bluuebunny/crossref_metadata_2025_split huggingface dataset:
IL-2 induction of IL-1 beta mRNA expression in monocytes. Regulation by agents that block second messenger pathways.
Authors: Kovacs E J , Brock B , Varesio L , Young H A 
Published: December 2022

Abstract
We have previously shown that in mixed cultures of PBL incubation with human rIL-2 induces the rapid expression of IL-1 alpha and IL-1 beta mRNA. Because studies have demonstrated that IL-2R can be expressed on the surface of human peripheral blood monocytes, we chose to investigate whether IL-1 beta mRNA could be directly induced in purified human monocytes by treatment with Il-2 and, if so, to analyze the second messenger pathways by which it may be controlled. Human monocytes do not spontaneously express IL-1 beta mRNA, but can express the gene as soon as 1 h after treatment with IL-2. The level of IL-1 beta mRNA induced by IL-2 at 5 h in human monocytes was about one-fourth that induced by LPS. LPS induction of IL-1 beta mRNA in human monocytes can be blocked by either an inhibitor of protein kinase C (PKc) 1-(5-isoquinolinesulfonyl)-2-methylpiperazine or an inhibitor of calcium/calmodulin (CaM) kinase N-(6-aminohexyl) 5-chloro-1-naphthalenesulfonamide, suggesting that both PKc and CaM kinase are involved in transducing signals initiated by LPS. In contrast, IL-2 induction of IL-1 beta mRNA expression is blocked only by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine, suggesting that PKc, and not CaM kinase, is activated by IL-2. These data suggest that overlapping but distinct second messenger pathways are involved in the transduction of signals initiated by IL-2 and LPS.
Mouse hepatitis virus 3 pathogenicity expressed by a lytic viral infection in bone marrow 14.8+ mu+ B lymphocyte subpopulations.
Authors: Jolicoeur P , Lamontagne L 
Published: December 2022

Abstract
Mouse hepatitis virus type 3 (MHV3) provides an excellent model for studying viral-B lymphocyte interaction in the immune system, which plays an important role in the outcome of an acute disease. Bone marrow B lymphocyte subpopulations, at various times postinfection, were studied in genetically C57BL/6 and resistant A/J mice, infected with pathogenic L2-MHV3 and its nonpathogenic variant, YAC-MHV3. B lineage cell subpopulations were identified by double immunofluorescence assays using mAb of terminal deoxynucleotidyl transferase, 14.8 and cytoplasmic (cu) or surface (su) Ig mu-chains. Results revealed diminished percentage and absolute number in the bone marrow 14.8+ mu+ B lymphocyte subpopulations, including pre-B (cu+ su-) and B (cu+ su+) cells of L2-MHV3-infected susceptible C57BL/6 mice; whereas, slight or no increase was evident in the cell subpopulations of L2-MHV3 infected resistant A/J mice or in YAC-MHV3 infected in both strains of mice. Abnormal large-sized forms of the 14.8+ mu+ cells occurred, at 48-h postinfection, in L2-MHV3-infected susceptible C57BL/6 mice only. In contrast, no change in the percentage and absolute number of precursor cells (terminal deoxynucleotidyl transferase positive) and pre pre-B cells (14.8+ mu-) were detected in all infected mice. In vitro L2-MHV3 infection of C57BL/6 bone marrow purified B lineage cell subpopulations showed that pre-B (cu+ su-) and B (cu+ su+) cells became abnormally large in size and depleted in number as a result of a productive and lytic viral replication. Low L2-MHV3 viral replication occurred in these cell subpopulations of A/J mice but no YAC-MHV3 virus was produced in the cells of both strains of mice. Pre pre-B (14.8+ mu-) cells in both strains were not permissive to L2-MHV3 or YAC-MHV3 viral replication. These results are discussed with regard to the role of humoral immunodeficiency in the pathogenic process.
Characterization of the thymus leukemia (TL) product encoded by the BALB/c T3c gene by DNA-mediated gene transfer. Comparison to the T13c product and BALB/c leukemia TL.
Authors: Chorney M J , Mashimo H , Bushkin Y , Nathenson S G 
Published: December 2022

