bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cellular dissemination of priming for a mucosal immune response to cholera toxin in rats.
Authors: Pierce N F , Cray W C 
Published: December 2022

Abstract
Using CT as the test antigen, we sought 1) to learn whether primary immunization at 1 mucosal site caused priming of distant nonstimulated mucosae, 2) to study the role of migrating memory cells in the dissemination of mucosal priming, and 3) to compare disseminated priming with priming that occurs at the site of initial immunization. CT given i.c. or i.d. caused priming in tracheal and nonexposed enteric mucosae; i.t. immunization, however, did not cause detectable enteric priming. Adoptive transfer of immune TDLs showed that priming was conveyed by migrating memory cells. These appeared to be of 2 types: those that recirculated briefly before settling in MALT, and those that continued to recirculate until recruited by antigen to the site of mucosal challenge. Both types were required for secondary responses at mucosae distant from the site of priming. The time-course of disseminated mucosal priming resembled that of priming at the site of initial CT exposure, both lasting at least 16 wk. Disseminated priming persisted better in jejunal than tracheal mucosa, suggesting that the subgroup of memory cells that did not continue to recirculate settled preferentially in jejunal MALT. Disseminated priming supported smaller challenge responses than priming at the site of initial CT exposure did, suggesting that sessile memory cells also contributed to the latter process. These observations extend the concept of a "common mucosal immune system" to include cellular dissemination of mucosal priming, but also show quantitative differences between local and disseminated priming that probably reflect the patterns of distribution of migrating and sessile memory cells.
Mitogenic and co-mitogenic properties of hemin.
Authors: Stenzel K H , Rubin A L , Novogrodsky A 
Published: December 2022

Abstract
We report here that hemin, an agent known to induce cellular differentiation in Friend erythroleukemia cells, induces mitogenesis in human T cells and enhances mitogenic responses to supraoptimal concentrations of Con A. Mitogenesis induced by suboptimal or optimal concentrations of Con A is not affected by concentrations of hemin that markedly potentiate responses to supraoptimal amounts of Con A. Maximum mitogenic responses are reached 4 to 5 days after initiation of the cultures. The mitogenic response is macrophage dependent, whereas enhancement of responses to supraoptimal concentrations of Con A is not. Indeed, a greater degree of enhancement is observed after removal of adherent cells. Responses to other mitogens (phytohemagglutinin, wheat germ agglutinin, and sodium periodate) are also enhanced by hemin. Compounds that are metabolically or structurally related to hemin are neither mitogenic nor co-mitogenic. Protoporphyrin IX, which is nonmitogenic, is rendered mitogenic by the chemical insertion of iron to form hemin. Hemin does not affect Con A binding to lymphocytes. These findings indicate that hemin is a macrophage-dependent T cell mitogen with the unusual and remarkable property of overcoming the inhibition of mitogenesis induced by high concentrations of Con A. Since hemin has a limited number of metabolic effects, it provides a useful probe for determination of molecular events associated with lymphocyte activation.
Early effects of low-doses exposure to asbestos on local cellular immune responses in the lung.
Authors: Rola-Pleszczynski M , Massé S , Sirois P , Lemaire I , Bégin R 
Published: December 2022

Abstract
We recently developed an animal model to study the pulmonary reactions after exposure to environmental pollutants. In this model, sheep received monthly intratracheal instillations of a suspension of varying amounts of chrysotile asbestos in saline. All animals were studied by pulmonary function tests, transbronchial biopsies, and bronchoalveolar lavage. During the 6 mo of the study, no changes were seen in the 2 former tests, but bronchoalveolar lavage yielded leukocytes that responded with enhanced proliferative activity to concanavalin A, pokeweed mitogen, and staphylococcal lysate. The response to phytohemagglutinin was poor but also enhanced in the asbestos-exposed animals. Enhanced responsiveness was dose-related, except for the highest dose used, 128 mg, which was associated with a less enhanced proliferative response or none. Our data suggest that the initial response to low-dose exposure to asbestos consists in a stimulation of lymphocyte function; the possibility that this phenomenon may be linked to the eventual fibrogenic response of asbestosis warrants further studies.
Phenotypes of human natural killer cell populations detected with monoclonal antibodies.
Authors: Zarling J M , Clouse K A , Biddison W E , Kung P C 
Published: December 2022

