bluuebunny/crossref_metadata_2025_split huggingface dataset:
Defective calcium response in B-chronic lymphocytic leukemia cells. Alteration of early protein tyrosine phosphorylation and of the mechanism responsible for cell calcium influx.
Authors: Michel F , Merle-Béral H , Legac E , Michel A , Debré P , Bismuth G 
Published: December 2022

Abstract
To study defective signal transduction via the Ag receptor of B-chronic lymphocytic leukemia cells (B-CLL), we examine in this report the Ca2+ response triggered by anti-mu antibody in 23 patients previously classified in three phenotypic groups. Altered Ca2+ changes are essentially found in CLL group II whose leukemic cells are characterized by a marked expression of the CD11b Ag. B-CLL cells from patients with a defective Ca2+ response present an altered pattern of protein tyrosine phosphorylation after anti-mu stimulation in comparison with normal human B cells and B-CLL cells from patients having a normal Ca2+ response. Most of the proteins usually tyrosine phosphorylated after the triggering of cell-surface IgM are concerned. This includes the gamma 1 isoform of phospholipase C, although the protein is normally present in B-CLL cells. These findings suggest that the interruption of the phosphoinositide pathway in B-CLL cells is very proximal, at the level in the signaling cascade between activated surface Ig receptors and protein tyrosine kinases. Simultaneously, we demonstrate that some low responding patients exhibit a decreased Ca2+ response to thapsigargin, an agent known to release intracellular Ca2+ without inositol 1,4,5-trisphosphate production. This suggests that an altered functioning of the mechanism leading to the cell Ca2+ influx in B cells can be also involved in the decreased Ca2+ response observed in B-CLL cells.
Modulation of in vivo immune response by selective depletion of neutrophils using a monoclonal antibody, RP-3. I. Inhibition by RP-3 treatment of the priming and effector phases of delayed type hypersensitivity to sheep red blood cells in rats.
Authors: Kudo C , Yamashita T , Araki A , Terashita M , Watanabe T , Atsumi M , Tamura M , Sendo F 
Published: December 2022

Abstract
Recent studies on neutrophils have revealed that these cells produce various cytokines, and may be involved in regulation of the immune response. We examined whether neutrophils are involved in delayed type hypersensitivity (DTH) to SRBC in rats by selective depletion of in vivo neutrophils using a mAb designated RP-3. When the rats had been treated with RP-3 at the time of priming with SRBC, DTH to these cells was inhibited. Furthermore, RP-3 treatment was effective in inhibiting the effector phase of the DTH response to SRBC. When spleen cells from rats that had been treated with RP-3 at the time of immunization were used for local transfer of DTH, footpad swelling was significantly less than that induced by spleen cells from the RP-3-untreated immune rats.
Modulation of in vivo immune response by selective depletion of neutrophils using a monoclonal antibody, RP-3. II. Inhibition by RP-3 treatment of mononuclear leukocyte recruitment in delayed-type hypersensitivity to sheep red blood cells in rats.
Authors: Kudo C , Yamashita T , Terashita M , Sendo F 
Published: December 2022

Abstract
We demonstrated in our previous paper that treatment of rats with RP-3, a mAb that depletes in vivo neutrophils selectively, resulted in inhibition of both the priming and effector phases of delayed type hypersensitivity (DTH) to SRBC. In order to clarify the mechanisms of this phenomenon, we examined the effect of RP-3 treatment on mononuclear leukocyte (MNL) recruitment in DTH. When rats had been treated with RP-3 at the time of Ag priming, MNL migration, which accompanies DTH, was inhibited. The prior infiltration of neutrophils was also partially required for MNL recruitment because migration was inhibited when the immune rats were treated with RP-3 at the time of DTH elicitation.
IFN-gamma influences the migration of thoracic duct B and T lymphocyte subsets in vivo. Random increase in disappearance from the blood and differential decrease in reappearance in the lymph.
Authors: Westermann J , Persin S , Matyas J , van der Meide P , Pabst R 
Published: December 2022

