bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of human natural killing. I. The role of monocytes, interferon, and prostaglandins.
Authors: Koren H S , Anderson S J , Fischer D G , Copeland C S , Jensen P J 
Published: December 2022

Abstract
We have found that human endogenous natural killer activity as measured in a rapid 51Cr release assay is unaffected by the presence of monocytes. Moreover, stimulation of natural killer cells by poly I:C is independent of monocytes. In contrast, the presence of monocytes in a mixed population of mononuclear cells that have been stimulated by poly I:C suppresses NK activity. The suppression is shown to be partially reversible if indomethacin (10(-6) M) is added to the cultures during stimulation. Culture supernatants of monocytes stimulated with poly I:C are shown to contain PGE1 in a radioimmunoassay, and have NK inhibitory activity comparable to that obtained with exogenous PGE1 added to NK assays at a concentration range of 10(-7) to 10(-9) M. Culture supernatants from poly I:C-stimulated monocytes do not have detectable levels of antiviral activity. In contrast, plastic nonadherent cells stimulated with poly I:C produce significant levels of interferon (100 to 200 U/ml/2 x 10(6) cells) but almost undetectable amounts of PGE. Supernatants of nonadherent cells incubated with indomethacin (10(-6) M) alone augment NK activity. Taken together, the results suggest that stimulation of mononuclear cells with poly I:C is dependent on and regulated by the relative levels of interferon produced by lymphocytes and PGE produced by monocytes.
Myelogenous production and maturation of B lymphocytes in the mouse.
Authors: Landreth K S , Rosse C , Clagett J 
Published: December 2022

Abstract
Cells of the B lymphocyte lineage in young adult murine bone marrow were identified and resolved into compartments based on cell size and the expression of the mu heavy chain of IgM in the cytoplasm (cmu) or on the cell surface (smu). The proliferative status, renewal rate, and intercompartmental transit of cells through the defined compartments were determined using established protocols of in vivo tritiated thymidine (3H-TdR) administration, followed by radioautography of bone marrow smears. In addition, we specifically tested whether any of the defined cell compartments were derived from long-lived lymphocytes that are known to enter the marrow. Only large cells immediately incorporated the DNA precursor and both small cmu+ smu- and cmu+ smu+ cells were postmitotic lymphocytes. Large cmu+ smu- cells were found to be a rapid transit compartment in which the last mitosis of B lymphocyte differentiation takes place. All large cmu+ smu- cells divided only once, and both daughter cells entered the postmitotic small cmu+ smu- population. Large cmu+ smu- cells relied for their maintenance entirely on cell input from an Ig- progenitor compartment. Progenitors of cmu+ smu- large cells were not small lymphocytes, proliferated less rapidly than their descendants, and maintained the input of large cmu+ smu- cells for up to 40 hr. Approximately 70% of small cmu+ smu- cells were the immediate division products of large cmu+ smu- cells, whereas the remainder were derived from a precursor with no detectable mu synthesis. Small cmu+ smu+ cells were the maturation products of small cmu+ smu- cells. This conversion appeared to take place at random rather than as a function of postmitotic age. Renewal times for small cmu+ cells without or with detectable smu were calculated to be 48 and 96 hr, respectively. Only the cmu- smu+ compartment included long-lived cells. All other mu+ populations either proliferated or were replaced by newly produced cells. A conspicuous minor population of large smu+ B cells were detected, and the data relating to these were subjected to several interpretations. These observations provide insight into the origin and fate of B lineage precursors in the marrow and suggest a scheme for the terminal stages of B lymphocytes formation that is similar to the myelogenous production of other hemopoietic cells.
Purification from guinea pig erythrocyte stroma of a decay-accelerating factor for the classical c3 convertase, C4b,2a.
Authors: Nicholson-Weller A , Burge J , Austen K F 
Published: December 2022