Abstract
Using DNA-mediated gene transfer, we have studied the TL protein products encoded by both the T3c and T13c BALB/c genes. Biochemically, the proteins differed in their m.w. and pI points; serologically, although both molecules were recognized by TL alloantiserum, only the T13c protein was recognized by monoclonal TL antibodies. Interestingly, both proteins were serologically and immunochemically recognized by leukemia-specific TL.4 antiserum. The quantity of cell surface T13 was significantly greater than T3 possibly due to the less efficient splicing of T3 transcripts in the L cell nucleus; both genes directed the synthesis of cytoplasmic RNA containing an unspliced intron 3 as assessed by S1 analysis. In toto, the results suggest that T3c is similar or perhaps identical with the novel TL product previously identified on the surface of certain x-ray-induced BALB/c leukemias.
Asparagine-linked glycosylation of cytochrome b558 large subunit varies in different human phagocytic cells.
Authors: Kleinberg M E , Rotrosen D , Malech H L 
Published: December 2022

Abstract
Cytochrome b558, an essential component of the respiratory burst of phagocytic cells, is the terminal electron donor to molecular oxygen that results in the formation of superoxide anion (O2-.). It is an integral membrane heterodimer that in neutrophils consists of a 22-kDa small subunit and a highly glycosylated 91-kDa large subunit. Identical core proteins often differ in glycosylation in different cell types and with some membrane glycoproteins, the glycosylation state may markedly affect function. In the present study, antisera reactive with cytochrome b558 large subunit was used for immunoblot analysis of the glycosylation pattern of this subunit from different types of phagocytic cells. Striking variability in the apparent m.w. of this broadly banding subunit was detected in five different phagocytic cell types (neutrophils 78,000 to 93,000; eosinophils 74,000 to 115,000; monocytes 82,000 to 99,000; dibutyryl cyclic AMP-induced HL-60 cells 79,000 to 103,000; dimethyl sulfoxide-induced HL-60 cells 77,000 to 110,000). However, after complete cleavage of N-linked oligosaccharides with endoglycosidase F, the core peptide of cytochrome b558 large subunit from these different cell types had the same Mr (58,000). Inhibition of N-glycosylation with tunicamycin in differentiating HL-60 cells resulted in the synthesis of immunoreactive protein of the same m.w. and banding pattern as seen after endoglycosidase F cleavage. These tunicamycin treated cells retained some capacity to generate superoxide anion when stimulated with PMA. We conclude that the identity of the N-linked oligosaccharides of the cytochrome b558 large subunit differ in various phagocytic cells. All N-linked glycans on cytochrome b558 in all cell types examined were of the complex type as defined by resistance to endoglycosidase H cleavage. N-linked glycosylation of the cytochrome b558 large subunit may not be essential for activation of the respiratory burst.
Mast cells chemotax to laminin with enhancement after IgE-mediated activation.
Authors: Thompson H L , Burbelo P D , Yamada Y , Kleinman H K , Metcalfe D D 
Published: December 2022

Abstract
The increase of mast cells at sites of tissue inflammation suggests the production of local factors chemotactic for mast cells. In this report, we demonstrate that the murine mast cell line PT18 and primary mouse bone marrow-derived mast cells chemotax to the basement membrane glycoprotein laminin, and that the synthetic laminin A chain-derived peptide, PA22-2, represents a region of laminin that contains a major chemoattractant site. Mast cell chemotaxis to laminin is enhanced after activation of mast cells by the calcium ionophore, A23187, or PMA and by sensitization of the cells with IgE followed by exposure to antigen. Chemotaxis is not increased in the presence of IL-3 and is independent of mast cell degranulation, as histamine release did not occur when cells were activated with PMA. Mast cell chemotaxis to laminin and its enhancement by IgE-dependent mast cell activation provides a mechanism by which these cells may be attracted to sites of tissue injury. Such activity may be particularly relevant in the response of host tissues to inflammation accompanying parasitic infestations, allergic reactions, and wound healing.
Induction of human lymphokine-activated killer cells by IFN-alpha and IFN-gamma.
Authors: Ellis T M , McKenzie R S , Simms P E , Helfrich B A , Fisher R I 
Published: December 2022

