bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of antigen-specific T cell responses in autoimmune MRL/Mp-lpr/lpr and MRL/Mp-+/+ mice.
Authors: Scott C F , Tsurufuji M , Lu C Y , Finberg R , Sy M S 
Published: December 2022

Abstract
The MRL-1 mouse develops severe autoimmune disease characterized by high titers of autoantibodies at an early age (3 to 5 mo). The congeneic MRL-n mouse, which differs only in the lymphoproliferative (lpr) gene, exhibits no such pathologic or serologic abnormalities at the same age. We examined antigen-specific T cell responses in the MRL-1 mouse and compared them to age- and sex-matched MRL-n controls. We found broad defects in these responses in the MRL-1 mouse; an inability to generate primary allospecific and hapten-specific cytolytic T lymphocytes (CTL), secondary hapten- and virus-specific CTL, as well as a deficient proliferative response to hapten and natural antigens and a weak delayed-type hypersensitivity response were demonstrated. Our data furthermore suggest a lack of interleukin 2 (IL 2) acceptor sites in the proliferating T cell, while suggesting no such lack on CTL precursors. In fact, the deficient CTL responses in MRL-1 mice can be restored to levels seen in MRL-n by the in vitro addition of IL 2. The implications of these findings and the possible explanations for the relative deficit in helper function in the MRL-1 mouse are discussed.
Interferon and natural killing of human lymphoma cell lines after induction of the Epstein Barr viral cycle by superinfection.
Authors: Blazar B A , Strome M , Schooley R 
Published: December 2022

Abstract
Interferon (IFN) production during natural killer (NK) cell assays with Raji, an EBV-carrying human lymphoma-derived cell line, was studied to determine whether IFN generated by effectors in vitro acted in target cell lysis. In 4-hr tests, Raji is insensitive to NK but becomes susceptible after superinfection with the P3HR-1 strain of EBV. IFN was not detectable by bioassay in supernatants from 4-hr assays, and the addition of antibody to IFN did not prevent the lysis of the superinfected Raji cells. In 18-hr tests the NK sensitivity of the superinfected Raji cells was markedly elevated, and a percent of the normal Raji cells was also killed. IFN alpha was found in supernatants from 18-hr tests. Antibody to IFN alpha markedly reduced the killing of superinfected Raji and slightly reduced cytotoxicity against control Raji in 18-hr tests. Taken together these results indicate that what is referred to as natural killing has IFN-related and IFN-nonrelated components.
Replication of herpes simplex virus in human T lymphocytes: characterization of the viral target cell.
Authors: Braun R W , Teute H K , Kirchner H , Munk K 
Published: December 2022

Abstract
Herpes simplex virus (HSV) replicated in mitogen-stimulated human T cells. Virus replication was obtained in highly enriched mitogen-stimulated T cells of the OKT 3+, OKT 4+, or OKT 8+ subtype, in stimulated B cells, and in macrophages precultured for 7 days. In contrast, no virus replication was obtained in unstimulated T or B cells, in macrophages grown in culture for 1 day, in Null/NK cells, or in granulocytes. Infectious center assays revealed that below 1% of the infected T cell subpopulations supported virus replication, whereas up to 42% of infected B cells and 80% of macrophages cultured for 1 wk were able to replicate HSV. By indirect double immunofluorescence studies, complement-mediated mass cytolysis, and positive selection experiments, it was shown that only T cells expressing Ia antigen actively replicated the virus. T cells activated in the mixed lymphocyte culture and with UV-inactivated HSV were also susceptible to HSV infection. Several human leukocyte cell lines were tested for their ability to support virus replication and were tested for a correlation with the expression of Ia antigen. Only cell lines expressing Ia antigen on more than about 5% of the total population produced new progeny virus. Ia-expressing T cells that spontaneously replicated HSV without any mitogenic prestimulation were found to occur in variable numbers in human cord blood. It is suggested, that such T cells, permissive for HSV replication, might contribute to an outspread of viral infection in vivo.
Mechanisms of contact photosensitivity in mice. IV. Antigen-specific suppressor T cells induced by preirradiation of photosensitizing site to UVB.
Authors: Takigawa M , Miyachi Y , Toda K , Yoshioka A 
Published: December 2022