Abstract
In our recent studies, human natural killer (NK) cell activity was found to be decreased 2- to 4-fold after treatment of monocyte-depleted peripheral mononuclear cells with monoclonal antibody OKM1 and complement (C). The present study was undertaken to determine whether there is an additional population of NK cells that is OKM1-, since treatment with OKM1 and C decreased, but did not eradicate, NK cell activity. Treatment of lymphocytes with monoclonal antibody OKT11A, which reacts with all sheep red blood cell rosetting lymphocytes, and C also decreased NK cell activity. Although approximately 90% of OKT11A+ cells are OKT3+, NK cell activity resides within the OKT11A+ cell population, which is OKT3- since OKT3-cell depletion fails to decrease NK cell activity. Double fluorescence analysis of OKT3-depleted lymphocytes revealed that 54% of the OKM1+ cells are OKT11A- and 45% of the OKT11A+ cells are OKM1-, thus demonstrating that within the OKT3-depleted population, approximately one-half the OKM1+ cells are OKT11A- and vice versa. Treatment of lymphocytes with OKM1 together with OKT11A and C decreased NK cell activity against 3 NK-sensitive leukemia lines--K562, MOLT-4, and HSB-2--more than did treatment with either antibody alone; virtually no lytic activity was retained after elimination of OKM1+ and OKT11A+ cells. The results thus provide strong evidence that there is at least 2 populations of human NK cells; one is OKM1+ and the other is OKT11A+
Specific anti-influenza virus antibody production in vitro by human peripheral blood mononuclear cells.
Authors: Yarchoan R , Murphy B R , Strober W , Schneider H S , Nelson D L 
Published: December 2022

Abstract
Cultures of human peripheral blood mononuclear cells stimulated in vitro with influenza virus were found to produce anti-influenza virus antibody. An enzyme-linked immunosorbent assay was used to measure cumulative antibody secretion into culture supernatants. Optimal antibody production was obtained with 2 x 10(6) peripheral blood mononuclear cells cultured in flat-bottomed wells for 12 days in 2 ml of RPMI 1640 medium supplemented with 10% fetal calf serum, antibiotics, and 4 mM L-glutamine. Antibody could be detected in cultures stimulated with live A/Hong Kong/68 (H3N2), purified formalin-inactivated A/Aichi/68 (H3N2), or live B/Hong Kong/68 influenza virus. Antibody of both IgG and IgM isotypes was produced. Under optimum conditions, the secreted IgG antibody was found to be directed preferentially at antigens on the stimulating virus. Antibody production was shown to require the cooperative interaction of B and T cells. Poisson analysis of B cell precursor frequency showed that approximately 1 in 40,000 B cells could be induced to produce IgG anti-influenza virus antibody in virus-stimulated cultures. Further investigation of this in vitro response should allow dissection of the cellular mechanisms involved in the regulation of antibody production in man.
Release of histamine from human leukocytes stimulated with the tumor-promoting phorbol diesters. II. Interaction with other stimuli.
Authors: Schleimer R P , Gillespie E , Daiuta R , Lichtenstein L M 
Published: December 2022

Abstract
The tumor promoter and irritant, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), previously shown to be a potent histamine releaser, has been used to further probe the mechanism of histamine release from human basophils. TPA and the calcium ionophore, A23187, produced a synergistic response in which subeffective concentrations of each stimulus (which alone produced less than 3% release) together produced over 70% histamine release. TPA also synergized with the IgE cross-linking stimulus anti-IgE. Desensitization of cells by incubation with anti-IgE in the absence of calcium rendered the cells unresponsive to anti-IgE and super-responsive to TPA. This marked increase in the TPA response was the result of an increase in the rate of TPA-induced histamine release, and occurred in the absence of extracellular calcium. The ability of various concentrations of anti-IgE to "sensitize" cells to TPA paralleled their ability to produce histamine release in untreated cells rather than their ability to desensitize the cells. These results suggest that in the absence of calcium, anti-IgE induces desensitization of some activation of other elements of the histamine-release process. The anti-IgE dose-response pattern of this activation event further suggests that it is an integral part of the anti-IgE-induced release process itself.
Chido and Rogers antigenic determinant on the fourth component of human complement.
Authors: Chu V F , Marsh W L , Gigli I 
Published: December 2022