Abstract
By traditional definitions, NK cells can be activated by cytokines to exhibit two functionally distinct levels of cytotoxicity. Whereas IL-2-mediated activation of NK cells leads to the development of lymphokine-activated killer (LAK) cytotoxicity, characterized by the acquisition of cytolytic activity against NK-resistant targets, IFN-treated NK cells become activated without the acquisition of novel cytolytic specificities. In this study we show that NK cells activated by 18 to 24 h of stimulation with either IFN-alpha or IFN-gamma do acquire LAK cytolytic activity, demonstrated by the ability of IFN-treated PBMC to lyse NK-resistant COLO 205 cells as well as fresh tumor targets. The level of IFN-alpha-induced LAK activity was significantly greater than that induced by IFN-gamma, although IL-2-induced LAK activity was considerably greater than IFN-alpha-induced LAK cytotoxicity. Maximal IFN-induced LAK cytotoxicity occurred after 24 h of culture, and occurred with the use of IFN-alpha at 500 U/ml and IFN-gamma at 1000 U/ml. Whereas neutralizing antibody experiments demonstrated that IFN-alpha-induced LAK activation did not involve the participation of endogenously produced IL-2, the partial inhibition (63%) of IFN-gamma-induced LAK cytotoxicity by anti-IL-2 and of IL-2-induced LAK by anti-IFN-gamma (33.3%) indicates that the induction of LAK cytotoxicity by either of these individual cytokines involves the endogenous production and participation of the other cytokine. Similar to IL-2-induced LAK cells, phenotypic analysis revealed that IFN-alpha/gamma LAK cells were Leu-19+, although the Leu 19"dim"+ subset exhibited greater IFN-induced LAK activity than the Leu-19"bright"+ subset. The results of this study clearly demonstrate that IFN-alpha and IFN-gamma induce classic LAK activity and IFN-gamma plays a participatory role in the optimal induction of LAK cells by IL-2.
Polymorphisms in human H chain V region genes from the VHIII gene family.
Authors: Souroujon M C , Rubinstein D B , Schwartz R S , Barrett K J 
Published: December 2022

Abstract
Polymorphisms of the Ig H chain V region (VH) genes were examined with probes from the coding and flanking regions of a gene from the largest VH gene family, VHIII. The 5'-flanking probe gave the simplest pattern and revealed the largest number of polymorphic fragments. Analysis of unrelated individuals and of families identified five polymorphic loci. Two alleles were detected for each of two of the loci, whereas a polymorphic band was scored as present or absent for the other three loci. The polymorphic fragments segregated in the expected Mendelian fashion and parental haplotypes could be assigned in all cases. Comparison of the patterns obtained with the flanking and coding region probes suggests that the human VHIII gene family is highly polymorphic and may contain several hundred V genes. This method, as well as the polymorphism detected, can be used to investigate the organization and germ-line variation of H chain V genes and their inheritance in normal individuals and in individuals with immunologic disorders.
A novel VHDJH to JH joining that induces H chain production in an Ig-null immature B cell line.
Authors: Komori T , Sugiyama H , Kishimoto S 
Published: December 2022