Abstract
A protein with decay-accelerating activity for the classical C3 convertase, C4b2a, has been isolated on the basis of this function from guinea pig erythrocyte stroma. The isolation procedure for decay-accelerating factor of stroma (DAF-S) utilizes butanol extraction and chromatography on DEAE-Sephacel, hydroxylapatite, and phenyl Sepharose. Purified DAF-S has a m.w. of 60,000 and 65,000 on reduced and unreduced SDS gels, respectively, and exhibits m.w. of 30,000 and 175,000 on alkaline gradient gels, suggesting multiples of a 60,000-65,000 subunit. Purified DAF-S elicited a monospecific antiserum whose IgG fraction neutralized the decay-accelerating activity for C4b,2a affixed to 10(7) sheep erythrocytes (EAC1,4,2) in a dose-response fashion. The monospecific antiserum diluted up to 1:5120 agglutinated 1 x 10(6) guinea pig erythrocytes, but not sheep or human erythrocytes, suggesting that DAF-S, an integral membrane protein, has species-specific antigens that are expressed on the surface of the guinea pig erythrocyte.
Enumeration of T lymphocyte subsets by monoclonal antibodies in young and aged humans.
Authors: Nagel J E , Chrest F J , Adler W H 
Published: December 2022

Abstract
The percentage and absolute number of peripheral blood mononuclear cells reactive with monoclonal antibodies identifying mature thymocytes and T cells (T3+), helper/inducer cells (T4+), and suppressor/cytotoxic cells (T8+) was determined in 19 young (mean age 35 yr) and 31 elderly (mean age 72 yr) individuals. The percent representation but not the absolute number of T cells (T3+) declined significantly (p less than 0.001) in the elderly, and the decline was attributable to both an absolute and relative decrease in the representation of the subpopulation of cytotoxic/suppressor (T8+) cells. The percentage and number of helper/inducer (T4+) T cells was comparable in both age groups.
Lymphokines and aging: interleukin-2 production and activity in aged animals.
Authors: Thoman M L , Weigle W O 
Published: December 2022

Abstract
The capacity of aged animals to produce and respond to the T cell-replacing factor, interleukin-2 (IL-2), has been examined. IL-2 activity in the supernatants of concanavalin A-activated aged spleen cells is 5- to 10-fold lower than comparable supernatants prepared using young spleen cells. This lesion in IL-2 synthesis may limit antibody production to T-dependent antigens, because supplementation with purified IL-2 markedly enhances the number of anti-SRBC plaques generated by aged spleen cells. The response of aged splenocytes can be fully restored to that obtained using young adult cells. However, there appears to be a defect in the ability of aged cells to effectively translate the IL-2 signal into B cell helper activity, in the absence of T lymphocytes. That is, although young adult, nylon wool-purified T cells can interact with aged T-depleted spleen cells, producing a normal high level anti-SRBC response, IL-2 is incapable of reconstituting the response in aged animals to this level. On the other hand, both young adult T cells and IL-2 can interact with young adult T-depleted splenic lymphocytes to produce a normal, high level anti-SRBC response.
Induction of immunoglobulin secreting cells in the human autologous mixed leukocyte reaction: regulation by helper and suppressor lymphocyte subsets defined with monoclonal antibodies.
Authors: Gatenby P A , Kotzin B L , Engleman E G 
Published: December 2022

Abstract
The generation of IgM- and IgG-secreting cells in the human autologous MLR has been confirmed by using a microwell culture system and a reverse hemolytic plaque assay. The regulation of this response by T cell subsets was examined by using monoclonal antibodies that have previously allowed the definition of a Leu-3 helper/inducer subpopulation and a Leu-2 suppressor/cytotoxic subpopulation. These subsets were isolated by "panning" with monoclonal antibodies and were then cultured with autologous non-T cells, which serve as both stimulators of the reaction and a B cell source. The induction of antibody-forming cells was found to be dependent upon the Leu-3 subset whereas the Leu-2 subset not only failed to support C cell maturation, it actively suppressed the Leu-3 induced response. The Leu-3 response was found to be partially sensitive to radiation doses of 1000 rad or greater, whereas Leu-2 mediated suppression, even at high doses of cells, was totally ablated by 1500 rad. Thus, the generation of antibody-forming cells in the human autologous MLR is regulated by a balance of Leu-3 cell help and Leu-2 cell suppression. Such a finding may prove to be of relevance to immunoregulation in both health and disease.
Cutaneous basophil responses and immune resistance of guinea pigs to ticks: passive transfer with peritoneal exudate cells or serum.
Authors: Brown S J , Askenase P W 
Published: December 2022

