bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of the J11d marker on peripheral T lymphocytes of MRL-lpr/lpr mice.
Authors: Seth A , Pyle R H , Nagarkatti M , Nagarkatti P S 
Published: December 2022

Abstract
MRL-lpr/lpr (lpr) mice spontaneously develop massive lymphadenopathy resulting from the expansion of a unique population of Thy-1+ cells which are CD4- and CD8- (double negative) and the nature of which is not clear. The antibody J11d has been shown to define a differentiation Ag found on immature thymocytes but not on mature and functional peripheral CD4+ or CD8+ T cells. To analyze the possible relationship between the lpr double-negative T cells and the thymocytes, we investigated the simultaneous expression of J11d and Thy 1 Ag on the double-negative lpr lymph node cells by using two-color immunofluorescent staining technique. We observed that lpr mice at 3 to 4 weeks of age, before the onset of lymphadenopathy, did not have significant numbers (less than 4%) of J11d+ T cells in the periphery, similar to the number found in the control MRL +/+ mice. However, with increasing age of approximately 8 to 10 weeks and coinciding with the appearance of lymphadenopathy, a significant number (approximately 35%) of J11d+ Thy-1+ cells started appearing in the periphery of lpr mice and was maintained until the mice died at 20 to 24 weeks of age. The J11d+ T cells belonged to the abnormal double-negative T cell pool, inasmuch as J11d+ CD4+ or J11d+ CD8+ cells were absent in the lymph nodes of 20-wk-old lpr mice. Furthermore, 20-wk-old lpr mice demonstrated increased numbers (approximately 41%) of double-negative T cells in the thymus, a significant proportion of which were J11d+. In contrast, the 20-wk-old +/+ mice or 4-wk-old lpr mice had only 4% double-negative T cells in the thymus. The present study suggests that a significant number of peripheral double-negative T cells of lpr mice bear the immature thymic differentiation Ag J11d. The possibility that the accumulation of double-negative T cells results from abnormal peripheralization of double-negative J11d+ thymocytes, before complete differentiation into CD4+ or CD8+ T cells, is discussed.
IL-4 regulates differentiation and proliferation of human precursor B cells.
Authors: Hofman F M , Brock M , Taylor C R , Lyons B 
Published: December 2022

Abstract
The mechanism by which precursor and pre-B cells undergo differentiation is unclear; however, it is known that growth factors play an important role in this maturation process. The lymphokine, IL-4 has been shown to increase expression of class II Ag on B cells and induce B cell proliferation. In the murine system, IL-4 induced differentiation of precursor B cells into pre-B cells. In order to analyze growth factors on B cell development we have established an in vitro culture system for human bone marrow cells. We found that in the presence of IL-4, normal human precursor and pre-B cells can be induced to differentiate in the absence of cell proliferation with four days of culture. Furthermore, IL-4 depressed proliferation induced by supernatant from a T cell line. The differentiation was measured by an increase in both the number of cytoplasmic mu and surface IgM-positive cells. The effect of IL-4 on precursor and pre-B cell differentiation was detected as soon as 14 h of exposure to the lymphokine in the absence of an adherent feeder layer. These data suggest that IL-4 directly affects the differentiation process of normal human precursor and pre-B cells, and may antagonistically affect cell proliferation.
Immunoglobulin heavy H chain isotypes in a teleost fish.
Authors: Lobb C J , Olson M O 
Published: December 2022

Abstract
Three mouse mAb were derived which identified different populations of the approximately 700,000-Da tetrameric Ig of channel catfish (Ictalurus punctatus). Immunoprecipitation analyses using the three mAb in various combinations showed that the catfish Ig population identified by each mAb was antigenically distinct. Each Ig population contained both classes of catfish L chains (F and G). Solid-phase binding assays indicated that the mAbs preferentially identified H chains rather than L chains. Comparative peptide mapping analyses of the H chains defined by each mAb indicated that H chains were different, although each had the same apparent mass (approximately 70,000 Da). This structural distinction was not based upon allotypic variation because the analysis of the serum from individual catfish showed the presence of each H chain in fish examined. Therefore, the different H chains represent different isotypes; each representing approximately 20% of the total serum Ig. There is at least one undefined additional H chain isotype found in the serum Ig population. Partial sequence information was obtained on the first variable framework region (FR1) of two of the three H chain isotypes. These results indicated that the variable region associated with each isotype was heterogeneous; two and sometimes three different residues were represented in the majority of positions. The sequence information also showed that the FR1 of one H chain was distinct from the other; there was less than a 50% match of the primary residues. The analyses suggest that the V region genes which code for the FR1 are differently associated with each H chain isotype. Finally, the relative levels of the three H chain isotypes were monitored during the temporal immune response of individual catfish to the dinitrophenyl hapten. These results indicated that one H chain isotype was preferentially expressed early in the immune response (approximately 3 wk) and remained the predominantly expressed isotype during the humoral immune response.
Specific H chain junctional diversity may be required for non-T15 antibodies to bind phosphorylcholine.
Authors: Feeney A J , Clarke S H , Mosier D E 
Published: December 2022

