bluuebunny/crossref_metadata_2025_split huggingface dataset:
Carbon Dioxide Studies
Authors: Valley George 
Published: January 2023

Abstract
In the preceding paper (Valley and McAlpine)1 it was shown that carbon dioxide exerts a very definite preserving action on serum alexin.2 It was further demonstrated that a displacement of atmospheric (molecular) oxygen by hydrogen, nitrogen and carbon monoxide exercised no greater preservative action than the mechanical removal of atmospheric air by evacuation, or by limiting the volume of enclosed air in an hermetically sealed tube. It is apparent, therefore, that aside from a mere mechanical displacement of molecular oxygen by carbon dioxide, this gas brought about other influences which favored alexin preservation. Hence the explanation of the phenomenon should be sought in the nature of carbon dioxide action on a serum complex.
Displacement of oxygen may be more efficiently effected by carbon dioxide than by other gases, due to the chemical nature of the former.
The Distribution of Antibodies in the Serum and Organs of Rabbits
Authors: Freund Jules , Whitney Caroline E. 
Published: January 2023

Abstract
In a previous study (1) on the distribution of immune agglutinins in the serum and organs of rabbits the following conclusions were drawn: Agglutinins accumulate in the organs of rabbits that have been passively immunized.The rate of accumulation of agglutinins in the liver, spleen, kidney and lungs is greater than in the uterus and skin.If the animal is killed within from five to seventeen hours after the injection of the immune serum, all or a large part of the agglutinins can be removed from the uterus and skin; after seventeen hours the agglutinins become perfusion-fast in these organs.
The demonstration of perfusion-fast antibodies in organs might seem to support the cellular (sessile receptor) theory of anaphylaxis, according to which the anaphylactic antibodies become fixed to the cells during the incubation period of passive anaphylaxis.
Effect of Exposure to Low Temperatures on Diphtheria Toxin-Antitoxin Mixtures
Authors: Robinson Elliott S. , White Benjamin 
Published: January 2023

Abstract
The dissociation by freezing of diphtheria toxin-antitoxin mixtures, with consequent increase in toxicity, was first reported in 1924 by White and Robinson (5). Kirkbride and Dow (3), in an article published simultaneously, stated that, under their experimental conditions, they were unable to produce this phenomenon. Anderson and Leonard (1) succeeded in bringing about such a dissociation, but only in experimental mixtures differing from those ordinarily employed for active immunization against diphtheria. Following the appearance of these papers, Glenny, Pope, Waddington and Wallace (2) suggested that an increased phenol concentration, brought about as the mixtures freeze, is the cause of the increased toxicity and that the discordant results reported “are due to the amount of protein present and other factors influencing the relative degree of destruction of antitoxin or of toxin by the local concentration of phenol that occurs when these mixtures are frozen.”
Intrathymic lymphoid precursor cells during fetal thymus development.
Authors: Antica M , Wu L , Shortman K , Scollay R 
Published: January 2023

Abstract
Our previous studies have demonstrated the presence, in the adult mouse thymus, of a population of early precursor cells able to give rise to T and B lymphocytes but not myeloid cells. This population of cells expresses low levels of CD4 and has been termed the "low CD4 precursors." All these precursors were found to be c-kit positive, and they precede the better known CD4-CD8- precursor stage. In this study, embryonic and neonatal thymuses were examined to see whether a similar low CD4 precursor was part of the pathway of T cell development during ontogeny. A population with the phenotypic characteristics of the adult low CD4 precursor was found from day 15 of embryonic development, although the expression of low levels of CD4 was apparent only from embryonic day 17. Functional tests of these putative precursors showed they had no thymus-reconstituting ability when isolated from thymuses at any time during embryonic life, and very low reconstituting ability even 24 days after birth. These results raise questions about the adult low CD4 precursor as an obligatory stage in the development of T cells in the thymus.
Functional effects of CD30 on a large granular lymphoma cell line, YT. Inhibition of cytotoxicity, regulation of CD28 and IL-2R, and induction of homotypic aggregation.
Authors: Bowen M A , Olsen K J , Cheng L , Avila D , Podack E R 
Published: January 2023