Abstract
Resistance to infestation by larval Amblyomma americanum or Rhipicephalus sanguineus ticks was transferred to naive guinea pigs with peritoneal exudate cells (PEC) or serum from donors immunized by prior infestation with homologous tick larvae. In the A. americanum system, PEC transfer induced 87% tick rejection, which was similar to the level of resistance in actively sensitized hosts. In the R. sanguineus system, PEC conferred resistance (39% rejection) that was weaker than in actively sensitized hosts (57% rejection). In both systems, immune serum conferred significant but weaker resistance (20 to 29% rejection). In actively sensitized hosts, resistance to each tick species was specific, but there was considerable cross-reactive resistance. Basophils dominated the 24-hr challenge feeding sites of A. americanum ticks in actively sensitized hosts (69% of the infiltrate) and recipients of sensitized PEC (69%). Mononuclear cells were dominant (69% of the infiltrate) in the challenged tissues of immune serum recipients that had a significant but weaker cutaneous basophil response (24%). Mononuclear cells also dominated (58% of the infiltrate) the 24-hr challenge feeding sites of R. sanguineus ticks in actively sensitized hosts, but there were also 24% basophils. These studies demonstrate that immune resistance to tick is dependent on sensitized lymphoid cells or serum components, and that sensitized cells or serum can transfer a cutaneous basophil response that is associated with immune resistance. Rejection of ticks is usually associated with large basophil infiltrates, but sometimes mononuclear cells are dominant. Thus, immune resistance of guinea pigs to ticks is a heterogeneous response in which immune cells and serum probably act to recruit diverse effector leukocytes to mediate rejection that is specific but significantly cross-reactive.
A monoclonal antibody-inhibiting FMLP-induced chemotaxis of human neutrophils.
Authors: Cotter T G , Keeling P J , Henson P M 
Published: December 2022

Abstract
A monoclonal IgG1 antibody, termed NCD3, was raised against human neutrophils and has been shown to inhibit neutrophil chemotaxis. NCD3 displayed a considerable degree of stimulus specificity in that it inhibited N-formyl-methionyl-leucyl-phenylalanine- (FMLP) induced chemotaxis up to 80%, C5a and zymosan-activated plasma induced chemotaxis by only 20% and had no effect on leukotriene B4- (LTB4) or casein-mediated chemotaxis. NCD3 did not inhibit granule enzyme release from neutrophils in response to stimulation by various secretagogues, including FMLP, in the presence or absence of cytochalasin B (CB). Neutrophil phagocytosis of 51Cr-labeled opsonized sheep erythrocytes (51Cr-EAC) and superoxide anion (O2-) production in response to FMLP or phorbol myristate acetate (PMA) stimulation were not affected by pretreating cells with NCD3. Divalency of NCD3 was necessary for inhibition of chemotaxis, suggesting a requirement for cross-linking of the antigenic determinants on the neutrophil membrane surface.
Suppressor cell activity in tumor-bearing mice. III. Co-purification of a factor inhibiting cellular DNA synthesis and DNA polymerase activity.
Authors: Farrar W L , Elgert K D , Foo A S 
Published: December 2022

Abstract
The factor(s) derived from fibrosarcoma-induced suppressor T cells was sensitive to pronase and neuraminidase, but not to trypsin, beta-galactosidase, DNase, or RNase. Protein and RNA, but not DNA, synthesis were required to mediate suppression. Suppressor T cell-derived factor(s) could be precipitated by a 50% saturated ammonium sulfate (SAS) solution. The 50% SAS fraction inhibited both in vitro and in vivo spleen cell blastogenesis, whereas the 80% and unprecipitated fractions had no inhibitory activity. Using Sephadex G-200 chromatography, the 2nd protein fraction (fraction II) contained an inhibitor of both DNA polymerases (IDP) and DNA synthesis (IDS) activity, which possessed no cytotoxic activity. In vitro DNA polymerase alpha activity was suppressed by fraction II, whereas DNA polymerase beta and gamma activities remained unchanged. Molecular weight of IDP/IDS, as determined by Sephadex G-200 gel filtration chromatography, was approximately 14,500. Attempts to separate IDP/IDS activities found in fraction II by anion-exchange chromatography and slab gel electrophoresis were not successful, which suggested that the 2 activities were the same or very similar molecules.
Genetic control of natural resistance to Mycobacterium bovis (BCG) in mice.
Authors: Gros P , Skamene E , Forget A 
Published: December 2022

