bluuebunny/crossref_metadata_2025_split huggingface dataset:
An antigen-specific T8+ human clone of cells with a nonspecific augmenting function on the T4 cell-B cell helper interaction.
Authors: Brines R D , Sia D Y , Lehner T 
Published: December 2022

Abstract
We isolated a T8+ T3+ Ia+ clone of cells from the peripheral blood mononuclear cells of a healthy subject. The clone was expanded and maintained with autologous feeder cells, interleukin 2, and a streptococcal antigen. The T8+ clone of cells responded specifically to the streptococcal antigen, in the absence of accessory cells, and released a soluble factor. Both the cloned cells and the corresponding soluble factor expressed augmenting helper but not suppressor activity. The augmenting helper activity for B cell antibody synthesis was demonstrable only in the presence of autologous T4 cells. Although stimulation of the T8+ cloned cells was antigen-specific, the resulting soluble factor elicited nonspecific antibody synthesis in the presence of T4 and B cells. The T8+ cloned cell-derived factor was adsorbed by B cells but not by T4 cells. Preliminary studies suggest that the factor has the properties of a B cell growth factor. We suggest that the T8+ population consists of functionally heterogeneous cell subsets, some that have suppressor function and others that augment the T4+ helper-inducer activity in B cell antibody synthesis.
Signal requirement for interleukin-1-dependent interleukin 2 production by a human leukemia-derived HSB.2 subclone.
Authors: Mukaida N , Kasahara T , Yagisawa H , Shioiri-Nakano K , Kawai T 
Published: December 2022

Abstract
We have previously established subclones from human leukemia-derived HSB.2 cell line that produced high levels of interleukin (IL) 2 when stimulated with phytohemagglutinin (PHA) and IL-1. Herein, we investigated the signal requirement for IL-2 production, particularly concerning the role of IL-1 in this system. PHA but not IL-1 rendered marked protein kinase C (PKC) activation and IL-2 production induced by PHA plus IL-1 was totally abrogated by a potent PKC inhibitor, H-7. Concomitantly, PHA alone caused marked Ca2+ influx, whereas IL-1 neither induced Ca2+ influx nor augmented PHA-induced Ca2+ influx. As expected, a signal delivered by PHA could be substituted by phorbol 12-myristate 13-acetate (PMA) and ionomycin while IL-1 was still indispensable, indicating that at least three signals, i.e., those delivered by IL-1 as well as PKC activation and Ca2+ influx were required for optimal IL-2 production. Kinetic study indicated that while PMA and ionomycin should be added at the initiation of culture, delayed addition of IL-1 up to 4 hr later induced even higher levels of IL-2 production, demonstrating the requirement for IL-1 after PKC activation and Ca2+ influx. In this system, it was revealed that IL-1 was not involved in PKC activation, Ca2+ influx, and breakdown of phosphatidylinositols. Whereas PMA, ionomycin, and IL-1 stimulated high levels of IL-2 production, those combinations of signals did not induce breakdown of phosphatidylinositols. It should be noted that IL-2 production induced by these three signals seemed to bypass hydrolysis of phosphatidylinositols in contrast to PHA plus IL-1 stimulation that was accompanied with a marked breakdown of phosphatidylinositols.
Synergistic and antagonistic effects of recombinant human interleukin (IL) 3, IL-1 alpha, granulocyte and macrophage colony-stimulating factors (G-CSF and M-CSF) on the growth of GM-CSF-dependent leukemic cell lines.
Authors: Santoli D , Yang Y C , Clark S C , Kreider B L , Caracciolo D , Rovera G 
Published: December 2022

