANA, in man-rodent somatic cell hybrids.
Authors: Slovin S F , Glassy M C , Dambaugh T , Catalano M A , Curry R A , Ferrone S , Kieff E , Vaughan J H , Carson D A 
Published: December 2022

Abstract
The Epstein Barr nuclear antigen (EBNA) and the rheumatoid arthritis nuclear antigen (RANA) develop in human B lymphocytes that have been infected and transformed by Epstein Barr virus (EBV). Antibodies to RANA and EBNA are found only in individuals with prior exposure to EBV. The purpose of the present studies was to determine the relation of the 2 antigens to each other and to EBV genetic material, in human-rodent somatic cell hybrids. Cultured human B lymphoblastoid cells, Raji, Daudi, and RPMI 4098 were fused with thymidine kinase-deficient mouse or hamster fibroblasts. After selection and cloning in ouabain-HAT medium, the hybrid nature of the surviving cells was confirmed by isozyme analysis. The hybrid clones were analyzed for EBNA by anti-complement im,munofluorescence, and for RANA by anti-immunoglobulin immunofluorescence and immunodiffusion. The results showed that RANA and EBNA segregated entirely independently of each other in the hybrid clones. Two methods were used to detect the presence of EBV DNA sequences in the intracellular DNA of hybrid clones. The 1st method relied on the hybridization of labeled cRNA prepared from virion DNA with DNA from 8 hybrid clones affixed to nitrocellulose filters. The 2nd approach was to hybridize labeled intracellular DNA from 3 hybrid clones to Southern blots of cloned fragments of EBV DNA. These results suggested that the presence of EBV DNA was not sufficient for the expression of either antigen. One stable RANA-positive hybrid cell line contained at least 80% of the EBV genome in the absence of detectable EBNA.
A murine stage-specific embryonic antigen (SSEA-2) is expressed on some murine SV40-transformed cells.
Authors: Shevinsky L H , Knowles B B , Howe C , Aden D P , Solter D 
Published: December 2022

Abstract
A stage-specific embryonic antigen-2 (SSEA-2) found on murine preimplantation embryos is maximally expressed on 4- to 8-cell stage embryos and is present in decreasing amounts of morulae and blastocysts. This antigenic determinant is also expressed on murine teratocarcinoma cells, sperm, and some, but not all, SV40-transformed mouse cell lines. Analysis of solubilized immunoprecipitates by SDS-gel electrophoresis indicates that this cell surface molecule is not the 54,000 m.w. protein shared by teratocarcinoma and SV40-transformed cell lines.
In vitro antibody response to influenza virus. II. Specificity of helper T cell recognizing hemagglutinin.
Authors: Anders E M , Katz J M , Jackson D C , White D O 
Published: December 2022

Abstract
Intraperitoneal immunization of mice with liver influenza virus was shown to induce helper T (TH) cells with specificity for the hemagglutinin (HA). The interaction of virus-primed TH cells with purified HA was studied independently of B cell reactivity to the same antigen by using the generation of nonspecific help as an index of activation of HA-specific TH cells. TH cells from mice primed with any of the H3 viruses A/Aichi/68 X A/Bel/42 (H3N1), A/Memphis/102/72 X A/Bel/42 (H3N1) or A/Port Chalmers/73 (H3N2) were strongly cross-reactive towards HA of other strains within the H3 subtype. In addition, several examples of cross-reactivity towards HA of a different subtype were observed, usually of a lower magnitude. TH cells from mice primed to any of the H3 viruses above or to A/Bel/42 (H1N1) virus cross-reacted with the HA of A/Japan/305/57 (H2); furthermore, priming with A/Bel/42 or with A/Jap/305/57 X A/Bel/42 (h2N1) virus yielded TH cells that cross-reacted with certain of the H3 HA preparations. The cross-reactivity observed between subtypes was not due to the common chicken host carbohydrate component of HA, since no response to the purified type A HA preparations was obtained with T cells from mice primed with egg-grown influenza B/Hong-Kong/8/73 virus. The results indicate that HA of different subtypes may share cross-reactive antigenic determinants recognized by TH cells. Within a subtype, HA are highly cross-reactive with respect to tH cell recognition.
Analysis of the cytotoxic T cell response to H-Y in CBA/H mice.
Authors: Brenan M , Müllbacher A 
Published: December 2022