Abstract
Mice of 12 inbred strains infected i.v. with Mycobacterium bovis (BCG) exhibited 2 distinct patterns of response as determined by the degree of BCG burden in the spleens of animals at 3 wk after infection with 10(4) viable bacilli: susceptible (C57BL/6J and related sublines, BALB/c and DBA/1J) and resistant (A/J, C3H/HeCr, DBA/2J, CBA/J, C57Br, AKR). Mendelian analysis of this trait on segregating backcross and F2 populations derived from the mating of resistant and susceptible progenitors was compatible with the hypothesis that resistance to BCG is controlled by a single, dominant, autosomal gene, which is being given the designation Bcg. The product of the Bcg gene was found to influence the early phase of host response resulting in the genetic advantage of the resistant host being demonstrable as early as 24 hr after infection.
Ir genes of different high responder haplotypes for staphylococcal nuclease are not allelic.
Authors: Berzofsky J A , Pisetsky D S , Killion D J , Hicks G , Sachs D H 
Published: December 2022

Abstract
The Ir gene controlling high responsiveness to staphylococcal nuclease in the H-2d haplotype has been mapped to the I-A subregion, in contrast to that in the H-2k and H-2a haplotypes, which maps in the I-B subregion. The nonallelic high responder genes also confer differences in fine specificity on the antibodies produced. This nonallelism of Ir genes for the same antigen in different haplotypes is consistent with Ir gene mechanisms involving associative recognition of antigen plus Ia by T lymphocytes. It further suggests that products of different subregions can perform the same function.
A shared alloantigenic determinant on Ia antigens encoded by the I-A and I-E subregions: evidence for I region gene duplication.
Authors: Bhattacharya A , Dorf M E , Springer T A 
Published: December 2022

Abstract
Two monoclonal antibodies to mouse Ia antigens were produced by fusion of xenoimmune rat spleen cells with the NSI myeloma. These monoclonal antibodies detect polymorphic determinants present on B cells and activated T lymphocytes from mice carrying the H-2b, H-2d, H-2k, H-2r, and H-2q haplotypes but not from mice carrying the H-2s or H-2r haplotypes. Antigenic site number determinations showed the positive haplotypes can be divided into 2 groups. Mice bearing the H-2b, H-2d, and H-2q haplotypes express a high number--40,000 to 80,000--of antigenic sites per B lymphocyte, and monoclonal antibody plus complement can lyse B cells from these mice. In contrast, mice bearing the H-2k and H-2r haplotypes express a low number of antigenic sites--about 5000 per cell. Spleen cells from mice carrying the latter haplotypes are not lysed with monoclonal antibody and complement. Genetic mapping demonstrated that high and low expression map to the I-A and I-E subregions, respectively. The monoclonal antibodies detect an Ia specificity on I-Ab, I-Ad, I-Ed, and I-Ek molecules. These observations were confirmed using several different experimental approaches, i.e., cytotoxicity, fluorescent staining, competitive inhibition of monoclonal antibody binding, and 2-dimensional gel electrophoresis of immunoprecipitates. The avidity for A alpha b A beta b and E alpha k E beta k is 5 to 7 x 10(-9) M-1. The antigenic determinant is heat labile, which suggests that it is not carbohydrate. The results imply that Ia antigens encoded by distinct subregions share sequence homology, which may be a consequence of ancestral gene duplication.
Genetic control of B cell function. II. Antibody responses of inbred mice to red blood cells are controlled at the B cell level.
Authors: Hetzelberger D , Simon M M , Eichmann K 
Published: December 2022

Abstract
Inbred strains of mice can be classified into high and low responders with respect to their antibody responses to RBC. In this paper, we investigate the cellular basis of the difference in responsiveness between high- and low-responder strains. In cell-mixing experiments with purified B cells, T cells, and macrophages from 2 different combinations of H-2-identical high- and low-responder strains, we find that the B cells determine high and low responsiveness, whereas T cells and macrophages from low responders function equally as well as those of high responders. We could also exclude that suppressor T cells play an important role in determining high and low responsiveness. It is therefore suggested that low responsiveness is a defect of B cells to become activated in a T helper cell-dependent antibody response. In the previous paper of this series we showed that a limited number of genes (possibly 2), 1 linked to the Igh gene complex and the other(s) of unknown linkage, control the level of responsiveness. Taken together, we think that this represents a novel example of a genetic polymorphism in B cell function that is sufficiently simple, genetically and functionally, to provide a genetic approach to the study of B cell activation.
Binding of C-reactive protein to human lymphocytes. II. Interaction with a subset of cells bearing the Fc receptor.
Authors: James K , Hansen B , Gewurz H 
Published: December 2022