Abstract
Mice were successfully contact photosensitized with 3,3',4',5-tetrachlorosalicylanilide (TCSA) plus black light irradiation. Pre-exposure of the photosensitizing site (ca 5 cm2) to UVB (280 to 320 nm; 400 mJ/cm2) rendered mice unresponsive to a challenge reaction. Cell transfer experiments demonstrated that the spleens from the nonreactive mice contained suppressor T cells (Ts) that were antigen-specific and that blocked the afferent limb of contact photosensitivity to TCSA. To exert suppressive functions, Ts required another population of cyclophosphamide-sensitive T cells that resided in the spleens of nonsensitized mice. The results provide evidence that UVB-induced aberrant homeostasis of the skin caused a marked suppression of immune system that is associated with the generation of Ts.
T cell regulation of B cell activation: MHC-restricted T augmenting cells enhance the B cell responses mediated by MHC-restricted cloned T helper cells.
Authors: Asano Y , Hodes R J 
Published: December 2022

Abstract
The present studies demonstrated that unprimed populations of Lyt-1+2- T cells are able to augment the responses generated by optimal numbers of antigen-specific and MHC-restricted cloned TH cells. The TA cells function early in the course of B cell responses. Responses mediated by (A X B)F1 (B + accessory) cells and parentA restricted cloned TH cells are augmented by TA cells from (A X B)F1 leads to parentA radiation bone marrow chimeras, but not by TA cells from (A X B)F1 leads to parentB chimeras. Thus, TA cell activation and function are MHC-restricted, but this restriction is not related to recognition of genotypically expressed B cell and/or accessory cell MHC products alone. Rather, TA cell function is intimately related to the MHC-restricted interaction between TH cells and responding (B + accessory) cells. Specifically, it was shown that TH cell interaction with B cells via an MHC-restricted and carrier-hapten-linked pathway is required for the function of TA cells expressing the same MHC restriction. Moreover, neither MHC homology nor TH cell recognition of MHC determinants on TA cells is required for TA cell function, and the activity of TA cells is not demonstrably influenced by non-MHC genes. It was further demonstrated that the function of cloned TH cells in B cell activation consists of at least two distinct components, one is radiosensitive and the other is radioresistant. TA cells are able either to replace the radiosensitive function of cloned TH cells directly or to bypass this requirement through an alternative pathway.
The cytotoxic effector cells in preparations of adherent mononuclear cells from human peripheral blood.
Authors: Freundlich B , Trinchieri G , Perussia B , Zurier R B 
Published: December 2022

Abstract
We have characterized the effector cells present in fresh adherent cell preparations from human peripheral blood that are responsible for the lysis of K562 and IgG antibody-sensitized P815Y target tumor cells. Purified lymphocytes and monocytes, separated from adherent cell preparations by using techniques that utilized light scatter properties and reactivity of the cells with monoclonal antibodies, were used as effectors for the spontaneous and antibody-dependent cytotoxicity. The role of monocytes was also studied at the single cell level. Our results indicate that when a subpopulation of adherent cells that is B73.1+ (NK cells), B44.1- (non-monocyte), with light scatter characteristics of lymphocytes, is removed from the total adherent cell population, the resultant purified monocytes are unable to spontaneously kill K562 target cells. This data suggests that fresh unstimulated adherent cell cytotoxicity against K562 cells is mediated by lymphocyte contamination in these preparations and that the cell responsible for this killing is probably the NK cell. In contrast antibody-dependent cellular cytotoxicity against P815Y target cells is mediated by monocytes and lymphocytes.
In vivo effects of antibodies against a high frequency idiotype of anti-DNA antibodies in MRL mice.
Authors: Teitelbaum D , Rauch J , Stollar B D , Schwartz R S 
Published: December 2022