Abstract
Three human leukemia cell lines (TALL-101, AML-193, and MV4-11) that require granulocyte/macrophage-colony stimulating factor (GM-CSF) for growth in a chemically defined medium were examined for their response to recombinant human (rh) cytokines. Either rh interleukin (IL)-3 or rhGM-CSF alone supported the long term growth of all three cell lines, and the two growth factors acted synergistically to stimulate the proliferation of the early T lymphoblastic leukemia (TALL-101) and of the monocytic leukemia (AML-193) cells. However, IL-3 antagonized the proliferation of the biphenotypic B-myelomonocytic leukemia (MV4-11) cells in the presence of GM-CSF when both factors were used at very low concentrations. The rh granulocyte (G)-CSF independently supported the long and short term growth of AML-193 and MV4-11, respectively, and synergized with GM-CSF in inducing proliferation of these cells. By contrast, G-CSF did not stimulate TALL-101 cell growth and antagonized the effect of GM-CSF such that proliferation was arrested. Although neither rh macrophage (M)-CSF nor rhIL-1 alpha independently promoted proliferation of the three leukemia cell lines, these cytokines were able to either up- or down-regulate the GM-CSF-dependent growth of these cells. Taken together, these data demonstrate that leukemic cells often require the synergistic action of several cytokines for optimal growth, whereas other combinations of factors may be growth-inhibitory. This raises the possibility that multiple hemopoietic growth factors sustain or control leukemic cell proliferation also in vivo. In addition, the observation the G-CSF, M-CSF, and IL-1 alpha can, in some cases, arrest cell proliferation without inducing differentiation suggests that the programs of proliferative arrest and differentiation in leukemic cells can be dissociated.
Reduced receptor binding by a human interferon-gamma fragment lacking 11 carboxyl-terminal amino acids.
Authors: Leinikki P O , Calderon J , Luquette M H , Schreiber R D 
Published: December 2022

Abstract
Treatment of recombinant human interferon-gamma (IFN-gamma) with either 1) the arginine-specific proteases clostripain or submaxillaris protease or 2) the broadly specific enzyme pronase produced a stable fragment with m.w. of 15,500. Structural analysis showed that the cleavage occurred between residues 129 and 130 and thus produced a fragment lacking only 11 carboxyl-terminal amino acids. The fragmented and untreated molecules showed identical amino-terminal amino acid sequences and were equally reactive with either polyclonal or monoclonal anti-IFN-gamma. IFN-gamma lacking carboxyl-terminal amino acids displayed a 1000- to 2000-fold reduction in its capacity to bind to cellular IFN-gamma receptors at 4 degrees C. Functionally the fragment showed a 50-fold reduction in its ability to induce antiviral activity in fibroblasts and a 10-fold reduction in its ability to induce Fc receptors on the human histiocytic lymphoma cell line U937. These results thus suggest that the carboxyl terminus of human IFN-gamma contributes significantly to the formation of the receptor-binding site of the molecule.
The role of Ca2+ in activation of mature cytotoxic T lymphocytes for lysis.
Authors: Ostergaard H , Clark W R 
Published: December 2022

Abstract
We carried out a detailed analysis of the requirement for Ca2+ in the lysis of target cells by cloned cytotoxic T lymphocytes (CTL). In direct, antigen-specific lysis we always observed an influx of Ca2+ into the CTL concomitant with target cell binding. However, we never observed an increase in CTL Ca2+ content during lectin-mediated lysis, or nonspecific lysis by phorbol myristate acetate-induced CTL. We found that in all three types of lysis (direct, lectin-mediated lysis, C or phorbol myristate acetate-induced) the requirement for Ca2+ in lysis was dictated by the target cell used; the same CTL can kill one target cell in the absence of detectable Ca2+, and absolutely require Ca2+ for the lysis of another target cell. Target cell killing, when it occurred in the absence of Ca2+, was accompanied by microtubule organizing center reorientation in the CTL, showing that this function is not uniformly Ca2+ dependent. These results provide further evidence that Ca2+ is not always required for activation of the lytic pathway in CTL, although Ca2+ may be absolutely required for other CTL functions such as interleukin production or expression of the interleukin 2 receptor.
The ability of cytotoxic T cells to recognize HLA-A2.1 or HLA-B7 antigens expressed on murine cells correlates with their epitope specificity.
Authors: Bernhard E J , Le A X , Yannelli J R , Holterman M J , Hogan K T , Parham P , Engelhard V H 
Published: December 2022

Abstract
Two groups of human and murine cytotoxic T lymphocyte (CTL) clones specific for human leukocyte antigen (HLA)-A2 or -B7 can be distinguished based on their ability to kill murine transfectants expressing these molecules. The clones which do not recognize murine transfectants exhibited greatly reduced conjugate formation with these cells, indicating that the inability to lyse these cells occurs in recognition and binding. No systematic differences in inhibitory titer between the two types of CTL clones were seen with anti-CD8 (Lyt-2), anti-LFA-1, or monoclonal antibodies against HLA class I molecules. However, blocking with anti-HLA class I monoclonal antibodies suggested that different CTL clones recognized spatially separate epitopes on HLA-A2 and -B7. In addition, a correlation between the inability to recognize murine transfectants and fine specificity was seen. Eight of nine clones which did not lyse murine transfectants also failed to recognize human cells expressing HLA-A2.2 or -A2.3. In contrast only 5 of 12 clones which lysed transfectants failed to recognize the variant molecules. Analogous data were obtained with human CTL clones raised against HLA-A2.1. These findings suggest that CTL clones that do not lyse murine cells expressing appropriate antigens recognize epitopes that have been altered or lost as a consequence of expression on the murine cell surface. It is suggested that the loss of HLA-associated epitopes on the murine cell surface may be due to differences between mouse and human cells in the processing or presentation of class I-associated peptides.
Physiology of natural killer cells. In vivo regulation of progenitors by interleukin 3.
Authors: Kalland T 
Published: December 2022