Abstract
A novel Ig H chain gene rearrangement, a VHDJH to JH joining, was observed in an Ig-null immature B cell line. The preexisting, nonproductive VHDJH complex was replaced by the productive VHJH complex which was generated by the novel joining between the rearranged VH and a germ line JH gene. This VHDJH to JH joining is thought to be a site-specific recombinational event mediated by a putative recombination signal sequence, CACAGCC-12-base-GCAAGAAAG, embedded in the rearranged VH gene including the N region. This sequence might be a novel recombination signal sequence, which had not yet been reported, for so-called recombinase.
Fine specificity of T cell recognition of the same peptide in association with different I-A molecules.
Authors: Brett S J , Cease K B , Ouyang C S , Berzofsky J A 
Published: December 2022

Abstract
The fine specificity of the response of T cell clones derived from B10.BR and B10.S congenic mouse strains restricted by I-Ak and I-As molecules, respectively, and which recognize the same 17 amino acid sequence (102-118) of myoglobin, has been investigated and compared with that of T cell clones specific for the same peptide with I-A.d The critical amino acid residues within the 102-118 region of myoglobin required for stimulation of I-Ak-and I-As-restricted T cell clones specific for this determinant were compared using a panel of synthetic peptide analogs. Residues 109, 113, and 116 were critical for stimulation of clones from both haplotypes, although the precise fine specificity varied, even among clones using the same restriction molecule. Residues 109 and 116 are also critical for stimulation of myoglobin-specific I-Ad-restricted clones (Berkower, I., L. A. Matis, G.K. Buckenmeyer, F.R. N. Gurd, D. L. Longo, and J. A. Berzofsky. J. Immunol. 132:1370, 1984). There was also considerable overlap in the size of the minimal determinant necessary for full activity: 106-118 for B10.BR and B10.D2 (Cease, K. B., I. Berkower, J. York-Jolley, and J. A. Berzofsky. J. Exp. Med. 164:1779, 1986) clones and 102-117 for B10.S clones. Despite this similarity in fine specificity, T cell clones were genetically restricted and could not be stimulated with the 102-118 peptide presented by Ia molecules of other haplotypes that could also present this epitope to syngeneic clones. These results suggest that binding of an immunogenic peptide to class II molecules is not sufficient to ensure recognition by a given T cell antigen receptor specific for the peptide, but do not indicate whether the major histocompatibility complex molecules interact directly with the T cell antigen receptor or induce a different recognizable conformation of the peptide.
Analysis of epitope expression and the functional repertoire of recombinant complement receptor 2 (CR2/CD21) in mouse and human cells.
Authors: Carel J C , Frazier B , Ley T J , Holers V M 
Published: December 2022

Abstract
We transfected human complement receptor 2 (CR2/CD21) cDNA containing eukaryotic expression constructs into CR2-negative mouse L cells and human K562 erythroleukemia cells. We subsequently selected stably transformed cells that expressed human CR2, as assessed by flow microfluorimetry analysis and immunoprecipitation of 125I-labeled surface membranes using the monoclonal anti-CR2 antibody, HB5. Utilizing flow microfluorimetry analysis, epitopes recognized by anti-CR2 mAb HB5, OKB7, B2, and four other anti-CR2 antibodies were detected on CR2 expressing transfectants but not parental cells. In addition, CR2 expressing transfected cells efficiently formed rosettes with sheep erythrocyte intermediates bearing human C3bi and C3d, but not C4b or C3b, consistent with the known ligand specificity of CR2. CR2 containing transfectants were also demonstrated to specifically bind EBV. Infection with EBV of CR2 expressing L cells and K562 cells resulted in mean expression of Epstein-Barr nuclear Ag (EBNA) at 48 h in 0.35% of CR2 expressing L cells and 3.7% of CR2 expressing K562 cells. Parental L cells and K562 cells did not express EBNA after EBV infection. These results indicate that CR2 alone is sufficient to transfer both C and EBV receptor functions to heterologous cells. In addition, expression of EBNA was found to be significantly higher in human K562 than mouse L cells, both expressing the same recombinant receptor. These results suggest that mechanisms other than CR2 binding lead to inefficient EBV infection and/or EBNA synthesis in mouse fibroblasts.
Destruction of pancreatic islet cells by cytotoxic T lymphocytes in nonobese diabetic mice.
Authors: Nagata M , Yokono K , Hayakawa M , Kawase Y , Hatamori N , Ogawa W , Yonezawa K , Shii K , Baba S 
Published: December 2022

