bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of thymectomy on peripheral lymphocyte subsets in myasthenia gravis: selective effect on T-cells in patients with thymic atrophy.
Authors: Haynes B F , Harden E A , Olanow C W , Eisenbarth G S , Wechsler A S , Hensley L L , Roses A D 
Published: December 2022

Abstract
Myasthenia gravis (MG) is an autoimmune disease affecting nicotinic acetylcholine receptors. The clinical improvement that follows thymectomy in some myasthenic patients implicates thymic factors as well in the pathogenesis of MG. We have studied circulating immunoregulatory T cell subsets before and after thymectomy in 11 adult patients with MG. Six patients had thymic hyperplasia and five patients had atrophic thymus at the time of thymectomy. Before thymectomy, patients who subsequently were shown to have an atrophic thymus, had lower lymphocyte counts than either patients later shown to have a hyperplastic thymus (1315 +/- 143 lymphocytes/mm3 vs. 2434 +/- 350 lymphocytes/mm3, p less than 0.01), or age-matched controls (1315 +/- 143 lymphocytes/mm3 vs. 2636 +/- 589 lymphocytes/mm3, p less than 0.02). Moreover, after thymectomy, in MG patients with an atrophic thymus, there was a significant rise in lymphocyte count (from 1315 +/- 143 lymphocytes/mm3 to 2279 +/- 292 lymphocytes/mm3, p less than 0.02) beginning 3 days postthymectomy and persisting for at least 6 weeks thereafter. In comparison, patients with a hyperplastic thymus showed no change in circulating lymphocyte counts (p greater than 0.1). Enumeration of lymphocyte subsets in MG patients with an atrophic thymus demonstrated normal B cell numbers before and after thymectomy (p greater than 0.1), whereas, T cells were significantly decreased before thymectomy compared with age-matched normal subjects (859 +/- 82 T cells/mm3 vs. 2215 +/- 545 T cells/mm3, p less than 0.05), and rose to near normal levels after thymectomy (1796 +/- 294 T cells/mm3, p less than 0.02 compared with prethymectomy levels). Using monoclonal anti-T cell antibodies 3A1, OKT4, and OKT8, we found that, before thymectomy in the atrophic thymus group, 3A 1+ T cells were significantly depressed compared with postthymectomy levels (620 +/- 173 cells/mm3 vs. 1627 +/- 331 cells/mm3, p less than 0.02) as were OKT4+ cells 436 +/- 88 cells/mm3 vs. 1112 +/- 63 cells/mm3, p less than 0.001), In contrast, no significant change was seen after thymectomy in the OKT8+ cell subset (p greater than 0.1). MG patients with an atrophic thymus had decreased plasma cortisol levels postthymectomy compared with prethymectomy levels, whereas thymectomy in MG patients with a hyperplastic thymus effected no change in plasma cortisol levels. These data demonstrate in MG patients with an atrophic thymus that thymectomy has an effect on the number of circulating T cells, and in particular, on those T cells expressing antigens 3A1 and OKT4. This effect may in part be mediated by changes in plasma adrenal corticosteroid levels after thymectomy or may be due to a factor produced by atrophic thymuses in MG.
Expansion of cyclophosphamide-resistant cytotoxic precursors in vitro and in vivo by purified human interleukin 2.
Authors: Merluzzi V J , Welte K , Savage D M , Last-Barney K , Mertelsmann R 
Published: December 2022

Abstract
Precursors of cytotoxic lymphoid cells obtained from mice treated with cyclophosphamide (CY) can be expanded in culture by alloantigens in the presence of purified human interleukin 2 (IL 2). Similarly, IL 2 delivered in vivo in a rate-controlled manner enhances cytotoxic activity in mice that are immunosuppressed by high doses of CY. The effector cells are Thy-1.2+ and are not elicited in the absence of antigen.
Tryptic peptide disparity between serologically indistinguishable guinea pig Ia.3,5 antigens.
Authors: Fuge Abruzzini L N , Zacheis M P , Schwartz B D 
Published: December 2022