Abstract
The blood group substances Chido (Cha) and Rogers (Rga) represent two electrophoretic variants of human C4. Based on the observation that anti-Cha and anti-Rga antisera agglutinated human red blood cells prepared in sucrose-activated autologous serum (LIS cells) at 37 degrees C, it has been assumed that the Cha and Rga antigenic determinants reside in the C4d fragment of C4. Here, we present evidence indicating that C4d is not present on those cells. In order to identify structurally the C4 fragments deposited, LIS cells were prepared at 37 degrees C and 4 degrees C in autologous serum to which 125I-C4 was added. Membranes of LIS cells were solubilized and analyzed by SDS-PAGE in 5 to 15% gradient gels followed by autoradiography. C4d was not deposited on LIS cells prepared at 37 degrees C, whereas C4c (beta, gamma, alpha 3 alpha 4) was. Cells prepared at 4 degrees C carried C4d (alpha 2) and C4c. Anti-Cha and anti-Rga antisera agglutinated both cell types, although C4d was not present on the cells prepared at 37 degrees C. Purified C4, C4c, C4d, and alpha-, beta- and gamma-chains of C4, as well as alpha 3 and alpha 4, were used to neutralize these antisera. C4 and the alpha-chain C4d and alpha 4 fragment of C4c, but neither the alpha 3 fragment nor the beta- or gamma-chains, were capable of neutralizing anti-Cha and anti-Rga antisera. These results strongly suggest that C4d and alpha 4 share an antigenic determinant, both of which are recognized by anti-Cha and anti-Rga antisera.
Biochemical and immunologic heterogeneity of Ia glycoproteins isolated from a chronic lymphocytic leukemia.
Authors: Letarte M , Falk J 
Published: December 2022

Abstract
Ia glycoproteins have been isolated from human chronic lymphocytic leukemic cells (CLL) by Lens culinaris chromatography and by filtration on ACA-34 Ultrogel. Ia antigenic activity, measured by inhibition of the cellular radioimmunoassay, was separated by gel filtration into 2 fractions, peak I and peak II. Monoclonal antibodies, produced against peak II glycoproteins, appear to recognize different antigenic determinants of Ia molecules. Monoclonal antibody 18a4 reacted with Ia molecules of peaks I and II, whereas monoclonal antibodies 18c2 and 18d5 reacted almost exclusively with peak II molecules both in the cellular radioimmunoassay and by immunoprecipitation. In addition to antigenic differences, minor variations in the apparent m.w. of the Ia polypeptide chains were observed between peaks I and II. These results indicate the existence of antigenically distinct subsets of Ia molecules that are separable by gel filtration.
Clonal analysis of restriction antigens for human TNP-specific cytotoxic T lymphocytes.
Authors: Neefe J R , Sullivan J E , Hartzman R J 
Published: December 2022

Abstract
Previous studies of populations of human TNP-specific cytotoxic T lymphocytes have shown a preference for HLA-matched, TNP-modified targets. However, substantial killing of modified targets mismatched for serologically defined HLA antigens is also observed. The present report concerns oligoclonal and monoclonal populations of TNP-specific cytotoxic lymphocytes from a single donor whose lymphocytes were primed in vitro to TNP-modified autologous lymphocytes and frozen in aliquots. Conditions for the expansion of precursors of cytotoxic cells to sufficient numbers for assay are described. Expansion required IL 2-containing supernatants and stimulator or feeder lymphocytes in great excess; PHA, present in the IL 2-containing supernatants, was not required. TNP modification of the stimulators in secondary cultures was not required but appeared to enhance activity. Oligoclonal populations showed marked preference for TNP-modified targets sharing any of 3 of the 4 HLA-A and -B antigens of the donor (Aw24, B8, Bw44) when compared with targets sharing only the 4th antigen (A1) or no antigens. Monoclonal TNP-specific populations showed marked preference for certain TNP-modified targets when tested against a panel, but the pattern often did not correspond with the serologically defined HLA-A and -B antigens. The data suggest that most or all TNP-specific cytotoxic clones are restricted in their killing patterns by determinants associated closely with but not necessarily identical to the serologically defined HLA-A and -B antigens.
Immunoglobulin expression by human B lymphocytes clonally transformed by Epstein Barr virus.
Authors: Brown N A , Miller G 
Published: December 2022