Abstract
Thoracic duct lymphocytes (TDL) continuously patrol through the body, facilitating immune responses at most sites. IFN-gamma might regulate immune responses by influencing the migration of TDL. Therefore, it was investigated in vivo whether IFN-gamma affects the migration of thoracic duct B, T, CD4+, and CD8+ lymphocytes from blood to lymph. Labeled TDL were injected i.v. into rats continuously receiving IFN-gamma via a central venous catheter. The numbers of B, T, CD4+, and CD8+ lymphocytes were determined in blood and thoracic duct lymph for 120 h. IFN-gamma increased the disappearance of TDL from the blood to a similar extent in all subsets. In contrast, the reappearance of B and T lymphocyte subsets in the lymph was decreased: B lymphocytes were affected significantly more than T lymphocytes, whereas CD4+ and CD8+ lymphocytes were affected to a similar extent. Our study suggests that differential retention within the tissue rather than preferential immigration into the tissue creates a microenvironment with a distinct composition of lymphocyte subsets.
Autoantibodies in Chagas' disease. An antibody cross-reactive with human and Trypanosoma cruzi ribosomal proteins.
Authors: Bonfa E , Viana V S , Barreto A C , Yoshinari N H , Cossermelli W 
Published: December 2022

Abstract
Sera from 102 patients with chronic Chagas' disease were studied for the presence of autoantibodies to intracellular proteins and nucleic acids by three different methods. Only four sera had autoantibodies detected by indirect immunofluorescence on HEp-2 cells. All of the sera were negative for anti-dsDNA, anti-Ro/SSA, anti-La/SSB, anti-Sm and anti-RNP autoantibodies but 12 (12%) of the sera had low to moderate levels of anti-histone antibodies. When Chagas sera were tested for autoantibodies to a total HeLa cell extract by Western blotting, weak reactivity was observed in 31 sera. Despite significant heterogeneity in the protein Ag targeted by these sera, seven recognized a 23-kDa protein. Strong binding to this 23 kDa protein was observed in one-third of the sera when isolated ribosomes were used as source of Ag. In contrast, no autoreactivity was detected with ribosomal proteins P0, P1, and P2. These findings confirm the presence of autoantibodies in chronic Chagas' disease and indicate a remarkable restricted humoral immune response to human ribosomal proteins. Furthermore, affinity-isolated anti-23-kDa antibody cross-reacted with a Trypanosoma cruzi ribosomal protein of similar molecular weight. This molecular mimicry may be responsible for the apparent breakdown of self-tolerance resulting in tissue damage. Indeed, experiments demonstrating that immunization of mice and rabbit with T. cruzi ribosomes have been reported to induce myocarditis.
Pneumocystis carinii stimulates tumor necrosis factor-alpha release from alveolar macrophages through a beta-glucan-mediated mechanism.
Authors: Hoffman O A , Standing J E , Limper A H 
Published: December 2022

Abstract
Recent studies suggest that TNF-alpha plays a central role in host defenses during Pneumocystis carinii pneumonia. To determine whether P. carinii directly stimulates TNF-alpha secretion, rat alveolar macrophages were cultured in the presence of purified P. carinii. Whereas unstimulated alveolar macrophages released only 13.0 +/- 2.7 pg/ml of TNF-alpha into the medium, macrophages stimulated with P. carinii released 108.2 +/- 20.4 pg/ml of TNF-alpha after overnight culture (p = 0.0001). Maximal TNF-alpha release was observed after 8 h of incubation and required a P. carinii: macrophage ratio of at least 2.5:1. Autoclaved P. carinii were also able to trigger TNF-alpha release from macrophages albeit at a reduced level. In view of recent evidence that P. carinii is phylogenetically related to the fungi and contains a beta-glucan-rich cell wall, we hypothesized that TNF-alpha release might in part be mediated by this cell wall component. Preincubation of macrophages with particulate beta-glucan derived from Baker's yeast resulted in complete inhibition of TNF-alpha release in response to P. carinii. In addition, digestion of P. carinii with zymolyase, a preparation containing predominantly beta-glucanase activity, substantially reduced the ability of P. carinii to cause TNF-alpha release from macrophages. In a similar manner, macrophages incubated with P. carinii in the presence of laminariheptaose, an oligosaccharide that binds to macrophage beta-glucan receptors, also displayed decreased TNF-alpha release. Interestingly, TNF-alpha release may not be completely linked to the adherence of the organism to macrophages. Particulate beta-glucan significantly reduced P. carinii adherence to macrophages and also impaired TNF-alpha release. However, yeast mannan also significantly reduced P. carinii adherence to macrophages and also impaired TNF-alpha release. However, yeast mannan also significantly reduced P. carinii adherence but had no effect on TNF-alpha release. These data demonstrate that P. carinii can directly stimulate the secretion of TNF-alpha from alveolar macrophages and that this effect is largely mediated by beta-glucan components of the P. carinii cell wall.
Isotype-specific antibody-secreting cells to transmissible gastroenteritis virus and porcine respiratory coronavirus in gut- and bronchus-associated lymphoid tissues of suckling pigs.
Authors: VanCott J L , Brim T A , Simkins R A , Saif L J 
Published: December 2022