Abstract
Studies are described revealing novel regulatory functions for the lymphocyte activation Ag CD30. A new mAb, C10, reactive with YT cells binds to CD30 and induces inhibition of the cytotoxicity of YT for Raji cells. C10 inhibition of cytotoxicity requires several hours preincubation of YT with C10; the antibody has no effect if added directly to YT cytotoxicity assays. CD30 stimulation by C10 down-regulates CD28 expression on YT by &gt; 80% within 48 h. Because CD28 is required for YT cytotoxicity toward Raji cells and other B7/BB1 bearing targets, it is suggested that inhibition of cytotoxicity of YT is mediated by control of CD28 expression and/or signaling via CD30. Accordingly, conjugation of YT with Raji is only slightly affected by CD30-mediated down-regulation of CD28, and perforin mRNA steady state levels are not changed at all. C10 treatment of YT cells additionally down-regulates the expression CD45 and up-regulates IL-2R p55. Moreover, CD30 stimulation by C10 causes homotypic aggregation of YT. Homotypic aggregation is slow, requiring gene transcription, translation, metabolic energy at elevated temperature (37 degrees C), magnesium ions, and an intact cytoskeleton. These studies offer insights into the function of CD30 as a complex regulator of T cells.
Production of soluble IL-4 receptors by murine spleen cells is regulated by T cell activation and IL-4.
Authors: Chilton P M , Fernandez-Botran R 
Published: January 2023

Abstract
Many cytokine receptors exist naturally as both membrane-bound and soluble forms. Whereas the membrane receptors have an obvious role in signal transduction, the putative immunoregulatory role played by the soluble receptors remains unclear. Although natural forms of soluble IL-4R (sIL-4R) are known to be present in the biologic fluids of normal mice, the mechanisms regulating the production of sIL-4R have not been characterized. In this study, we have developed an ELISA that allows the measurement of sIL-4R without interference from endogenous IL-4, and have analyzed the effect of cellular activation and several cytokines on the secretion of sIL-4R by murine splenic cells. Although normal spleen cells in culture produced low, but detectable levels of sIL-4R under basal conditions, stimulation with the T cell-mitogens, Con A or soluble anti-CD3 antibodies, caused a 10- to 40-fold increase in the production of sIL-4R. Stimulation of B lymphocytes with LPS, however, did not result in significant up-regulation of sIL-4R secretion. Moreover, IL-4, but not other cytokines, was also a potent inducer of sIL-4R production by spleen cells, even in the absence of other stimuli. Blocking experiments with an anti-IL-4 antibody, 11B11, demonstrated that the effect of T cell-mitogens is partially mediated by endogenously produced IL-4. Cell depletion experiments suggested that although the effect of T cell-mitogens was dependent on the presence of viable T cells, all major cell types including T cells, B cells, and macrophages, either resting or activated, were able to up-regulate their secretion of sIL-4R in response to IL-4. Unlike many activities of IL-4, the secretion of sIL-4R by IL-4-stimulated splenic cells was not antagonized by IFN-gamma. These results suggest that the production of sIL-4R is regulated by stimuli leading to T cell activation and IL-4 secretion and are consistent with sIL-4R having an important role in the regulation of IL-4 activity in vivo.
Reversion of the SCID phenotype by human T cell grafts. Development of cross-species immunocompetence.
Authors: Donjon C M , Morkowski H , Cheung R K , Leeder J S , Dosch H M 
Published: January 2023

Abstract
Due to defective recombinase function, mice with severe combined immunodeficiency (SCID) lack functional lymphocytes and can accept human lymphoid xenografts. Xenografted animals (SCIDhum) are thought to provide a neutral environment for in vivo studies of normal, malignant or HIV-infected human cells. SCIDhum often develop endogenous, EBV+ lymphomas in the graft and in the our study two-thirds of 142 SCIDhum mice did so. Surprisingly, one-third of animals developed reversion of the SCID phenotype rapidly after human T cell engraftment. 90% of tumors occurred in nonrevertant and only 10% in revertant mice. These revertant animals showed immunologic tolerance for normal human B lymphocytes, maintained stable levels of mouse and human IgM and IgG. In addition, they generated competent mouse T cells able to kill transformed (EBV+) but not fresh B cells from the same donor nor unrelated human B cell lines. The tolerance for human lymphoid cells and the cross-species antitumor competence of host T lymphocytes imply unexpected recognition and selection events. Rather than a neutral "bioreactor," these observations mark the SCID host as potentially active participant in a composite immune system generated by xenografting.
A lymphostromal molecule, thymic shared Ag-1, regulates early thymocyte development in fetal thymus organ culture.
Authors: Randle E S , Waanders G A , Masciantonio M , Godfrey D I , Boyd R L 
Published: January 2023