Abstract
Epstein Barr virus (EBV) immortalizes human B lymphocytes, resulting in long-term lymphoblastoid cell lines. To date, such cell lines have typically been derived by suspension culture of mixed mononuclear cells, infected in vivo or in vitro with EBV. We have derived 208 lymphoblastoid lines by clonal transformation of peripheral blood lymphocytes from 3 neonates, 3 normal adults, and 1 patient with systemic lupus erythematosus (SLE), utilizing colony formation in agarose and then separate propagation of the colonies in liquid medium. A total of 180 lines have been analyzed for expression of cytoplasmic and/or secreted immunoglobulin isotypes. Such analysis reveals that 167 (92%) of the lines are monoclonal with respect to isotype expression. All clonally derived lines from neonates produce only IgM. Most clonal transformants from normal adults also produce IgM (81%), but clones producing IgG (16%) or IgA (3%) were also found. Clonal transformation of lymphocytes from the SLE patient revealed a shift in isotype expression, with increased numbers of IgG-secreting clones (48%) and IgA-secreting clones (13%). The data support the use of EBV-mediated clonal transformation as a probe for the analysis of states of isotype differentiation among circulating B cells, and as a method for deriving immortalized, monoclonal human B cell lines.
Defective regulation of B lymphocyte colony formation in patients with systemic lupus erythematosus.
Authors: Kumagai S , Sredni B , House S , Steinberg A D , Green I 
Published: December 2022

Abstract
We have succeeded in generating B cell colonies from freshly separated human peripheral blood by the double agar layer technique and expanding them in liquid culture for several weeks. Populations of cells enriched in B cells were placed into the upper layer with or without bacterial LPS. Although B cell colonies were observed without LPS, the addition of LPS to the cells in the upper agar layer increased the number of colonies. Also necessary for optimal B cell colony formation was the presence in the lower agar layer of either culture supernatant of PHA-stimulated mononuclear cells or purified T cells and PHA. Without such helper factors in the lower layer, only a few B cell colonies were observed in the upper layer. By using these techniques, peripheral blood lymphocytes from normal individuals and patients with active systemic lupus erythematosus (SLE) were studied for the generation of B cell colonies. Significantly more B cell colonies were observed in patients with SLE, using either kind of "helper" factor. In addition, T cells from normal individuals and patients were tested for their ability to help B cell colony formation. The SLE T cells were found to be defective in this function relative to normal T cells. Thus, although patients with SLE were hyperactive in forming B cell colonies, thier T cells were defective in supporting the formation of B cell colonies from normal individuals.
Immunochemical studies on thymosin: radioimmunoassay of thymosin alpha 1.
Authors: McClure J E , Lameris N , Wara D W , Goldstein A L 
Published: December 2022

Abstract
A sensitive and specific radioimmunoassay (RIA) has been developed to measure thymosin alpha 1 in human blood and tissue extracts. Thymosin alpha 1, originally isolated from bovine thymosin fraction 5, has an identical primary structure in bovine and human species. Antiserum to synthetic thymosin alpha 1 was prepared in rabbits. A synthetic analogue, N-Ac-(Tyr1)thymosin alpha 1 was radioiodinated by utilizing Na125I and soluble lactoperoxidase. The RIA is capable of detecting as small an amount as 40 pg thymosin alpha 1 in serum/plasma and does not significantly cross-react with other putative thymic hormones or other purified blood proteins that have been assayed. Proteolytic degradation of thymosin alpha 1 does not occur during the collection, storage, or assay of serum or plasma. The concentration of thymosin alpha 1 in the blood is highest in utero, decreases sharply after birth, and appears to remain fairly constant during the first 15 yr of life. Maternal blood levels of thymosin alpha 1 appear to be above normal during pregnancy.
Delayed hypersensitivity granuloma formation and modulation around Schistosoma mansoni eggs in vitro. II. Regulatory T cell subsets.
Authors: Doughty B L , Phillips S M 
Published: December 2022