Abstract
In the preceding paper we reported that C-reactive protein (CRP) in the presence of a multimeric binding specificity such as C-polysaccharide (CPS) binds to a small percentage of peripheral blood lymphocytes (PBL). In the present paper additional methods for demonstrating this binding were developed and utilized to help characterize the CRP-binding cell. Heat-modified CRP and E-CPS-CRP each were found to bind to a similar percentage of PBL by microscopic visualization, and an identical degree of binding was observed by cytofluorimetric analysis. Multiple marker studies indicated that CRP-binding cells are found in the T cell, B cell, and null cell categories in a ratio of 2:1:1, respectively. Preferential overlap was seen with IgG FcR-bearing cells, which accounted for 70% of the CRP-binding cells; however, only 12% of the FcR cells bound CRP. These studies indicate that CRP-binding cells predominantly represent a subset of cells bearing FcR, and these cells have the morphologic characteristics of large granular lymphocytes. CRP in the presence of CPS bound to cells of multiple human and murine cultured lines shown to have IgG FcR reactivity, but showed lesser or no binding to cell lines negative for FcR. The precise morphologic and functional characterization of the CRP-binding cells and the nature of the binding site are yet to be established.
Inhibition of C1-mediated immune hemolysis by monomeric and dimeric peptides from the second constant domain of human immunoglobulin G.
Authors: Lukas T J , Muñoz H , Erickson B W 
Published: December 2022

Abstract
Activation of the classical complement cascade by immunoglobulin G involves binding of the first complement component (C1) to a multivalent antigen-IgG complex. Binding occurs by interaction of a site on the surface of the C gamma 2 domain of IgG with a globular head of the C1q subcomponent of C1. Previously we found that the synthetic decapeptide consisting of residues 281-290 from the second constant domain of the gamma-chain of the human IgG1 protein Eu inhibited the binding of human C1 to sensitized erythrocytes. The present study describes inhibition of monomeric and dimeric peptides containing residues 289-292 or 282-292: (formula: see text). On a molar basis, monomeric peptide 282-292 is just as active an inhibitor of C1 binding as peptide 281-290, whereas monomeric peptide 289-292 (tuftsin) is 4 times less active. Peptides 282-292 and 289-292 were each cross-linked at the amino terminus through terephthaloyl-bis(iminodiacetic acid) (Tid). Each dimeric peptide is twice as active on a molar basis as the corresponding monomeric peptide. Dimeric peptide Tid(282-292)2 is just as active on a molar basis as the monomeric 7S form of human IgG1 and 60% as active as the Fc fragment of IgG in inhibiting the binding of human C1 to sensitized erythrocytes. These results suggest that the positively charged residues His-285, Lys-288, Lys-290, and Arg-292, which are located on the outer surface of the C gamma 2 domain, may be involved in the C1q-binding site of human IgG.
T cell recognition of Moloney leukemia virus proteins. III. T cell proliferative responses against gp70 are associated with the production of a lymphokine inducing 20 alpha-hydroxysteroid dehydrogenase in splenic lymphocytes.
Authors: Ihle J N , Lee J C , Rebar L 
Published: December 2022

Abstract
One of the characteristic cellular immune responses associated with the regression of Moloney leukemia/sarcoma virus-induced tumors is a T cell proliferative response against the major viral envelope glycoprotein, gp70. The results described here demonstrated that associated with this proliferative response is the production of a lymphokine, Interleukin 3 (IL-3). The production of IL-3 was immunologically specific and showed the same specificity as that observed in blastogenic responses. IL-3 production was dependent upon an antigen-specific Thy-1.2+, Lyt-1+, 2- lymphocyte subpopulation but did not require the presence of an Ia+ or an adherent accessory cell. The results also suggested that IL-3 may constitute one of the blastogenic factors previously shown to be involved in the proliferative response to gp70. In particular, purified IL-3 was found to induce proliferation of both normal and immune nylon wool purified splenic lymphocytes. The phenotype of the responding lymphocyte subpopulation was Thy-1.2-, Lyt-1-, 2-, Ig-, and Ia-. Maximal IL-3 production occurred approximately 48 hr after the addition of antigen and its production was significantly blocked by mitomycin C. These characteristics were unlike those for the general production of blastogenic factor activity suggesting that IL-3 is responsible for only a minor component of the proliferative response.