Abstract
The in vivo effects of a rabbit antiserum against the dominant idiotype of MRL-lpr/lpr anti-DNA antibodies (termed H130) were studied in MRL-lpr/lpr, MRL/++, and BALB/c mice. Under the conditions we examined, the anti-idiotype did not suppress anti-DNA antibodies or the H130 idiotype in either MRL-lpr/lpr or MRL/++ mice. By contrast, MRL/++ and BALB/c mice responded to the antiserum by producing antibodies with the H130 idiotype. The increase in levels of the idiotype was accompanied by a rise in anti-DNA antibodies only when F(ab')2 fragments of the rabbit antiserum were administered. Only about 10% of the induced H130+ immunoglobulins were anti-DNA antibodies. An immunoregulatory disturbance in MRL-lpr/lpr mice may account for their resistance to anti-idiotypic antibodies. Treatment of autoimmune diseases with anti-idiotypes may have the undesired effect of augmenting the production of autoantibodies.
TRF requirements for in vitro PFC responses to SRBC and R36a. I. TRF is distinct from IL 2 but indistinguishable from polyclonal BCSF.
Authors: Eisenberg L , Prystowsky M B , Dick R F , Sosman J A , Fitch F W , Quintáns J 
Published: December 2022

Abstract
In vitro PFC responses to the thymus-independent (TI) antigen Streptococcus pneumoniae R36a require T cell replacing factor(s) (TRF). This requirement for TRF is as significant as for the thymus-dependent (TD) antigen SRBC. TRF is shown to be distinct from IL 2 by the following observations: 1) culture supernatants from the cloned T cell line L2, collected over an 8-day period after allogeneic stimulation, transiently contain IL 2 activity but maintain high levels of TRF activity throughout 192 hr; 2) L2V, a variant subclone of L2, produces much higher levels of TRF activity than the parental line but no detectable IL 2 activity; 3) the addition of IL2+, TRF- supernatants from the T cell hybridoma FS6-14.13 does not affect the L2V SF-driven PFC responses to R36a or SRBC; and 4) the addition of contaminating T cells to cultures containing T cell-depleted spleen cells, L2V SF, and antigen does not affect the PFC response. TRF does appear to be indistinguishable from polyclonal B cell stimulating factor (BCSF), which stimulates polyclonal PFC responses in the absence of antigen, mitogen, or anti-Ig. The TRF and BCSF activities of L2V SF could not be separated by ion-exchange, hydrophobic-interaction, and gel-filtration chromatography. TRF and BCSF have an apparent m.w. of approximately 40,000.
Antibody 3G8, specific for the human neutrophil Fc receptor, reacts with natural killer cells.
Authors: Perussia B , Trinchieri G 
Published: December 2022

Abstract
Antibody 3G8 reacts with the receptor for the Fc fragment of aggregated IgG present on the majority of neutrophilic granulocytes and on a small proportion of lymphocytes. In this report, we compare the pattern of reactivity of antibody 3G8 on peripheral blood lymphocytes (PBL) and on polymorphonuclear leukocytes (PMN) with that of antibody B73.1, which reacts with the Fc receptor of natural killer (NK) cells or with a molecule functionally associated with it. We show that 3G8 reacts with the same PBL subset detected by antibody B73.1 and is responsible for virtually all NK cytotoxic activity. The lymphocyte subset recognized by the two antibodies has the morphology of large granular lymphocytes and includes neither B nor T cells. Our results indicate that NK cells and PMN express the same Fc receptor for immune complexes, and that B73.1 and 3G8 recognize on the same receptor two distinct epitopes that are preferentially expressed on NK cells and on PMN, respectively.
Glioblastoma cells release interleukin 1 and factors inhibiting interleukin 2-mediated effects.
Authors: Fontana A , Hengartner H , de Tribolet N , Weber E 
Published: December 2022

Abstract
Studies were designed to investigate whether the cellular immunodeficiency state observed in human glioblastoma patients could be due to inhibitory factors released by the tumor cells. Cultured human glioblastoma cells were found to secrete an interleukin 1-like factor (m.w. 22,000) and a factor (m.w. 97,000) that inhibits interleukin 2 (IL 2)-dependent T cell mechanisms. This is demonstrated by its inhibitory effect on the IL 2-induced proliferation of T cell clones and on the induction of alloreactive cytotoxic T cells in mixed lymphocyte cultures. Additionally the glioblastoma cell-derived 97,000-m.w. factor inhibited growth of neuroblasts but not of fibroblasts and thus shares the characteristics of the neuroblast growth inhibition factor (NGIF) previously detected in the supernatant of fetal rat glia cell cultures. If released by glioblastoma cells in vivo, the factor may contribute to impaired immunosurveillance and to the cellular immunodeficiency state detected in the patients.
Antigen-independent activation of memory cytotoxic T cells by interleukin 2.
Authors: Lefrancois L , Klein J R , Paetkau V , Bevan M J 
Published: December 2022