Abstract
The secondary antibody response of mice to phosphorylcholine (PC) shows a markedly different clonal profile than the primary response. In particular, the T15 antibodies that dominate the primary response are a minor part of secondary IgG antibodies, whereas 511 and 603 antibodies become a more prominent part of the PC-specific secondary response. These three anti-PC families differ only in L chain usage. We partially sequenced the IgH chain mRNA of a series of secondary T15 and 511 hybridomas to determine the role of somatic mutation and affinity maturation in these changes in clonal profile. None of the sequenced T15 antibodies showed somatic mutations or affinity increases. In contrast, all of the 511 antibodies had extensive somatic mutation and most had significantly increased affinity for nitrophenyl-PC. The failure of T15-expressing B cells to contribute to the secondary IgG response thus is likely to be explained by their inability to undergo (or tolerate) substantial somatic mutation and affinity maturation. We also noted that all 511 antibodies sequenced by us or others had an extra amino acid encoded at the VH-D junction by either N region addition or diversity of VH-D joining. Published sequences also show a 603 family-specific change at the VH-D junction. The frequency with which these changes, which appear obligate for PC binding, occur may determine the under-representation of these clonotypes in the primary anti-PC response. The affinity maturation in 511 antibodies after somatic mutation appears to account for their expansion in the secondary response.
Histamine release from human basophils by synthetic block co-polymers composed of polyoxyethylene and polyoxypropylene and synergy with immunologic and non-immunologic stimuli.
Authors: Atkinson T P , Smith T F , Hunter R L 
Published: December 2022

Abstract
Co-polymers composed of polyoxyethylene and polyoxypropylene have been shown previously to trigger histamine release from mouse peritoneal mast cells; this property quantitatively is directly related to the ionophorous ability of these compounds to cause a functional exchange of intracellular K+ for extracellular Na+ across the cell membrane. We investigated the effect of an inflammatory copolymer, T130R2, on human basophils. The data demonstrate that T130R2 can cause calcium-dependent histamine release from human basophils in vitro. Further, at concentrations that do not cause histamine release, this co-polymer markedly augments release by suboptimal concentrations of the lectin Con A or anti-IgE antibody and the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate but not the calcium ionophore A23187. Thus, these co-polymers induce mediator release from cells of both rodents and humans. In both instances it is likely that calcium-dependent cell triggering is the result of an influx of sodium ions with concomitant depolarization of the transmembrane potential. In common with the calcium ionophore A23187, the co-polymer T130R2 has the ability to synergize with stimuli which trigger the IgE receptor as well as those which directly activate the cellular calcium- and phospholipid-dependent protein kinase.
A newly characterized HLA-DP beta-chain allele. Evidence for DP beta heterogeneity within the DPw4 specificity.
Authors: Lair B , Alber C , Yu W Y , Watts R , Bahl M , Karr R W 
Published: December 2022