Abstract
Schistosoma mansoni granuloma modulation was first described in an in vivo murine model of schistosomiasis and was characterized as a diminished cellular responsiveness to newly formed eggs in chronic infections. This phenomenon of modulation was studied using an in vitro model of granuloma formation. Negative selection procedures using anti-Lyt-1.2, 2.2, and Qa-1 sera and complement on spleen cell populations from normal or S. mansoni-infected C57BL/6 or (C57BL/6 X A/J)F1 mice were examined for their effect on in vitro granuloma formation or modulation. These data suggest that there is a Lyt-1+2-, Qa-1+ T cell present in chronically infected spleen cells that is capable of inducing feedback suppression. In addition, selective removal of a population of Lyt-1-2+ T cells from chronically infected spleen cells augmented the ability of that population to form granulomas in vitro. The selective removal of Lyt-1+2- cells ablated the ability of chronically infected spleen cells to form in vitro granulomas. Granuloma formation is primarily dependent on a population of Lyt-1+, Qa-1+ cells, and modulation is dependent on 2 populations, 1 acting directly (Lyt-1-2+) and the other through a (Lyt-1+2-, Qa-1+) feedback mechanism of suppression.
The selective role of membrane IgG in the antigen-induced inhibition of human in vitro antibody synthesis.
Authors: Stevens R H , Benveniste E , Pineda E 
Published: December 2022

Abstract
IgG-anti-tetanus toxoid-producing B cell precursors from recently immunized individuals can be stimulated by pokeweed mitogen and T cells to produce IgG-Tet antibodies in vitro. Treatment of these cells with tetanus toxoid selectively inhibits the synthesis of IgG-Tet. Because the IgG-Tet precursors display heterogeneity in their surface isotypes (mu, delta, gamma), the aim of this study was to determine the surface isotype responsible for transmitting this antigen-induced inhibitory signal to the B cell. B cells were fractionated by rosetting techniques on the basis of surface IgM or IgD. The 4 resulting B cell subsets (SIgM+, sIgM-, sIgD+, sIgD-) were found to be equally susceptible to antigen-induced inhibition. Experiments were then performed with anti-isotype antibodies to investigate further the roles of sIgM, sIgD, and sIgG in antigen inhibition. Treatment of peripheral blood lymphocytes with 10 micrograms/ml of anti-gamma antibody inhibited IgG-Tet antibody production, whereas the addition of up to 100 micrograms of anti-mu or anti-delta antibodies did not. Tetanus toxoid and anti-gamma antibody inhibition of IgG-Tet synthesis in vitro followed similar temporal kinetics, with the IgG-Tet precursors being sensitive to inhibition by either tetanus toxoid or anti-gamma antibodies during the first 3 days of culture and not becoming totally resistant to these agents until day 5 of culture. Capping off of sIgG receptors, with the subsequent addition of tetanus toxoid, abolished the antigen-induced inhibition of IgG-Tet seen previously, whereas capping off of sIgD or sIgM did not affect antigen inhibition of IgG-Tet antibodies. These results implicate sIgG molecules as those responsible for rendering IgG-Tet precursors susceptible to antigen-induced inhibition.
Arming of mononuclear phagocytes by eosinophil peroxidase bound to Staphylococcus aureus.
Authors: Ramsey P G , Martin T , Chi E , Klebanoff S J 
Published: December 2022

Abstract
When eosinophil peroxidase (EPO) was incubated with Staphylococcus aureus (staph) approximately 40% remained firmly bound to the bacteria as indicated by guaiacol assay. The staph-EPO complex was killed readily by concentrations of H2O2 and a halide that did not alter the viability of control (non-EPO-coated) organisms or organisms pretreated with another basic protein, protamine. This toxic effect was abolished by omitting either H2O2 or halide and was inhibited by azide, cyanide, or aminotriazole. Peroxidase activity was evident on the surface of the organism after ingestion by rabbit blood monocytes. The staph-EPO complex was killed at a greater rate by both rabbit blood monocytes and alveolar macrophages than were control organisms, an effect that did not appear to be secondary to improved phagocytosis. The peroxidase inhibitor azide inhibited the killing of staph-EPO by these mononuclear phagocytes without affecting the killing of control staphylococci; in the presence azide, the killing curve with staph-EPO returned to that seen with control organisms. Further, aerosolized EPO-coated organisms were cleared more rapidly from rat lung than were uncoated organisms or organisms pretreated with protamine. These findings suggest mononuclear phagocytes can utilize EPO bound to the surface of ingested microorganisms to enhance their microbicidal activity.