Abstract
Culture supernatants from mitogen- or antigen-activated murine spleen cells are capable of causing reexpression of specific cytolytic activity from inactive memory cytotoxic T lymphocytes (CTL) in the absence of the original priming antigen. We have demonstrated that memory CTL from cytolytically inactive day 14 MLC cells are induced to reexpress high levels of specific cytotoxic activity after incubation with IL 2. Highly purified IL 2 was shown to induce levels of lytic activity comparable with that induced by supernatants from secondary mixed lymphocyte cultures (secondary MLC SN), suggesting that only IL 2 is necessary for the reactivation process. Moreover, only Lyt-2+ cells are necessary for reactivation inasmuch as inactive MLC cells depleted of Lyt-1+ cells by treatment with antibody and complement, followed by FACS selection of Lyt-2+ cells, were efficiently reactivated by IL 2. Because IL 2 is considered a proliferative signal, we examined whether proliferation was requisite for reactivation of memory CTL by IL 2. In the presence of cytosine arabinoside, which effectively inhibited proliferation, IL 2 was capable of reactivating memory CTL as efficiently as antigen, thus implying a differentiative role for IL 2 in secondary CTL activation. Reactivation of CTL by IL 2 and antigen appear to be functionally distinct events, because antigen but not IL 2 could trigger immune interferon release, although either IL 2 or antigen induced high levels of cytotoxicity. We propose that resting, memory CTL retain a heightened level of expression of IL 2 receptors as compared with naive CTL precursors, and thus are able to respond directly to exogenous IL 2. The consequences of this are proliferation and reexpression of specific killing activity, but this signal is not sufficient to induce immune interferon secretion. Rather, it appears that a signal via the antigen receptor is necessary for release of this lymphokine.
Interferon inhibits prostaglandin biosynthesis in macrophages: effects on arachidonic acid metabolism.
Authors: Boraschi D , Censini S , Bartalini M , Scapigliati G , Barbarulli G , Vicenzi E , Donati M B , Tagliabue A 
Published: December 2022

Abstract
Mouse resident peritoneal M phi produced considerable amounts of PGE when triggered in vitro with soluble or particulate stimuli. Preexposure of M phi to IFN-beta dramatically decreased PGE production. This effect depended on the dose of IFN-beta used and was abolished by anti-IFN-beta globulin. In addition to PGE, other AA metabolites of the cyclooxygenase pathway, namely TXB2 and 6-keto PGF1 alpha, were decreased in IFN-beta-treated M phi. However, IFN-beta did not have any effect on cyclooxygenase activity of M phi, indicating that an earlier step of PG biosynthesis was likely to be the target of its inhibitory action. Indeed, the release of radioactive compounds from M phi prelabeled with [14C]AA was strongly impaired by IFN-beta, suggesting that IFN-beta would decrease PG production in M phi by blocking phospholipase activation. The possibility that the IFN-beta effect on phospholipase could be mediated through the increase of the intracellular levels of cAMP is suggested.
Characterization of a B lymphoblastoid cell line mutant that secretes HLA-A2.
Authors: Krangel M S , Pious D , Strominger J L 
Published: December 2022

Abstract
HLA-A2 antigen mutants were obtained previously from the B lymphoblastoid cell line T5-1 by mutagenesis followed by immunoselection. Here we present biochemical studies of one particular mutant, clone 8.14.1. These cells synthesize two forms of HLA-A2: a minor form, which remains cell-associated at all times, and an abundant form, which is secreted. The former appears by SDS-PAGE to be slightly larger than T5-1 HLA-A2, whereas the latter appears to be 4000 to 5000 daltons smaller. In vitro translation and in vivo pulse-chase studies suggest that these species are not related to each other by post-translational processing. Proteolytic digestion studies localize the resulting structural alteration in the mobility difference between wild-type and secreted HLA-A2 to a region near the carboxy terminus of the HLA-A2 heavy chain; however, their extreme carboxy termini appear similar, if not identical. We suggest that the secreted form may result from a pattern of RNA splicing in which the exon encoding the hydrophobic, membrane-spanning region is frequently deleted.
Glycoproteins of 210,000 and 130,000 m.w. on activated T cells: cell distribution and antigenic relation to components on resting cells and T cell lines.
Authors: Hemler M E , Sanchez-Madrid F , Flotte T J , Krensky A M , Burakoff S J , Bhan A K , Springer T A , Strominger J L 
Published: December 2022