Abstract
cDNA clones corresponding to the DPw4 alpha- and DPw4 beta-chains were isolated from a cDNA library prepared from a DPw4 homozygous cell line, their nucleotide sequences were determined, and the corresponding amino acid sequences were deduced. This DPw4 alpha-chain is identical to the conserved DP alpha-chains from DPw4 and DPw2 haplotypes, although the DPw4 beta-chain (referred to as DPw4b beta) differs from all reported DP beta-chain sequences. The DPw4b beta-chain differs from the reported DPw4 beta sequence (referred to as DPw4a beta) at three amino acid positions in the first domain (36, 55, and 56). The DPw4b beta-chain sequence differs from the DPw2 beta-chain sequence only at position 69 in the first domain, suggesting that the lysine at position 69 in DPw4b beta and the glutamic acid at position 69 in DPw2 beta contribute to the epitopes that define "DPw4-ness" and "DPw2-ness," respectively. In addition, the patterns of sequence identities and differences among the DPw4b beta-, DPw4a beta-, DPw2 beta-, and DPw3 beta-chains suggest that the DPw4b beta sequence arose via a gene conversion event or a point mutation. The I-LR1 mAb, which was previously found to bind only to DPw2, DPw3, and DR5 molecules, binds to an L cell transfectant expressing the DPw4 alpha:DPw4b beta molecule. The DPw4b beta sequence provides the first evidence for structural heterogeneity within the DPw4 specificity.
Remethylation at sites 5' of the murine Lyt-2 gene in association with shutdown of Lyt-2 expression.
Authors: Carbone A M , Marrack P , Kappler J W 
Published: December 2022

Abstract
We have used hybridomas made by fusing the Lyt-2- AKR thymoma, BW5147, to Lyt-2+ SJL/J lymph node cells to study the regulation of Lyt-2 expression. Fusions of this type yielded hybridomas, the majority of which failed to express Lyt-2. In the minority of hybridomas that did express surface Lyt-2, expression was transient and greatly diminished in terms of molecules of Lyt-2 per cell. Lack of Lyt-2 expression was not due to loss of the gene encoding this cell surface molecule; rather, negative regulation of Lyt-2 appeared to be at the level of transcription (i.e., no Lyt-2 transcripts were detected in these hybridomas). We have shown that the Lyt-2 gene is undermethylated in normal Lyt-2+ T cells, whereas the gene is heavily methylated in Lyt-2- liver cells and in BW5147. Loss of Lyt-2 expression in (BW5147 x Lyt-2+ SJL/J lymph node cell) hybridomas was associated with remethylation of DNA within the Lyt-2 gene and at sites 5' of the Lyt-2 gene.
Production of a fibronectin-associated lymphokine by cloned mouse T cells.
Authors: Godfrey H P , Canfield L S , Kindler H L , Angadi C V , Tomasek J J , Goodman J W 
Published: December 2022

Abstract
Azobenzenearsonate-specific cloned mouse T cells able to transfer delayed hypersensitivity reactions in vivo produced macrophage agglutination factor (MaggF) after stimulation with mitogen or antigen in vitro. Mitogen (Con A) elicited MAggF production directly from T cells. Responses to Ag were Ag-specific, required syngeneic accessory cells in addition to T cells, and were independent of T cell fine specificity for azobenzenearsonate. Mouse MAggF shared a number of biochemical and immunochemical properties with the fibronectins (FN): 1) high Mr similar to that of plasma FN; 2) binding to gelatin, heparin, and polyclonal antibodies and mAb specific for cellular and plasma FN; 3) inhibition of activity in solution by monoclonal anti-human FN directed against plasma FN gelatin-binding domain; and 4) action on peritoneal exudate macrophages mediated through a FN-receptor cross reactive with one on human monocytes. MAggF production required active protein synthesis and was associated with significant increases in gelatin-binding immunoreactive FN (Mr 440 kDa on immunoblotting) in culture supernatants and T cell lysates. Metabolically labeled peptides could be precipitated by anti-FN from culture supernatants of activated T cells. Stimulated cultures contained significantly more cells with immunohistologically demonstrable cytoplasmic FN than unstimulated control cultures. We suggest that T cell FN is a distinct species of cellular FN which may play an important role in mediating delayed hypersensitivity inflammatory reactions in vivo.
Human recombinant IL-1 alters glucocorticoid receptor function in Reuber hepatoma cells.
Authors: Hill M R , Stith R D , McCallum R E 
Published: December 2022