Abstract
The dose response, kinetics, and target cell specificity of the H-Y immune Tc-cell response of fp-primed CBA/H mice was analyzed. Non-MHC genes were shown to influence responsiveness in fp-primed H-2k strains of mice. The possibility that dominant T-suppressor cells mask responsiveness in i.p. primed CBA/H mice was not confirmed in mixing experiments. Female spleen-adherent cells injected with male spleen cells i.p. elicited H-Y immune Tc-cell responses.
Helper cells in the autologous mixed lymphocyte reaction. I. Generation of cytotoxic T cells recognizing modified self H-2.
Authors: Wolos J A , Smith J B 
Published: December 2022

Abstract
The autologous mixed lymphocyte reaction (AMLR) in mice measures the proliferative response of T cells to determinants on syngeneic non-T spleen cells. Normally, cytotoxic T lymphocytes (CTL) are not generated in this reaction. However, the addition of trinitrophenyl-modified mitomycin C-treated syngeneic T cells (TNP-Tm) to the AMLR results in the generation of TNP-specific CTL but does not alter the proliferative response. Significant cytotoxic activity is not detectable against TNP in association with Ia unless TNP is present on cells bearing those determinants. Thus, if unselected spleen cells are TNP-modified and used as stimulators in the AMLR, the proliferative response is enhanced and CTL are generated that recognize TNP in association with K, D, and I region-encoded determinants. The CTL generated in the AMLR are H-2 restricted and dependent on the presence of adherent cells in the sensitization cultures. The experiments presented here suggest that the AMLR can provide the help necessary for generating cytotoxic T cells in vitro.
Hapten-specific T cell response to 4-hydroxy-3-nitrophenyl acetyl. X. Characterization of distinct T cell subsets mediating cutaneous sensitivity responses.
Authors: Sunday M E , Dorf M E 
Published: December 2022

Abstract
NP-O-Succinimide-induced cutaneous sensitivity (CS) responses can be adoptively transferred by NP-primed lymphoid cells into naive K-, I-, or D-compatible recipients. The distinct fine specificities of I- versus D-restricted T cell clones from various strains of mice suggested that presence of different idiotypic receptors on these T cell subsets. We now demonstrate that NP-O-Su immune lymphoid cells are composed of 2 T cell subsets with distinct antigen recognition patterns, as well as different Lyt 2 phenotypes. Thus, I-restricted cells respond to NP-coupled to a protein carrier but not to NP-coupled cells, whereas D-restricted clones react to NP-cells, but not to NP-protein conjugates.
T lymphocyte-mediated cytolysis. I. A common mechanism for target recognition in specific and lectin-dependent cytolysis.
Authors: Berke G , Hu V , McVey E , Clark W R 
Published: December 2022

Abstract
In this and the accompanying paper we examine the nature of the interactions between effector cells and target cells leading to lysis in T cell-mediated cytolysis reactions. In the first paper, we re-examine the role of lectin (Con A) in the process of lectin-dependent cell-mediated cytotoxicity (LDCC). Lectin has generally been thought to act simply as a bridge between the cytotoxic effector cell (EC) and the target cell (TC), thus bypassing the need for receptor-antigen interaction and accounting for the nonspecific character of this lytic reaction. A role for lectin in the activation of cytotoxic function in the EC has also been suggested. In this paper we confirm that LDCC occurs when TC alone are pretreated with lectin, but not when EC alone are pretreated with lectin, unless free lectin is also present in the assay mixture. In addition, we demonstrate that the failure of lectin-pretreated EC to bind to and lyse TC is not caused by agglutination or self-destruction of the EC. Moreover, lectin-pretreated EC are not inherently deficient in the ability to bind or lyse TC, if the latter are pretreated with lectin, or if free lectin is present in the assay. Finally, when EC are used as both effectors and targets in LDCC, lysis is observed only in the direction of the lectin-pretreated partner. From these results we conclude that in LDCC, as in specific CTL cytolysis, CTL-TC recognition proceeds through interaction of an EC surface receptor (distinct from the lectin receptor), and a TC antigen perhaps modified by, but distinct from, the lectin itself. In the accompanying paper we present evidence that this receptor-determinant interaction involves TC MHC antigen.
T lymphocyte-mediated cytolysis. II. Role of target cell histocompatibility antigens in recognition and lysis.
Authors: Berke G , McVey E , Hu V , Clark W R 
Published: December 2022