Abstract
Antibody-secreting cells (ASC) were enumerated in gut- and bronchus-associated lymphoid tissues of pigs exposed to three antigenically related coronaviruses: virulent transmissible gastroenteritis virus (TGEV), attenuated TGEV, and porcine respiratory coronavirus (PRCV). Exposure of 11-day-old pigs to virulent TGEV resulted in severe gastroenteritis and virus shedding mainly in feces but also to a limited extent in nasal secretions. PRCV and attenuated TGEV exposure produced no clinical signs and only one pig given a high dose of attenuated TGEV shed virus in feces, but virus was shed from the nasal passages. Nasal virus titers were highest after PRCV inoculation of pigs. Mononuclear cells were isolated from spleens, mesenteric, and bronchial lymph nodes of pigs and assayed for virus-specific IgG and IgA antibody secretion by an enzyme-linked immunospot assay. Virus-specific ASC peaked at postinoculation days 12 to 24 and IgG-ASC outnumbered IgA-ASC in all tissues tested. The greatest numbers of ASC were in mesenteric lymph nodes of virulent TGEV-exposed pigs and in BLN of PRCV-exposed pigs. Attenuated TGEV induced intermediate ASC responses in the gut and respiratory tract. Secondary in vitro ASC responses to inactivated TGEV or PRCV paralleled the primary responses except in BLN where the numbers of memory ASC were high for both TGEV- and PRCV-exposed pigs. We conclude that: 1) a single exposure of pigs to PRCV either oral-nasally or by aerosol leads to potent systemic and bronchus-associated, but not gut-associated, ASC responses; 2) a high dose of attenuated TGEV (4 x 10(8) plaque-forming units) is more effective than PRCV (6 x 10(5) or 2 x 10(8) plaque-forming units) or a lower dose of attenuated TGEV (7 x 10(6) plaque-forming units) in eliciting gut-associated ASC; 3) although virulent and a high dose of attenuated TGEV induce high numbers of ASC in the tissues tested, virulent TGEV induces the most ASC in the gut and IgA-ASC in all lymphoid tissues; and 4) virus replication in the gut or respiratory tract is a major factor affecting the magnitude of an ASC response at that site and may be necessary for the recruitment of IgG- and IgA-ASC and memory cells in large numbers from other mucosal inductive sites. This unique model of mucosal immunity using antigenically related viruses with distinct tissue tropisms may help to clarify interactions of the various components of the common mucosal immune system.
Anti-KCA-3, a monoclonal antibody reactive with a rat complement C3 receptor, distinguishes Kupffer cells from other macrophages.
Authors: Maruiwa M , Mizoguchi A , Russell G J , Narula N , Stronska M , Mizoguchi E , Rabb H , Arnaout M A , Bhan A K 
Published: December 2022

Abstract
A new mAb, designated anti-KCA-3, was developed against rat Kupffer cells. The reactivity of anti-KCA-3 was restricted to macrophages with preferential binding to Kupffer cells; only a few macrophages in the spleen, lymph nodes, lungs, and intestine stained with the antibody. A very small number of peritoneal resident and exudate macrophages reacted with the antibody and no reactivity was seen within the thymus, skin, heart, kidneys, brain, peripheral blood, and bone marrow. KCA-3 was expressed predominantly by the Kupffer cells in the periportal region rather than in the centrilobular region of the hepatic lobules. The cells in the portal tract did not stain with the antibody. The staining of the cytosmears and FACS analysis of the Kupffer cell fraction isolated from hepatic sinusoidal cells by centrifugal elutriation revealed that as many as 62% and 49% of the cells were stained with anti-KCA-3, respectively. Immunoelectron microscopic study of the liver indicated that expression of KCA-3 on Kupffer cells was limited to the plasma membrane facing the sinusoid rather than the space of Disse. Immunoprecipitation and SDS-PAGE analysis demonstrated KCA-3 to have a m.w. of approximately 50 kDa under both reducing and nonreducing conditions. After treatment of KCA-3 with N-glycanase, there was no significant change in the m.w., indicating KCA-3 was not highly glycosylated. C3b- and iC3b-mediated rosette formation between Kupffer cells and sensitized SRBC was inhibited by the antibody, implying that KCA-3 functioned as a complement C3 receptor or complement receptor-associated molecule. Furthermore, KCA-3 was eluted from C3b-Sepharose but not HSA-Sepharose after incubation with Kupffer cell lysate, indicating that KCA-3 directly binds C3b. The cell distribution, ligand-binding specificity, and biochemical properties of the protein were found to be different from the complement C3 receptors previously described. Because OX42 (antibody reactive with the rat CR3 receptor) inhibited complement C3-mediated rosette formation with peritoneal resident macrophages but not with Kupffer cells, the findings suggest that C3-mediated binding to Kupffer cells and to peritoneal macrophages is mediated by two different receptors. We conclude that anti-KCA-3 recognizes a novel type of complement C3 receptor preferentially expressed on Kupffer cells.
Heterologous desensitization of the high affinity receptor for IgE (Fc epsilon R1) on RBL cells.
Authors: Weetall M , Holowka D , Baird B 
Published: December 2022