Abstract
Proliferation of islet-associated leukocytes occurred when isolated islets from 20-wk-old female nonobese diabetic (NOD) mice were cultured with 10 U/ml rIL-2 for 7 days. Co-culture of these leukocytes with freshly isolated islets from 6- to 8-wk-old NOD donors in the presence of 1 U/ml rIL-2 produced islet structural deformation within 24 h and islet cytolysis within 48 h. Three lines of evidence suggest that these leukocytes were composed mainly of CTL specific for islet cells. First, morphologically, these proliferating cells adhered to NOD islets at 6 h and killed islets within 48 h of culture, but these phenomena could not be observed in the other tissues from NOD mice. These islet-derived cells were cytotoxic to NOD islet cells in a 51Cr-release assay, whereas no appreciable cytotoxicity was observed when NOD Con A-induced splenic blasts or fibroblasts were used as targets. Second, a flow cytometric analysis showed that these cells consisted of 97% Thy-1.2, 69% Lyt-2, 8% L3T4, and 4% asialo-GM1-positive cells, whereas Mac-1-positive cells could not be seen in these assays. After treatment with anti-Thy-1.2 or Lyt-2 mAb and C, these cells lost their activity to lyse NOD islet cells. However, these cells still had a full killing activity after the depletion of L3T4 or asialo GM1-positive cells. Third, islet cells from BALB/c, DBA/2, and B10.GD mice which share the same H-2K Ag with NOD mice were susceptible to cytolytic activity of these cells, whereas islet cells from NON, C57BL/6, C57BL/10, and C3H mice remained intact. Furthermore, anti-Kd antibody was capable of blocking this cytolysis. These results suggest that CTL expressing Thy-1.2 and Lyt-2 phenotypes appear to recognize the islet cell Ag with the restriction of MHC class I Kd, and then destroy NOD islet cells.
The structure of the rabbit macrophage defensin genes and their organ-specific expression.
Authors: Ganz T , Rayner J R , Valore E V , Tumolo A , Talmadge K , Fuller F 
Published: December 2022

Abstract
Defensins are a family of microbicidal and cytotoxic peptides abundant in the lysosomal granules of mammalian phagocytes. We present the cDNA and genomic sequences of two rabbit defensins, macrophage cationic peptides MCP-1 and MCP-2. Their cDNA and genomic sequences are highly homologous, reflecting the homology between the two defensins (32 of 33 amino acids). The MCP genes are closely linked (within 13 kb) suggesting that they evolved by a recent tandem gene duplication. Their cDNA sequences indicate that the peptides are synthesized as 95 amino acid prepro-MCPs, consistent with their lysosomal location. The MCP genes are separated into three exons encoding distinct domains: the 5' untranslated region, the prepropeptide domain, and the mature defensin sequence. Fully developed polymorphonuclear leukocytes, short-lived phagocytes with limited capacity for protein and nucleic acid synthesis, contained MCPs but lacked MCP mRNA. MCP mRNA was found in bone marrow and spleen, organs which contained immature polymorphonuclear leukocytes. MCP and MCP mRNA were detected in lung macrophages, but not in macrophages from other organs, nor in monocytes, the putative macrophage precursors. In macrophages, the expression of MCPs appears to be a marker of lung-specific differentiation.
Effect of membrane phospholipids on activation of the alternative complement pathway.
Authors: Mold C 
Published: December 2022