Abstract
Although compelling genetic and serologic evidence implicate target cell (TC) MHC antigens in specific cytotoxic T lymphocyte (CTL)-TC interaction leading to lysis, it is not entirely clear whether TC recognition through an MHC determinant(s) is a prerequisite for lysis to occur. In fact the finding that both specific and nonspecific TC are lysed equally well in lectin-dependent cell-mediated cytotoxicity (LDCC) challenges the necessity for TC MHC involvement in the cytolytic process beyond providing the basis for specificity in direct (nonlectin-dependent) CTL-mediated lysis. In the present paper we present evidence suggesting that even in nonspecific LDCC, as well as in nonspecific lymphocyte-mediated lysis of TC oxidized by periodate treatment or by galactose oxidase (ODCC), TC MHC components are required for lytic interactions with cytotoxic effector cells. This conclusion is based on 3 types of experimental evidence: 1) cells displaying reduced amounts of MHC proteins are poor targets in LDCC; 2) removal of H-2 by papain renders murine target cells refractory to lysis in LDCC, even though Con A binding is only slightly reduced; 3) antisera to target cell H-2-coded products block lysis in both LDCC and ODCC, whereas antisera to other cell surface antigens do not. A theory explaining nonspecific effector target interaction leading to lysis based on involvement of CTL receptor(s) and TC MHC components is presented.
Long-term in vitro culture of murine mast cells. II. Purification of a mast cell growth factor and its dissociation from TCGF.
Authors: Yung Y P , Eger R , Tertian G , Moore M A 
Published: December 2022

Abstract
Procedures are described for the isolation of a mast cell growth factor (MCGF) from medium conditioned by mitogen-activated splenic leukocytes (CM). Although optimal conditions for the production of MCGF in CM are identical to those for the production of T cell growth factor (TCGF), MCGF can be dissociated from TCGF after the first stage of purification on a DEAE-cellulose column. MCGF elutes from the column in the breakthrough fraction, whereas TCGF binds avidly to DEAE and is eluted only at high salt concentration. MCGF also differs from TCGF with respect to m.w. (as estimated by Sephadex G-150 chromatography) and sensitivity to trypsin. In addition, MCGF is produced by the murine myelomonocytic leukemia WEHI-3 and the radiation induced thymic lymphoma LBRM-33 cells, whereas TCGF is produced only by the latter in the presence of a mitogen. Another hemopoietically active factor, granulocyte colony-stimulating factor (G-CSF) present in media conditioned by WEHI-3 and LBRM-33 cells, however, shares a number of properties with MCGF. Although studies with purified or partially purified MCGF have thus far failed to reveal a correlation between MCGF and G-CSF, further biochemical analyses are necessary to dissociate MCGF from G-CSF.
Immunotherapy of murine leukemias by monoclonal antibody. I. Effect of passively administered antibody on growth of transplanted tumor cells.
Authors: Kirch M E , Hammerling U 
Published: December 2022

Abstract
The objective of the present study was to establish a model system for the evaluation of passive immunotherapy of murine leukemias. Monoclonal antibodies directed at T lymphocyte differentiation antigens (Thy 1 and Lyt 2) were tested for their effect on tumors that were grown in hosts congenic for the target antigen. Tumor challenges were selected that were at least 500 times the dose that was lethal in 50% of untreated controls. The A strain leukemia, ASL.1, was transplanted subcutaneously into a/Thy 1.1 congenic hosts. Intraperitoneal administration of anti-Thy 1.2 monoclonal antibodies of the IgG3 and IgM classes reduced tumor growth. Up to 90% of the mice receiving antibody of the IgG3 subclass failed to develop tumors, whereas IgM antibodies prolonged survival time, but the mice eventually died of tumors. Antibody was most effective if administered within 24 hr of tumor inoculation; delay of antibody injection for 48 hr prolonged host survival but did not eradicate cells at the injection site or prevent metastases. The C57BL/6-derived tumors, ERLD and EL4, were evaluated for susceptibility to treatment with antibody directed at the Lyt 2.2 alloantigen using the protocol that was effective in treating aSL.1. Monoclonal antibody of the IgG2a subclass was effective in the case of C57BL/6/Lyt 2.1 congenic mice bearing ERLD, but caused a decrease in survival time of mice bearing the transplanted EL4 tumor. Thus, antibody of the appropriate immunoglobulin subclass can be effective in controlling tumor growth if administered in the optimal treatment regimen, but inherent features of the tumor cell ultimately determine whether abrogation or enhancement of growth will occur.