Abstract
Exposure of Reuber hepatoma cells (RHC) to 30 and 300 fM human rIL-1 (hurIL-1) for 4 h significantly decreased cytosolic glucocorticoid binding. Scatchard analysis indicated that the 30 and 300 fM doses of hurIL-1 significantly decreased the Bmax (maximum number of available binding sites), but did not alter the Kd (affinity of the glucocorticoid receptor for ligand). The decrease in cytosolic glucocorticoid binding, expressed relative to cytosol protein, did not result from increased intracellular protein in hurIL-1-treated RHC. In addition, the receptor binding reaction in RHC treated with 300 fM hurIL-1 could be resolved only by computer application of a three-parameter model. Sucrose density gradient ultracentrifugation analysis confirmed significantly less untransformed (8 to 10S) receptor-ligand complexes in hurIL-1-treated RHC, which is biologically significant because hurIL-1 (300 fM) also inhibited the glucocorticoid induction of the gluconeogenic enzyme, phosphoenolpyruvate carboxykinase (PEPCK). Altered transformation of the receptor-ligand complex, a possible mechanism of action for hurIL-1-mediated inhibition of PEPCK induction, was examined. However, receptor transformation, verified by in vitro activation by high salt (0.3 M KCl) of glucocorticoid receptor-ligand complexes and subsequent sucrose density gradient ultracentrifugation analysis, was not affected by hurIL-1. Furthermore, cytoplasmic glucocorticoid binding, determined in intact cell dexamethasone uptake experiments, was decreased in hurIL-1-treated RHC. The decrease in cytoplasmic glucocorticoid binding was reflected subsequently in decreased nuclear binding. The results support our hypothesis that, during acute infection and inflammation, mediators alter metabolic pathways in the liver by interfering with glucocorticoid action.
IL-6/BSF-2 functions as a killer helper factor in the in vitro induction of cytotoxic T cells.
Authors: Okada M , Kitahara M , Kishimoto S , Matsuda T , Hirano T , Kishimoto T 
Published: December 2022

Abstract
rIL-6/B cell stimulatory factor 2 was found to augment CTL generation from mature as well as immature human T cells stimulated with UV-treated allogeneic cells. rIL-6 also acted on peanut agglutinin-positive murine thymocytes and Lyt-2-positive splenic T cells to give rise to CTL. rIL-6 alone could not induce CTL generation, the presence of IL-2 during the early phase of culture period was found to be essential for the IL-6 activity in the induction of CTL. The effect of rIL-6 was not mediated by the induction of IL-2 inasmuch as rIL-6 did not augment IL-2 production in MLC and anti-IL-2 antibody could not neutralize IL-6 activity. rIL-6 augmented CTL generation even when added 72 h after the initiation of cultures. The enhancing activity of rIL-6 could be neutralized with anti-IL-6 antibodies even when added 72 h after the initiation of cultures. The present data indicate that IL-6 acts in the late phase of CTL generation.
The characterization of four monoclonal antibodies specific for mouse IL-5 and development of mouse and human IL-5 enzyme-linked immunosorbent.
Authors: Schumacher J H , O'Garra A , Shrader B , van Kimmenade A , Bond M W , Mosmann T R , Coffman R L 
Published: December 2022

Abstract
Four rat mAb directed against mouse IL-5 have been characterized by their ability to remove and neutralize mouse IL-5 activity in various bioassays. All four mAb absorbed IL-5 activity from solution. Although all were able to neutralize mouse IL-5 bioactivity, two were significantly more effective. These two were also able to neutralize the activity of mouse IL-5 delivered to B cells during a cognate-linked interaction with a Th cell clone. A two-site sandwich ELISA specific for mouse IL-5 was developed by using pairs of mAb. The mouse IL-5 ELISA is capable of detecting natural or mouse rIL-5 in supernatants, crude bacterial lysates, and high concentrations of mouse serum, and has a detection limit of less than 20 pg. Two of these antibodies cross-reacted with and neutralized human rIL-5, and one of these was used for development of an ELISA for human IL-5.
A rabbit Ig lambda L chain C region gene encoding C21 allotopes.
Authors: Duvoisin R M , Hayzer D J , Belin D , Jaton J C 
Published: December 2022