Abstract
To study the properties of Fc epsilon RI desensitization induced by aggregation of that receptor, RBL cells were sensitized with a mixture of two different IgE mAb to create two different populations of IgE-receptor complexes. Cross-linking of one receptor population containing anti-dinitrophenyl (DNP) IgE with a bivalent Ag, 1-DNP-amino-12-biotinamidododecane)2-avidin ((DNP)2-avidin), results in desensitization of a subsequent response, both of the same receptor population (homologous desensitization) and of the second receptor population containing anti-5-dimethylaminonaphthalene-1-sulfonyl (dansyl) IgE (heterologous desensitization). The extent of heterologous desensitization is dependent on several parameters, including the concentration of both the first and the second Ag and the densities of the respective IgE populations. Heterologous desensitization of the Ca2+ response is more sensitive to the concentration of the second stimulus (dansyl-BSA) than heterologous desensitization of the degranulation response. AlF4-, which activates GTP-binding proteins, can effectively replace (DNP)2-avidin as the initial stimulant and desensitizing agent. Other agents that mobilize intracellular Ca2+ including thrombin and a Ca2+ ionophore are less effective at replacing (DNP)2-avidin. Because prestimulation with Ag does not desensitize subsequent responses to AlF4- or Ca2+ ionophore, it appears that signal transduction via Fc epsilon RI is impaired at an early step. Addition of monovalent DNP hapten within approximately 10 min after cross-linking by (DNP)2-avidin completely prevents the desensitization of the subsequent Ca2+ or degranulation response to dansyl-BSA. After longer times of incubation with DNP Ag, the DNP hapten becomes increasingly less effective at preventing the desensitization of the dansyl-BSA response, even though ongoing signal transduction by the DNP Ag is halted. These results suggest a form of cellular memory for the desensitized state.
Human Ig production and isotype switching in severe combined immunodeficient-human mice.
Authors: Vandekerckhove B A , Jones D , Punnonen J , Schols D , Lin H C , Duncan B , Bacchetta R , de Vries J E , Roncarolo M G 
Published: December 2022

Abstract
Severe combined immunodeficient (SCID) mice were transplanted with different human fetal organs (SCID-hu mice), including thymus, liver, spleen, and omentum, and the serum levels of human IgM, IgG, IgE, and IgA were measured. In all SCID-hu mice significant levels (up to 590 ng/ml) of IgM were detected, irrespective of the organs transplanted. In contrast, IgG was present (up to 530 ng/ml) only when the fetal thymus was transplanted together with the fetal liver, indicating that the presence of human T cell is a prerequisite for in vivo isotypes switching by human B cells in SCID-hu mice. Additional transplantation of fetal spleen did not significantly increase IgG levels. was observed 4 months after transplantation. At that time, analysis by IEF showed that human IgG present in SCID-hu serum was at least oligoclonal. Furthermore, all IgG subclasses were represented in the human IgG pool. Human B cells were undetectable in the peripheral blood, spleen, and bone marrow of these SCID-hu mice; in contrast, B cells expressing CD19 could be isolated from the SCID-hu thymus. Considerable proportions of the CD19+ B cells coexpressed CD5, CD7, CD10, CD40, and CD2. These B cells spontaneously produced IgM and IgG in vitro and could be induced to switch to IgE-producing cells when cocultured with cloned activated CD4+ T cells in the presence of IL-4. Collectively, these data demonstrate that functionally mature B cells able to produce IgM and IgG in vivo, and IgE in vitro, are present in the SCID-hu human thymus.
Expansion of genes that encode MHC class I molecules in cyprinid fishes.
Authors: Okamura K , Nakanishi T , Kurosawa Y , Hashimoto K 
Published: December 2022