Abstract
Previously, we detailed the characterization of thymic shared Ag-1, a unique marker of immature thymocytes and isolated thymic stromal cells, defined by the mAb MTS 35. In this study, the functional relevance of this molecule to thymopoiesis was investigated by the addition of purified MTS 35 to fetal thymus organ culture. It down-regulated thymic shared Ag-1 expression and dramatically reduced thymocyte cell yield through inhibition of alpha beta-TcR+ T cell differentiation, post CD3-CD4-CD8- triple negative thymocytes. These effects were specific for the mAb MTS 35, because controls, which include both isotype-matched and other lymphostromal mAb, showed no similar effects. These results demonstrate that thymic shared Ag-1 is a functionally important marker of early thymocyte differentiation, particularly with regard to the alpha beta-TcR lineage.
Role of CD4+ T cells in the expansion of the CD4-, CD8- gamma delta T cell subset in the spleens of mice during blood-stage malaria.
Authors: van der Heyde H C , Manning D D , Weidanz W P 
Published: January 2023

Abstract
The previously observed expansion of the splenic gamma delta T cell subset was examined during the course of murine malaria to determine whether CD4+ T cells are required. Flow cytometric analysis during the course of Plasmodium chabaudi adami malaria in both C57BL/6 and BALB/c mice revealed that the maximal percentage of CD4+ T cells that were blasts occurred during the period of ascending parasitemia, whereas the maximal numbers of gamma delta T cells and blast cells occurred during the period of descending parasitemia. Transfer of enriched populations of CD4+ cells (&gt; 75%) containing &lt; 0.9% gamma delta T cells from immune BALB/c donor to SCID mice led to a population of gamma delta T cells that constituted 37% of the splenic T cells in the recipients and allowed them to resolve their infections. Transfer of the CD4- fraction did not suppress parasitemia. These results suggest that CD4+ T cells are activated early during the infection and are required for the subsequent expansion of the gamma delta T cell population. Furthermore, the maximal gamma delta T cell blast response during the period of descending parasitemia and the detection of high levels of these cells only in models that resolved their infections suggest that these cells may function in the resolution of blood-stage malaria.
Antigen-dependent stimulation by bone marrow-derived mast cells of MHC class II-restricted T cell hybridoma.
Authors: Frandji P , Oskéritzian C , Cacaraci F , Lapeyre J , Peronet R , David B , Guillet J G , Mécheri S 
Published: January 2023

Abstract
This paper describes a new role for mast cells as being able to present Ag to immune T cells. A mouse bone marrow-derived mast cell population obtained after 3 wk of culture in a conditioned medium has been shown to express a variety of membrane-associated Ag, including MHC class II and class I Ag, CD23, CD32, high affinity receptor for IgE, and CD4. Expression of MHC class II molecules was up-regulated upon stimulation with LPS but not with IFN-gamma and was down-regulated after exposure of mast cells to IL-3 treatment. We have demonstrated that mast cells were able to present native Ag as well as immunogenic peptides to MHC class II-restricted T cell hybridoma. The inhibition of Ag presentation after mast cells have been treated with ammonia suggests that Ag catabolism in intracytoplasmic compartment as a key step in Ag handling takes place in these cells. The MHC class II molecule is the restricting element for the presentation of OVA and the lambda repressor from bacteriophage lambda to a panel of specific T cell hybridomas, as demonstrated by the blocking effect of anti-MHC class II mAb on the Ag-presenting function. A characteristic feature of mast cells is the generation of a narrower immunogenic peptide repertoire as compared with A20 and LBB 3.4.16, a B lymphoma cell line, and a B cell hybridoma, respectively. This novel function of mast cells brings to a much closer connection inflammatory and immunologic processes and sheds new light on the biology of mast cells and particularly on the specific allergic responses.
Intravenous interleukin-8 inhibits granulocyte emigration from rabbit mesenteric venules without altering L-selectin expression or leukocyte rolling.
Authors: Ley K , Baker J B , Cybulsky M I , Gimbrone M A , Luscinskas F W 
Published: January 2023