Abstract
Serological studies have suggested that the DHCBA strain guinea pig expresses an I region which is identical to that of strain 13. However, chemical characterization of Ia.3,5 molecules isolated from these two strains has indicated that these serologically indistinguishable Ia molecules are actually chemically distinct. Ia.3,5 molecules biosynthetically labeled with either [3H]leucine, [3H]arginine, or [3H]lysine were purified by ricin affinity chromatography and isolated by indirect immunoprecipitation with specific alloantisera. Initial examination of the two Ia.3,5 molecules by SDS-PAGE, isoelectric focusing, and two-dimensional gel analyses revealed no strain-specific differences. Furthermore, comparative peptide mapping of the DHCBA and strain 13 radiolabeled Ia.3,5 alpha-chains demonstrated complete peptide homology. In contrast, tryptic peptide maps of amino acid radiolabeled beta-chains revealed two peptides unique to the strain 13 beta-chain and one peptide unique to the DHCBA beta-chain. Analysis of [3H] mannose-labeled beta-chain tryptic peptides verified that the peptide differences observed using 3H-amino acids were not due to variation in N-linked glycosylation. However, strain-specific variability was also noted in the profiles of [3H]mannose-labeled beta-chains. These data indicate that the strain 13 and DHCBA alpha-chains are probably structurally identical, while the beta-chains show strain specific alterations in their chemical structure.
IgE-dependent and ionophore-induced generation of leukotrienes by dog mastocytoma cells.
Authors: Phillips M J , Gold W M , Goetzl E J 
Published: December 2022

Abstract
Isolated dog mastocytoma cells sensitized with dog anti-ragweed IgE and challenged with ragweed antigen generate the C-6 peptide leukotriene (LT) constituents of the slow-reacting substance of anaphylaxis (SRS-A), LTC4 and LTD4, and the potent leukocyte chemotactic factor, LTB4, as well as 15-hydroxyeicosatetraenoic acid (15-HETE), 12-HETE, and 5-HETE. Antigen challenge evoked a mean maximum production of LTC4, LTD4, and LTB4, respectively, of 16.3 ng, 4.6 ng, and 6.7 ng per 10(6) mastocytoma cells within 5 min at 37 degrees C, which was maintained for up to 45 min. The maximum production of leukotrienes by mastocytoma cells activated with optimum concentrations of 0.2 to 1 microM calcium ionophore A23187 was 35% to 50% greater than that achieved by antigen challenge, without alterations in the relative quantities of leukotrienes, but was realized only after 30 min at 37 degrees C. The leukotriene products of mastocytoma cells were identified by high-performance liquid chromatography, spectral properties, and immunoreactivity with mono-specific antisera, and exhibited the same concentration-dependence of biologic activity as authentic synthetic standards. The ratio of quantities of C-6 peptide leukotrienes generated was attributable in part to the rate of peptidolytic conversion of LTC4 to LTD4 in the mastocytoma cells, which was 33% per 30 min at 37 degrees C. The rapid maximum response to IgE-dependent stimulation and the unique spectrum of products distinguishes the secretion of leukotrienes by dog mastocytoma cells from that by basophils and some other types of mast cells and suggests diverse contributions of mast cell leukotrienes to immediate and late hypersensitivity reactions.
Frequency of mast cell precursors in normal tissues determined by an in vitro assay: antigen induces parallel increases in the frequency of P cell precursors and mast cells.
Authors: Crapper R M , Schrader J W 
Published: December 2022