Abstract
We have analyzed the genomic genes and the mRNA that encode MHC class I molecules in cyprinid fishes, namely, the ginbuna crucian carp (Carassius auratus langsdorfii) and the carp (Cyprinus carpio). The presence of several distinct class I genes was revealed in the genome of cyprinid fishes, and distinct class I genes that are expressed in carp cells were identified. The sequences of the alpha 3 domain of these class I genes are relatively well conserved, whereas the sequences of the respective alpha 1 and alpha 2 domains have diverged from one another. A comparison of the sequences expressed in carp with the sequences of the human classical class I molecules revealed that several amino acids in the peptide-binding region, including those that have been proposed to interact with antigenic peptide termini, are highly conserved. The present study demonstrated a dynamic expansion of the genes that encode MHC class I molecules in teleost fish whose ancestor branched off from the vertebrate line leading to mammals more than 400 million years ago.
Rejection of K1735 murine melanoma in syngeneic hosts requires expression of MHC class I antigens and either class II antigens or IL-2.
Authors: Chen P W , Ananthaswamy H N 
Published: December 2022

Abstract
Tumor specific immunity is mediated by CTL that recognize peptide Ag in the context of MHC class I molecules and by Th cells that recognize peptide Ag in the context of MHC class II molecules. To clarify the relative importance of MHC class I and II Ag in tumor rejection, we transfected a K1735 melanoma that did not express constitutively either MHC class I or II Ag with H-2Kk and/or I-Ak genes and determined their tumorigenicity. K1735 transfectants expressing either Kk or Ak Ag alone produced tumors in normal C3H mice, whereas most transfectants that expressed both molecules were rejected in normal C3H mice but produced tumors in nude mice. However, the Ak Ag requirement can be substituted by IL-2 because transfection of Kk-positive/Ak-negative K1735 cells with the IL-2 gene also resulted in abrogation of tumorigenicity in normal C3H mice but not in nude mice. Similarly, transfection of Kk-negative/Ak-positive K1735 cells with IFN-gamma gene resulted in induction of MHC class I Ag as well as rejection of these tumors in normal C3H mice. The rejection of K1735 transfectants expressing Kk and Ak Ag in normal C3H mice required both CD4+ and CD8+ T cells. In addition, the transplantation immunity induced by K1735 transfectants expressing both Kk and Ak Ag completely cross-protected mice against challenge with Kk-positive transfectants but only weakly protected them against challenge with parental K1735 cells or Ak-positive transfectants. These results indicate that expression of either MHC class I or II Ag alone is insufficient to cause the rejection of K1735 melanoma in syngeneic hosts and that both Ag are necessary. In addition, our data suggest that the failure of Kk-positive K1735 cells to induce a primary tumor rejection response in normal C3H mice may result from their inability to induce the helper arm of the antitumor immune response.
A novel population of natural killer progenitor cells isolated from human umbilical cord blood.
Authors: Cicuttini F M , Martin M , Petrie H T , Boyd A W 
Published: December 2022

Abstract
In this report, we describe the isolation of a unique subpopulation of CD7+ cells from human fetal blood. Umbilical cord blood was first immuno-rosette-depleted using T cell, B cell, granulocyte, and macrophage markers to isolate a Lin- population. The Lin- cells were further characterized by cell sorting. As expected, the CD34+Lin- population (30%) was homogeneous and highly enriched for hemopoietic progenitors. Somewhat surprisingly, the CD34-Lin- population was also shown to be relatively homogeneous, with over 95% of cells expressing CD7. This CD34-Lin-CD7+ population was shown to be negative for all other T cell markers tested (i.e., CD7+1-2-3-4-8-). However, approximately 30% of these cells were positive for the NK cell surface markers CD16 and CD56 (CD7+NK+). Both CD7+NK+ and CD7+NK- populations proliferated in response to stimulation in vitro with IL-2/PHA/PHA-conditioned medium. After such treatment, approximately 40% of the CD7+NK- acquired CD56 and 20% CD16, whereas about 20% of the CD7+NK+ population became CD2+. The significance of the 60% of CD7+NK- cells that did not acquire other markers remains to be determined. In addition, although neither population was cytotoxic when first isolated, both populations acquired the ability to lyse the NK target cell line K562 while cultured under these conditions. These data suggest that these two populations may represent a developmental sequence among NK cell precursors in human umbilical cord blood. Additional analysis of such precursors may be useful in understanding the ontogeny of NK cells in vivo.