Abstract
Adoptive transfer of bone marrow cells to syngeneic lethally irradiated C57BL/6 mice was used to study the maturation of natural killer (NK) cells from their progenitors. The NK progenitor cell was found to be asialomonoganglioside-negative, (aGM1-) Thy-1-, NK-1-, Ly-1-, Ly-2-, and L3T4-. The NK cells emerging from the bone marrow grafts were aGM1+, NK-1+, Thy-1+/-, Ly-1-, Ly-2-, and L3T4- and to have a target specter similar to that of NK cells isolated from the spleen of normal mice. The regulatory role of interleukin 2 (IL-2) and interleukin 3 (IL-3) for the maturation of NK cells was examined by exposure of the bone marrow cells to the lymphokines in vitro before bone marrow grafting or by treatment of bone marrow-grafted mice with lymphokines through s.c. implanted miniosmotic pumps. IL-3 antagonized the IL-2-induced maturation of NK cells in vitro and strongly inhibited the generation of NK cells after adoptive transfer of bone marrow cells in vivo. The suppressive effect of IL-3 was evident throughout the treatment period (8 or 16 days) but was apparently reversible because NK activity returned to control levels within 8 days after cessation of treatment. The inhibition of cytotoxic activity was accompanied by a reduced appearance of cells with the NK phenotypic markers aGM1 or NK-1, indicating that not only the cytotoxic activity of NK cells but also their actual formation was inhibited. Concomitantly, a moderate increase in cells expressing the T cell marker L3T4 and an increased proliferative response to the T cell mitogen concanavalin A was observed. A direct estimate of the effect of IL-3 on the frequency of NK cell progenitors was obtained by limiting dilution analysis of bone marrow cells at day 8 after bone marrow transplantation. The estimated minimal frequency of NK cell progenitors was reduced from 1/11,800 in control to 1/41,900 in IL-3-exposed mice. IL-3 may take part in the homeostasis of NK cells by the down-regulation of their progenitors.
Histamine-producing cell-stimulating activity. Interleukin 3 and granulocyte-macrophage colony-stimulating factor induce de novo synthesis of histidine decarboxylase in hemopoietic progenitor cells.
Authors: Schneider E , Pollard H , Lepault F , Guy-Grand D , Minkowski M , Dy M 
Published: December 2022

Abstract
Both interleukin 3 (IL-3) and granulocyte-macrophage colony-stimulating factor (GM-CSF) induce increased histamine production by murine hemopoietic cells. Histidine-free culture conditions or addition of alpha-fluoromethylhistidine, an irreversible inhibitor of histidine decarboxylase, completely abrogate this phenomenon, indicating that increased histamine levels result from an augmentation of the rate of its synthesis. L-Histidine decarboxylase (HDC) (EC 4.1.1.22) activity is detected in normal bone marrow cell lysates. It is markedly increased following incubation of the cells with IL-3 or GM-CSF. The cells responding by the most important enhancement of HDC activity are located in the less dense layers of a discontinuous Ficoll gradient containing the majority of the hemopoietic progenitor cell types, such as colony-forming units (spleen), granulocyte-macrophage colony-forming cells, and mast cell precursors. In comparison with other HDC-containing cell populations tested, the enzymatic activity contained in these cells is particularly high after IL-3 or GM-CSF treatment and similar to the HDC levels observed in murine fetal liver. The time course of IL-3 and GM-CSF-induced HDC activation at comparable concentrations is slightly different. In response to GM-CSF, HDC activation is more rapid, with a significant enhancement after 4 hr of incubation, as compared with IL-3-induced HDC activation. Moreover, in the latter case the activation increases more progressively up to 48 hr of incubation, whereas GM-CSF-induced increase of HDC activity reaches a plateau more rapidly. In addition, maximal increase in histamine production in response to IL-3 is always higher than in response to GM-CSF. Moreover, the simultaneous presence of both factors at optimal concentration induces only a partially cumulative effect. These results suggest that IL-3 and GM-CSF induce HDC activation in two distinct ways, possibly reflecting the involvement of distinct target cells. However, both mediators act by inducing the transcription of the HDC gene and de novo synthesis of this enzyme since actinomycin D or cycloheximide abolish GM-CSF-or IL-3-induced histamine-producing cell-stimulating activity. This synthesis is independent from cell proliferation as demonstrated by the lack of effect of bone marrow cell irradiation. Finally, the observation that cholera toxin, prostaglandin E2, and N6,2'-O-dibutyryl adenosine 3',5'-cyclic monophosphate mimic the effects of IL-3 and GM-CSF on bone marrow cell HDC suggests an involvement of cyclic adenosine monophosphate in factor-induced histamine-producing cell-stimulating activity.
Strain-dependent IgG subclass response patterns.
Authors: Slack J H 
Published: December 2022