Abstract
Injection (i.v.) of the granulocyte chemoattractant/activator IL-8 has been shown to reduce neutrophil recruitment into dermal inflammatory sites in vivo. To further investigate the mechanism of this phenomenon, we examined the effect of i.v. [Ser-IL-8]72 (12-20 micrograms/kg) on leukocyte rolling and chemoattractant-induced emigration in mesenteric venules of New Zealand White rabbits and on expression of L-selectin (mAb LAM1-3) and CD18 (mAb 60.3) on circulating rabbit granulocytes. Within 1 min of IL-8 i.v., granulocytes virtually disappeared from carotid blood samples for approximately 5 min. Concomitantly, the flux of rolling leukocytes in mesenteric venules fell from 83 +/- 21 to 2 +/- 1 leukocytes/min. Both rolling leukocyte flux and systemic granulocyte count returned to or exceeded control values within less than 30 min. The chemoattractant/activator FMLP (0.15 microgram/kg i.v.) produced similar results. A second i.v. injection of IL-8 or FMLP, 90 min after the first challenge, had equipotent effects. Local extravascular application of IL-8 via micropipette close to a venule induced adhesion and emigration of 63 +/- 21 leukocytes per site before, but only 26 +/- 9 leukocytes per site 50 to 75 min after i.v. IL-8, when systemic granulocyte count and rolling leukocyte flux had reached or exceeded control values. This was not due to agonist-specific desensitization, because a similar reduction of leukocyte emigration was seen after FMLP i.v. Rabbit granulocytes circulating in vivo uniformly expressed near-control levels of L-selectin at all times between 3 and 360 min after IL-8 i.v. CD18 expression transiently increased after IL-8 i.v. and returned to base line by 90 min. These findings show that IL-8 i.v. reduces granulocyte recruitment to inflammatory sites by inhibiting function(s) necessary for transmigration that are independent of L-selectin and subsequent to rolling.
Macrophage progenitors from mouse bone marrow and spleen differ in their expression of the Ly-6C differentiation antigen.
Authors: McCormack J M , Leenen P J , Walker W S 
Published: January 2023

Abstract
Using mAb and magnetic and fluorescence-activated cell sorting, together with culturing in semisolid culture medium, we show that essentially all splenic macrophage progenitors are Ly-6ChiMac-1-. By contrast, bone marrow macrophage progenitors were more heterogeneous in Ly-6C expression, the majority being restricted to the Ly-6CdimMac-1- and the Ly-6C-Mac-1- subsets. These findings provide immunophenotype evidence that macrophages in the spleen and bone marrow arise from different progenitors.
Binding of monomeric human IgG defines an expression polymorphism of Fc gamma RIII on large granular lymphocyte/natural killer cells.
Authors: Vance B A , Huizinga T W , Wardwell K , Guyre P M 
Published: January 2023

Abstract
Human PBL express one or more of the three classes of Fc receptors for IgG (Fc gamma receptors, I, II, and III). Each type of Fc gamma receptor has a characteristic binding pattern for isotypes of human and mouse IgG. Large granular lymphocyte/NK cells (LGL/NK cells) express the transmembrane form of Fc gamma RIII (Fc gamma RIIIa) on their surface, whereas polymorphonuclear neutrophils (PMN) express the glycosyl phosphatidyl inositol-linked receptor that is the product of the Fc gamma RIIIB gene. Fc gamma RIII has been reported to have low affinity for monomeric IgG, regardless of the cell type on which it is expressed. This study demonstrates specific and saturable binding of monomeric human IgG (M-IgG) to Fc gamma RIIIa on LGL/NK cells but not to Fc gamma RIIIb on PMN. M-IgG binding revealed an expression polymorphism between individuals, those with either high (12,000 to 15,000) or low (4,000 to 7,000) binding sites per cell. Both high and low M-IgG-binding LGL/NK cells bound hulgG1 and IgG3 but did not bind IgG2 or IgG4. The high/low Fc gamma RIIIA expression polymorphism correlated with the ability of an individual's LGL/NK cells to perform antibody-dependent cellular cytotoxicity of erythroid cell targets.
Interferon-gamma prevents graft-versus-host disease after allogeneic bone marrow transplantation in mice.
Authors: Brok H P , Heidt P J , van der Meide P H , Zurcher C , Vossen J M 
Published: January 2023