Abstract
A glycoprotein complex of 210,000 and 130,000 m.w., found on mitogen or alloantigen-stimulated human T cells and not on other hematopoietic cells, has been defined by a monoclonal antibody (Mab). The components of this complex are a subset of a larger family of proteins (210,000, 165,000 and 130,000 m.w.) defined by a second Mab. In a panel of hematopoietic cell lines and cell types, only activated T cells (including the cell line HUT-102) express the 210,000/130,000 complex and these cells also express the IL 2 receptor, a characteristic marker for activated T cells. The 210,000/130,000 m.w. complex (reactive with the Mab TS2/7) is present on all long-term activated T cells, including both the OKT4 and OKT8 subsets. The 210,000 m.w. subunit is expressed only on activated T cells. Other lymphoid cells express either the 130,000 m.w. subunit alone (unactivated lymphocytes, thymocytes, HUT-78) or the 130,000 subunit together with a 165,000 subunit (MOLT-4, HSB, and other leukemic T cell lines). The 210,000/130,000 m.w., 165,000/130,000 m.w. and 130,000 m.w. complexes are antigenically related in that all share reactivity with the Mab A- 1A5 . Among non-lymphoid hematopoietic cells and cell lines, none express the 210,000 m.w. chain; adherent cells (monocytes) and myeloid cell lines each express single proteins of 130,000 to 155,000 m.w. Granulocytes and red blood cells are negative and platelets express multiple bands (165,000 and 140,000 m.w.). Immunoperoxidase staining of tissue sections showed that a broad range of tissues and cell types had material cross-reactive with the lymphoid 130,000 m.w. protein. However, only a discrete subset of those tissues and cells including blood vessel walls, connective tissue, smooth muscle, kidney mesangial cells, and some non-cellular matrix tissue, had material cross-reactive with the 210,000 m.w. protein on activated T lymphocytes.
Primary structural variation among serologically indistinguishable DS antigens: the MB3-bearing molecule in DR4 cells differs from the MB3-bearing molecule in DR5 cells.
Authors: Giles R C , Hurley C K , Capra J D 
Published: December 2022

Abstract
HLA-DS molecules bearing the MB3 supertypic specificity have been isolated from two DR4 and two DR5 homozygous cell lines by using the monoclonal antibody IVD12 . Limited amino-terminal amino acid sequence analysis of these molecules demonstrates polymorphism of the HLA-DS subregion. Although the distribution of amino-terminal tyrosine residues in the alpha-chains of all IVD12 -reactive molecules was identical, amino-terminal amino acid sequence differences existed between DS beta-chains isolated from these two groups of cell lines bearing different DR specificities. These studies indicate that two DS molecules bearing the same serologic determinant ( MB3 ), although similar to one another, may be structurally distinct.
Suppression of the immune response to Listeria monocytogenes. I. Immune complexes inhibit resistance.
Authors: Virgin H W , Unanue E R 
Published: December 2022

Abstract
Murine infection with the facultative intracellular pathogen Listeria monocytogenes was studied as a model of cell-mediated immunity. Overwhelming lethal infection with Listeria developed when mice were given a secondary challenge with a protein antigen at the same time as Listeria infection. Three days after infection, mice immunized with ovalbumin and then challenged with Listeria and ovalbumin had up to 2.1(10)6 times as many viable Listeria organisms in their spleens as mice challenged only with Listeria. The suppressive effect of secondary challenge with a protein antigen was found to be antigen-specific, transient, and not dependent on route of challenge with either Listeria or ovalbumin. Secondary challenge with a protein antigen suppressed both the primary and the secondary responses to Listeria. Immune serum, or affinity-purified antibody, was found to transfer the suppressive effect to nonimmune mice. These findings demonstrate that acute formation of immune complexes causes a transient state of high susceptibility to infection with an intracellular pathogen. Possible mechanisms for, and implications of, these findings are discussed.