Abstract
Persisting (P) cells, homogeneous populations of cells that grow in vitro for prolonged periods provided a specific growth factor is present, resemble mast cells in many respects. An in vitro assay based on limit dilution was used to determine the frequency of precursors capable of giving rise to P cells. The incidences of P cell precursors per 10(6) cells in tissues of CBA mice in representative experiments were as follows: bone marrow, 291; spleen, 30; mononuclear blood cells, 11; popliteal lymph node, 0.5; and mesenteric lymph node, 18. P cell precursors appeared to be relatively undifferentiated, non-granulated cells; no cells with metachromatically staining granules were detected in the bone marrow or peripheral blood. Furthermore, mice of the Wf/Wf genotype that were grossly deficient in mast cells had the same frequencies of P cell precursors in bone marrow and spleen as their normal +/+ littermates. In many tissues in which we found P cell precursors, pluripotential hemopoietic stem cells are present. Among nonepithelial cells from the gut mucosa, however, in which there was a 10-fold higher frequency of P cell precursors than in bone marrow cells, pluripotential hemopoietic stem cells were undetectable, indicating the existence of committed P cell precursors distinct from pluripotential hemopoietic stem cells. The frequency of P cell precursors in mesenteric lymph nodes was more than 30-fold higher than in the popliteal lymph nodes, suggesting that antigenic stimulation influences their numbers. This latter notion is supported by the observation that after immunization in the footpad, the number of P cell precursors in ipsilateral popliteal lymph nodes rose about 35-fold. Immunization was also accompanied by a rise in mast cell numbers in draining popliteal nodes. This correlation between P cell precursors and the local production of mast cells was strengthened by the observation that the frequency of P cell precursors in cells from the gut mucosa of mice of Wf/Wf genotype, which are unable to mount an intestinal mastocytosis, was more than 1000-fold lower than in wild type mice. Thus, the precursors of P cells and probably of at least the T cell-dependent subset of mast cells appear to be generated in the bone marrow and seed as non-granulated cells via the blood to peripheral tissues such as spleen, lymph node, and mucosal surfaces. P cells appear to be in vitro counterparts of the mucosal subset of mast cells.
Macrophages as effector cells of protective immunity in murine schistosomiasis. V. Variation in macrophage schistosomulacidal and tumoricidal activities among mouse strains and correlation with resistance to reinfection.
Authors: James S L , Skamene E , Meltzer M S 
Published: December 2022

Abstract
Mice of several inbred strains previously characterized as defective in various aspects of macrophage activation for tumor cell killing were utilized to compare the genetic control of induction of macrophage tumoricidal and schistosomulacidal activity and to examine the role of activated macrophages in concomitant immunity to Schistosoma mansoni infection. In all mouse strains tested, macrophage larvicidal activity developed concurrently with tumoricidal activity after in vivo bacillus Calmette Guérin or Corynebacterium parvum treatment. Lpsd strains, A/J, and P/N mice failed to develop macrophages capable of killing either tumor cells or helminth larvae in vitro, whereas C57BL/6J, C3H/HeN, and BALB/c mice all demonstrated strongly cytotoxic cells. In fact, analysis of the reactivity of peritoneal cells from C. parvum-treated F1 hybrids between H-2 congeneic high responder (B10.A) and low responder (A) strains of mice, as well as from F1 hybrid X parent backcross animals, suggested that macrophage activation for killing of these two unrelated extracellular targets is controlled by the same autosomal dominant gene. Strains of mice that failed to develop activated macrophages after in vivo treatment with bacterial stimuli also failed to develop tumoricidal and larvicidal macrophages as a result of S. mansoni infection. The addition of antischistosome sera to the cultures did not reverse the unresponsiveness of macrophages from S. mansoni-infected C3H/HeJ, A/J, or P/N mice in in vitro larvicidal assays. Furthermore, the pattern of concomitant immunity at 6 wk after primary S. mansoni infection correlated closely with the pattern of induction of activated macrophages in these strains of mice. Whereas animals with normal macrophage function developed highly significant levels of concomitant immunity, strains with the Lps defect demonstrated lower levels of acquired resistance, and A/J and P/N mice were not significantly resistant to S. mansoni challenge infection. These results indicate that the genes controlling macrophage activation for the killing of extracellular targets also influence the development of concomitant immunity in schistosomiasis, and suggest that macrophages activated as a consequence of primary S. mansoni infection may be involved in the in vivo effector mechanism of resistance to challenge infection.
Trypanosoma cruzi: description of a highly purified surface antigen defined by human antibodies.
Authors: Scharfstein J , Rodrigues M M , Alves C A , de Souza W , Previato J O , Mendonça-Previato L 
Published: December 2022

Abstract
A glycoprotein of 25,000 daltons (G25) purified from T. cruzi extracts is recognized by serum antibodies of Chagas' disease patients. These human antibodies were isolated by affinity chromatography and were used to demonstrate that G25 antigenic determinants are i) represented at the parasite surface, and ii) are expressed in all developmental stages of the parasite's life cycle, as well as in several T. cruzi strains. This antigen-antibody system may be useful for the diagnosis of Chagas' disease because antibodies to radiolabeled G25 are found in the serum of 96.5% of 173 chagasic patients from different endemic areas, but are not found in the serum from other individuals. Taken collectively, the data suggest that antibodies to G25 define highly conserved determinants of the species T. cruzi. Moreover, its remarkable immunogenicity to infected humans offers an opportunity to investigate the role of specific immunologic responses in the pathogenicity of Chagas' disease.
Epinephrine-induced changes in the distribution of lymphocyte subsets in peripheral blood of humans.
Authors: Crary B , Hauser S L , Borysenko M , Kutz I , Hoban C , Ault K A , Weiner H L , Benson H 
Published: December 2022