Abstract
Although some of the membrane glycoproteins that serve as activators or regulators of C activation have been identified, the influence of membrane lipids has not been studied extensively. A model of alternative C pathway activation was established using liposomes composed of cholesterol and synthetic phospholipids. Liposomes containing phosphatidylcholine (PC) as the sole phospholipid did not activate C as measured by C3 binding after incubation in normal human serum containing 2.5 mM MgCl2 and 10 mM EGTA. When phosphatidylethanolamine (PE) was included as 20% or more of the phospholipid, C3 binding was observed. C3 binding to liposomes was inhibited by salicylhydroxamic acid indicating binding through the C3 thioester bond. The phospholipid composition did not influence C3 binding to liposomes in an unregulated system of C3, B, D, and P indicating equivalent C3b binding sites on activating and nonactivating liposomes. When the regulatory proteins H and I were added to the other components, liposomes containing PE bound three times more C3 than PC liposomes suggesting that the phospholipid affects C3 regulation. This was tested directly in a radiolabeled H binding assay. In the presence of equal amounts of C3b, PC liposomes showed a greater number of high affinity H binding sites than PE liposomes. Using different PE derivatives, C activation could be directly related to the phospholipid polar head group. Liposomes containing PE, trinitrophenyl-PE or monomethyl-PE did activate the alternative C pathway, whereas those containing dimethyl-PE, PC, or phosphatidylserine did not. These studies provide evidence that primary and secondary amino groups on lipid membranes can decrease the interaction between H and C3b and provide sites for alternative pathway activation.
Cognate interactions between helper T cells and B cells. III. Contact-dependent, lymphokine-independent induction of B cell cycle entry by activated helper T cells.
Authors: Noelle R J , McCann J , Marshall L , Bartlett W C 
Published: December 2022

Abstract
An Ag-specific, IL-2-dependent Th clone induced the growth of B cells in a class II-restricted, Ag-specific, IL-2-dependent manner. The formation of stable Th-3.1-B cell conjugates was restricted by Ag and class II MHC. After activation of Th-3.1 by insolubilized anti-T3 (Th-3.1T3), Th-3.1T3 induced the growth of B cells in a class II unrestricted, Ag nonspecific manner. The formation of stable conjugates between Th-3.1T3 and B cells was also class II unrestricted and Ag nonspecific. Although the interaction of Th-3.1T3 and B cells was class II unrestricted, the interaction was inhibited by the combination of anti-IA and anti-IE mAb. This suggested that monomorphic domains of class II MHC molecules were involved in Th-3.1T3-B cell interaction. Fixed Th-3.1T3 but not fixed resting Th-3.1 induced B cell cycle entry, as measured by an increase in B cell RNA synthesis. Trypsin-treatment of Th-3.1T3 before fixation reduced their ability to activate B cells, indicating that cell surface proteins on Th-3.1T3 were required for enhanced B cell RNA synthesis. Anti-IL-4, anti-IL-2R, or anti-IFN-gamma did not affect the ability of Th-3.1T3 to induce heightened B cell RNA synthesis. Progression into S phase by B cells activated with fixed Th-3.1T3 was supported by the addition of soluble factors. When stimulated with fixed Th-3.1T3, EL4 supernatant (SN) enhanced B cell DNA synthesis. Depletion of IL-4, but not IL-2, from EL4 SN ablated its supportive capabilities. IL-4 alone was completely ineffective in supporting entry into S phase. Therefore, IL-4 and another activity(ies) in EL4 SN were necessary for B cell cycle progression into S phase. Taken together, these data suggest that after Th activation, Th cell surface proteins are expressed that mediate the binding of Th to B cells via recognition of nonpolymorphic domains of class II MHC molecules. Contact of Th-3.1T3 with B cells, not lymphokines, results in the entry of B cells into the cell cycle and heightened B cell lymphokine responsiveness. The addition of exogenous lymphokines supports the progression of Th-3.1T3-activated B cells into S phase.