Abstract
Previous studies have shown that antigens preferentially stimulate IgG subclasses. However, the immunologic processes responsible for the patterns of IgG subclasses stimulated by antigens are probably complex and are certainly unclear. To define some of the genetic controls of IgG subclass expression in mice, we have studied the patterns of IgG subclasses elicited by antigens in BALB/cAn, C57BL/6N, derived recombinant inbred strains, and derived Ig congenic strains. This study shows that both thymus-independent antigens and thymus-dependent antigens stimulate different patterns of IgG subclasses in BALB/cAn and C57BL/6N. Furthermore, analysis using recombinant inbred strains and Ig congenic strains shows that the patterns of IgG subclasses stimulated by all antigens are linked to Ig allotype. In contrast, only the IgG subclass patterns stimulated by thymus-dependent antigens are linked to major histocompatibility complex haplotype. This study also shows that the Ig allotype-linked controls of IgG subclass response patterns are located telomeric to a BAB14 intra-heavy chain variable region recombinant site. Therefore, this region of mouse chromosome 12 may contribute to the control of IgG subclass selection in the B cell.
The neutrophil glycoprotein Mo1 is an integral membrane protein of plasma membranes and specific granules.
Authors: Stevenson K B , Nauseef W M , Clark R A 
Published: December 2022

Abstract
The glycoprotein Mo1 has previously been demonstrated to be on the cell surface and in the specific granule fraction of neutrophils and to be translocated to the cell surface during degranulation. It is not known, however, whether Mo1 is an integral membrane protein or a soluble, intragranular constituent loosely associated with the specific granule membrane. Purified neutrophils were disrupted by nitrogen cavitation and separated on Percoll density gradients into four fractions enriched for azurophilic granules, specific granules, plasma membrane, and cytosol, respectively. The glycoproteins in these fractions were labeled with 3H-borohydride reduction, extracted with Triton X-114, and immunoprecipitated with 60.3, an anti-Mo1 monoclonal antibody Mo1 was detected only in the specific granule and plasma membrane fractions and partitioned exclusively into the detergent-rich fraction consistent with Mo1 being an integral membrane protein. In addition, treatment of specific granule membranes with a high salt, high urea buffer to remove absorbed or peripheral proteins failed to dissociate Mo1. These data support the hypothesis that Mo1 is an integral membrane protein of plasma and specific granule membranes in human neutrophils.
Differential expression of the c-myb proto-oncogene marks the pre-B cell/B cell junction in murine B lymphoid tumors.
Authors: Bender T P , Kuehl W M 
Published: December 2022

Abstract
A series of murine B lymphoid tumor cell lines which are representative of the pre-B cell, immature and mature B cell, and plasma cell stages of B cell development have been examined for expression of c-myb proto-oncogene mRNA. The pre-B cell lymphoma cell lines express equivalent high steady state levels of c-myb mRNA. In contrast, the B cell lymphoma and plasmacytoma cell lines express steady state c-myb mRNA at levels which are 0.005 to 0.1 times that of the pre-B cell lymphoma lines. These results correlate high levels of c-myb mRNA expression with the pre-B cell stage of development. Subclones of the 1881 pre-B cell lymphoma which express K light chain and are surface IgM-positive as well as two types of hybrid B lymphoid cell lines have been used to demonstrate that surface immunoglobulin expression is not sufficient to result in the down-regulation of c-myb mRNA levels or changes in the expression N-myc mRNA, lambda 5 mRNA, or the BP-1 surface antigen which are markers of the pre-B cell stage of development. Thus, changes in the expression of genes which are independent of immunoglobulin expression are associated with transition from the pre-B cell to the immature B cell stage of development.
Molecular cloning of the liver-specific rat F antigen.
Authors: Gershwin M E , Coppel R L , Bearer E , Peterson M G , Sturgess A , Mackay I R 
Published: December 2022