Abstract
Lethally irradiated C3H/Law mice were injected (i.v.) with C57BL/Rij allogeneic bone marrow cells to induce a delayed type graft-vs-host disease (GVHD). Signs of GVHD first became apparent in the third week after transplantation. The disease resulted in a mortality rate of 70% at 80 days. Treatment with IFN-gamma twice weekly, for a period of 6 wk, starting at the time of bone marrow transplantation (BMT), completely prevented overt GVHD, as evidenced by a lack of diarrhea and no mortality during the follow-up period of 100 days after BMT. Also, the histologic GVHD lesions in the gastrointestinal tract were almost completely abrogated by the IFN-gamma treatment. All long term survivors were proven to be chimeras. During the induction phase of GVHD, the number of Con A-induced, IFN-gamma-producing cells in the spleen was significantly reduced in the IFN-gamma-treated mice as compared with control mice. These results suggest that the normally enhanced production of endogenous IFN-gamma in the spleen at the time of hematopoietic reconstitution after BMT is down-regulated by exogenously administered IFN-gamma. This cytokine-mediated strategy to prevent GVHD might be an alternative to the current strategy of in vitro depletion of T cells for allogeneic BMT.
Human T cell clones reactive against U-small nuclear ribonucleoprotein autoantigens from connective tissue disease patients and healthy individuals.
Authors: Hoffman R W , Takeda Y , Sharp G C , Lee D R , Hill D L , Kaneoka H , Caldwell C W 
Published: January 2023

Abstract
SLE and mixed connective tissue disease (MCTD) are characterized by the presence of high titers of autoantibodies against uridine-rich RNA-small nuclear ribonucleoprotein (snRNP) Ag. Because the presence of such snRNP-reactive autoantibodies has recently been shown to be associated with polymorphisms of HLA, this study was undertaken to determine whether snRNP-reactive T cells could be identified and characterized from patients. PBMC were stimulated with affinity-purified snRNP Ag and cloned by limiting dilution in the presence of rIL-2 and rIL-4, snRNP-reactive human T cell clones were generated from three patients and two healthy blood donors who possessed disease-associated HLA genotypes. The cell surface phenotype of clones determined by flow cytometry was CD3+, CD4+, CD45RO+, TCR V alpha beta+. TCR V beta analysis, performed using V beta-specific primers and polymerase chain reaction, revealed that the T cell lines generated were clonal; a limited number of TCR V beta genes were expressed among the clones tested. All clones tested by mAb blocking of Ag-induced proliferation were restricted by HLA-DR. Several T cell clones were identified that were specific for B'/B or D polypeptides. These results demonstrate that snRNP-reactive T cells can be isolated from SLE and MCTD patients in vitro, and that Ag-driven expansion of such T cells could play a role in the immunopathogenesis of these diseases in vivo.
Regulation of human CD44H and CD44E isoform binding to hyaluronan by phorbol myristate acetate and anti-CD44 monoclonal and polyclonal antibodies.
Authors: Liao H X , Levesque M C , Patton K , Bergamo B , Jones D , Moody M A , Telen M J , Haynes B F 
Published: January 2023

Abstract
CD44 molecules are comprised of multiple alternatively spliced forms and are associated with diverse functions such as mediation of carcinoma metastasis and T cell coactivation. To study the function of individual CD44 isoforms, we have transfected CD44 isoforms into CD44-negative Jurkat T cells and produced cloned Jurkat cell lines that are stably transfected with either a CD44 isoform containing no alternatively spliced insert (CD44H) or a CD44 variant (CD44E) containing an insert of 132 amino acids derived from exons 12, 13, and 14 of the CD44 gene. We found that neither CD44H- nor CD44E-transfected Jurkat T cells constitutively bound hyaluronan (HA), whereas PMA treatment induced Jurkat cells transfected with CD44H but not CD44E to bind HA. CD44 mAb against noninsert regions of the CD44 extracellular domain (A3D8, A1G3) and polyclonal antisera against the COOH-terminal extracellular glycosaminoglycan region of CD44H (anti-6A serum) both induced CD44H-transfected cells to bind HA, whereas only one CD44 mAb (A1G3) induced CD44E-transfected Jurkat T cells to bind HA. Studies of Jurkat cells transfected with CD44H forms with truncations of the CD44 cytoplasmic domain demonstrated that the cytoplasmic COOH-terminal 52 amino acids were critical for binding of HA to the CD44 extracellular domain. Thus, these data underscore the importance of the CD44 cytoplasmic domain in the function of the extracellular portion of CD44H, and demonstrate a role for ligation of human CD44 isoforms at multiple distinct sites in regulation of expression of CD44 binding to HA.