Abstract
Southern blot analyses of germ-line DNA obtained from rabbits expressing lambda chains of C7 and/or C21 allotypes were performed with a rabbit C lambda region-specific probe; a 12-kbp EcoRI- and a 2-kbp BamHI-hybridizing fragment were detected only in the DNA from rabbits expressing the C21 allotype. The 12-kbp EcoRI fragment was cloned and shown to contain two C lambda region-encoding genes in the same orientation. Each is preceded by a J lambda gene segment. Nonamer-12-bp spacer-heptamer recombination signal sequences were found 5' of each J lambda segment, and splicing signals were identified at the 3' ends of the J lambda segments and the 5' ends of the corresponding C lambda genes. The C lambda 5 gene, which exhibits a sequence identical with that found in several cDNA clones, is carried by the 2-kbp BamHI fragment missing from the genomic DNA of rabbits which do not express the C21 allotype. The second C lambda gene, C lambda 6, lies 3' of C lambda 5, in a 1.6-kbp BamHI fragment which is present in genomic DNAs of all tested rabbits, irrespective of their phenotype. Its sequence is identical with that found in one cDNA clone and differs from that of C lambda 5 in 17 base positions resulting in four amino acid substitutions. A fragment of a cDNA, with a J-C region sequence identical with that encoded by the J lambda 5-C lambda 5 gene pair, was subcloned into a plasmid expression vector. The resulting polypeptide product could be specifically immunoprecipitated by anti-C21 but not anti-C7 alloantisera, showing that some, if not all, C21 allotopes are encoded by the C lambda 5 gene. In contrast, the C lambda 6 gene product was not precipitable, either by anti-C7 or by anti-C21 alloantisera, although it was readily immunoprecipitated by a goat anti-rabbit lambda chain antiserum.
Disruption of the internal thioester bond in the third component of complement (C3) results in the exposure of neodeterminants also present on activation products of C3. An analysis with monoclonal antibodies.
Authors: Hack C E , Paardekooper J , Smeenk R J , Abbink J , Eerenberg A J , Nuijens J H 
Published: December 2022

Abstract
Hydrolysis of the internal thioester bond in native C3 is thought to be a key event in initiating the alternative pathway of C activation, because the resulting C3(H2O) acquires "C3b-like" properties. Therefore, disruption of the internal thioester bond is probably accompanied by conformational changes in the C3 molecule. In this study, we demonstrate that such conformational changes indeed occur; 7 of the 19 mAb raised against C3 or C3 activation products recognized epitopes exposed on C3(H2O) but not on native C3. One of these epitopes is located on the C3a part, three on the C3c part, and another three on the C3d,g part. Because the 7 mAb bound equally well to C3 incubated either with MgCl2 or with methylamine (which primarily disrupts the thioester), the conformational changes detected by the mAb apparently occur after disruption of the thioester. Furthermore, the epitopes were also present on the corresponding C3 activation products. Immunoblotting experiments revealed that the epitopes for the three anti-C3d,g mAb were located on the C3d part, C-terminal to the thioester. The epitopes for 2 of the 3 anti-C3c mAb were located on the C-terminal alpha-chain fragment of C3c. Thus, this study provides immunochemical evidence for the biologic resemblance between C3(H2O) and C3 activation products. Implications of these findings for the activation process of C3 are discussed.
Regulation of complement factor H synthesis in U-937 cells by phorbol myristate acetate, lipopolysaccharide, and IL-1.
Authors: Minta J O 
Published: December 2022

Abstract
The capacity of the human monocyte cell line U-937 to synthesize complement factor H was examined. The kinetics of secretion of factor H into cell culture supernatant were followed by a sensitive solid phase RIA capable of measuring 0.1 ng of protein. Daily secretion of factor H was low and almost linear and was approximately 3 ng of factor H per 10(6) cells. Factor H synthesis was inhibited by cycloheximide but returned to the levels seen in untreated cultures after removal of the inhibitor. LPS and IL-1 both effected a time- and dose-dependent enhancement of factor H synthesis. Induction of U-937 cells with PMA to differentiate into macrophage-like cells also resulted in increased factor H synthesis. RIA of cell lysates, immunofluorescence microscopy, as well as FACS analysis all revealed that factor H Ag was also associated with the U-937 cell membrane. The population of U-937 cells bearing membrane-associated factor H was decreased from 77 to 43% after stimulation for 48 h with LPS (1 microgram/ml). [35S]Methionine metabolic labeling and SDS-PAGE analysis of factor H immunoprecipitates from unstimulated and stimulated culture supernatants and cell lysates demonstrated a major polypeptide, m.w. 150,000, and a minor component, m.w. 42,000. Western blot analysis of factor H in fresh normal plasma also detected both 150,000 and 42,000 m.w. factor H proteins. This is in agreement with the recent demonstration of a 4.4- and 1.8-kb mRNA for factor H in human liver. These data demonstrate that U-937 cells synthesize factor H that is structurally and antigenically similar to factor H in normal plasma. The exact nature of the membrane-bound factor H and its functions and mechanism of attachment to the cell membrane remain to be elucidated.