Abstract
F antigen is a 43-kDa widely conserved liver protein that has been intensively used in studies of immunogenicity and tolerance; two murine allotypes have been identified. Immunization of specific responder inbred strains with liver homogenates from the opposite allotype leads to precipitating antibody and cell-mediated immunity against F. The antibodies produced are autoantibodies as they react equally well with self. We have identified a cDNA clone from rat liver that reacts with alloantisera to F. The fused polypeptide produced by the clone was shown to correspond to F by several experiments. First, alloantisera to F antigen reacted with the cloned fused polypeptide, but not control recombinant clones. Second, mice immunized with the fused polypeptide generate an antibody response that reacts specifically with the 43-kDa protein of mouse liver homogenates and with highly purified F antigen. Finally, both anti-F allosera and sera from mice immunized with the fused polypeptide react with the same 43-kDa liver protein on two-dimensional immunoblots. The nucleotide and deduced amino acid sequence of the clone are presented and the sequence was found to have a significant homology with L28, an Escherichia coli ribosomal protein. The availability of recombinant F antigen will allow definitive questions to be addressed with respect to epitopes and specifically the identification of the T cell epitope which allows for autoimmune responses.
Differential expression of the human thymosin-beta 4 gene in lymphocytes, macrophages, and granulocytes.
Authors: Gondo H , Kudo J , White J W , Barr C , Selvanayagam P , Saunders G F 
Published: December 2022

Abstract
A cDNA clone encoding human thymosin-beta 4 was isolated from a cDNA library prepared from peripheral blood leukocytes of a patient with acute lymphocytic leukemia. This clone contained the entire coding sequence of 43 amino acid residues of thymosin-beta 4 and had an initiation codon and two termination codons. The amino acid and nucleotide sequences in the coding region were well conserved between rat and human. Nine of 132 nucleotides were different in the coding sequences (93% homology), but the deduced amino acid sequences were identical. No signal peptide was found in the deduced protein sequence. Human thymosin-beta 4 mRNA, approximately 830 nucleotides in length, was about 30 nucleotides larger than rat thymosin-beta 4 mRNA. Expression of the human thymosin-beta 4 gene in various primary myeloid and lymphoid malignant cells and in a few human hemopoietic cell lines was studied. Northern blot analyses of different neoplastic B lymphocytes revealed that steady state levels of thymosin-beta 4 mRNA varied as a function of differentiation stage. Thymosin-beta 4 mRNA levels were decreased in myeloma cells as are class II human leukocyte antigen, Fc receptor, and complement receptor, suggesting a relationship between thymosin-beta 4 and the immune response. Thymosin-beta 4 mRNA was more highly expressed in mature granulocytes than in immature blastic cells. Treatment of THP-1 cells, a human monocytic cell line, with recombinant human interferon-lambda reduced the levels of thymosin-beta 4 mRNA. Its level decreased after differentiation of THP-1 cells into Ia+ macrophages, but increased after differentiation of HL-60 cells into Ia- macrophages. The pattern of thymosin-beta 4 gene expression suggests that it may play a fundamental role in the host defense mechanism.
T lymphocyte response to bacteriophage lambda repressor cI protein. Recognition of the same peptide presented by Ia molecules of different haplotypes.
Authors: Lai M Z , Ross D T , Guillet J G , Briner T J , Gefter M L , Smith J A 
Published: December 2022

Abstract
The murine T cell response to bacteriophage lambda cI repressor protein has been investigated. Isolation and characterization of class II-restricted T cell hybridomas from BALB/c and A/J mice undergoing a primary response has revealed that a single region of the protein, residues 12-26, is the immunodominant site. Fine specificity analysis using truncated peptides (P12-24 and P15-26) reveals a great deal of heterogeneity at the clonal level of I-Ad-restricted T cells. I-Ek-restricted T cells are less heterogeneous in their reactivity toward P12-24 and P15-26, but show diversity in their responses to peptide analogues with substitution at Tyr22. The specificity difference between T cell hybridomas of I-Ad-restriction and I-Ek-restriction and the inhibition effect of different inactive peptides suggest that the same peptide is presented in different configurations by different Ia molecules. Further, no cross-reactivity can be detected between T cells of these two haplotypes, Ia molecules and Ia bound-peptides.