Abstract
We have previously demonstrated that mitogen responsiveness of mononuclear cells (MNC) from peripheral blood is reduced after a single injection of epinephrine to human subjects. The purpose of the present study was to characterize the relative distributions of MNC subsets after epinephrine administration using monoclonal antibodies and conventional cell markers. The absolute number of circulating MNC increased 64% within 30 min after injection of epinephrine, and returned to baseline by 2 hr. Analysis of MNC subsets revealed that there were no changes in the relative percentages of total T lymphocytes [T3+ cells, or neuraminidase-treated sheep red blood cell rosettes (EN-rosettes)], B lymphocytes (B1+, or cells with surface-bound immunoglobulin), or monocytes (by morphologic criteria) after epinephrine administration. The percentage of inducer T cells (T4+) declined at 30 and 60 min postinjection. Overall, the percentage of suppressor/cytotoxic T cells (T8+) did not change after injection of epinephrine; however, analysis of individual subjects revealed opposing responses of this subset. The T4:T8 ratio was 2.19 before injection, declined to 1.56 at 60 min, then increased to 3.10 2 hr postinjection. The percentage of natural killer/killer cells (HNK-1+) increased from a baseline of 15.5% before epinephrine injection to 29.6% at 30 min postinjection, then declined to 11.4% at 2 hr. Therefore, the administration of physiologic doses of epinephrine results in changes in the relative proportions of lymphocyte subsets in peripheral blood, in addition to reduced mitogen responsiveness as reported previously.
Two phenotypically distinct suppressor T cell subpopulations inhibit the induction of B cell differentiation by phytohemagglutinin.
Authors: Clement L T , Dagg M K , Lehmeyer J E , Kiyotaki M 
Published: December 2022

Abstract
Human B lymphocytes can be induced to differentiate into antibody-secreting plasma cells by Leu-3+ T lymphocytes stimulated with pokeweed mitogen (PWM), a polyclonal T cell activator. In contrast, other polyclonal T cell mitogens, such as phytohemagglutinin (PHA), also activate Leu-3+ T cells but are relatively ineffective inducers of B cell differentiation. We have performed a series of experiments to investigate the mechanism underlying this apparent paradox. When human B cells were cultured with unfractionated T cells and PWM or PHA, only PWM was able to induce plasma cell formation and immunoglobulin (Ig) secretion. However, when the T cells were treated with mitomycin C (MMC) before culture, both PWM and PHA were able to induce significant B cell differentiation. These data indicated that both mitogens were able to activate the helper T cells required for B lymphocyte differentiation and suggested that MMC-sensitive suppressor T cells were responsible for inhibiting the induction of antibody-secreting cells by MMC-untreated T cells stimulated with PHA. Phenotypic analysis of the T cells capable of suppressing PHA-induced B cell differentiation revealed that small numbers of either Leu-2+ or Leu-3+ T cells could profoundly suppress the B cell differentiation induced by PHA. In contrast, significant suppression of PWM-stimulated B cell differentiation was observed only with relatively large numbers of Leu-2+ T cells. These data confirm previous reports that OKT4+/Leu-3+ T cells can suppress human B cell differentiation and indicate that the difference in B cell differentiation induced by PWM and PHA with MMC-untreated T cells is largely a reflection of the relative potency of these mitogens to activate these phenotypically distinct suppressor T cell subpopulations.
Defective B cell function associated with inherited interstitial deletion of the short arm of the X chromosome.
Authors: Eskola J , Nurmi T , Ruuskanen O 
Published: December 2022

Abstract
The B cell function of a patient with low serum immunoglobulin (Ig) levels and with an interstitial deletion in the short arm of one of her X chromosomes (del(Xp] and the B cell function of her relatives were analyzed by indirect protein A plaque-forming cell (PFC) assay and by measuring immunoglobulin secretion in vitro by ELISA. B cells were activated by pokeweed mitogen (PWM) with or without hydrocortisone (HC) to inhibit HC-sensitive suppressor cells. The patient, her mother, and one sister, all of them having del(Xp), generated very few PFC induced by PWM, even in the presence of HC, whereas normal PFC responses were found in the patient's cytogenetically normal sisters. The B cells of the subjects with del(Xp) secreted very low amounts, if any, of IgA, IgG, and IgM. Co-culture experiments with B cells from del(Xp) subjects and normal OKT 4+ cells revealed no or very low Ig production. The function of the del(Xp) subjects' OKT 4+ cells was slightly reduced, whereas the activity of their OKT 8+ cells was normal. The cell subset analysis in the peripheral blood revealed decreased OKT 4+:8+ ratios in all del(Xp) subjects. The results indicate an intrinsic B cell defect with a possible concomitant immunoregulatory defect associated with del(Xp). Moreover, the results support the hypothesis that antibody production is at least partially controlled by genes located in the short arm of the X chromosome.
Monocyte receptors for the Fc portion of IgG increase in number in autoimmune hemolytic anemia and other hemolytic states and are decreased by glucocorticoid therapy.
Authors: Fries L F , Brickman C M , Frank M M 
Published: December 2022

Abstract
Peripheral blood monocyte receptors for the Fc portion of IgG were quantitatively studied in 43 normal subjects, in 14 patients with warm antibody autoimmune hemolysis (AIHA), and in nine individuals with nonantibody-mediated hemolysis. Monocytes of normal females expressed significantly greater numbers of Fc gamma receptors than did similar cells from male subjects, with no difference in affinity for the IgG1 probe. Monocyte Fc gamma receptor number was increased in patients of both sexes with AIHA; a similar, but smaller, increase in monocyte Fc gamma receptor number was noted in patients with nonantibody-mediated hemolysis. Glucocorticoid administration was associated with a dose-dependent decrease in monocyte Fc gamma receptor number in normal volunteers and patients. Possible etiologic mechanisms and pathogenetic consequences of enhanced monocyte Fc gamma binding in AIHA are discussed.
Regulatory function of Thy-1- cells. IV. Biologic and Biochemical characterization of B cell clone-derived lymphokine (BEF).
Authors: del Guercio P , Poirier M F 
Published: December 2022

Abstract
Studies were made on the immunoregulatory activity of a lymphokine produced by a B cell clone that does not express immunoglobulin heavy or light chains. The B factor (BEF; B cell-derived enhancing factor), was effective in augmenting the primary and the anamnestic response to SRBC and/or in prolonging the IgG anamnestic response to SRBC and the response to DNP-LE, provided it was added at early stages of culture. The BEF seems to act mainly by preventing the activation of T suppressor cells rather than by counteracting the activity of already activated suppressor cells. Indeed, thymocytes and virgin T cells, but not Con A-activated thymocytes, Con A-activated T cells or B cells, express acceptors for the BEF. The biochemical properties of the BEF were also reported. The apparent m.w. of the factor was 450,000 to 500,000 by gel chromatography. The BEF was sensitive to digestion by papain, trypsin, and subtilisin, indicating that it was protein in nature. The regulatory activity was precipitated by 50% (NH4)2SO4 and was destroyed by heating at 70 degrees C for 30 min or by exposure to pH 2.2 for 6 hr.
Restoration of LPS responsiveness of C3H/HeJ mouse lymphocytes by microinjection of cytoplasmic factor(s) from LPS-stimulated normal lymphocytes.
Authors: Eda Y , Ohara J , Watanabe T 
Published: December 2022

Abstract
Cytosol fractions of lymphocytes from LPS-responder mice (C3H/HeN) were prepared and injected into B lymphocytes of LPS-nonresponder mice (C3H/HeJ) by a microinjection technique utilizing polyethyleneglycol-mediated cell fusion. The B lymphocytes of C3H/HeJ mice microinjected with cytosol prepared from LPS-stimulated C3H/HeN cells became normally responsive to LPS. Microinjection of cytosol itself did not stimulate C3H/HeJ cells to proliferate or differentiate into immunoglobulin-producing cells, and the cells injected with cytosol had to be restimulated with LPS in order to proliferate and differentiate. These data suggested that C3H/HeJ B cells acquired LPS responsiveness by microinjection of cytoplasmic factor(s) from LPS-stimulated C3H/HeN cells and that these factor(s) may be one of the components involved in normal signal transmission from cell surface to nucleus in the early stages of the LPS response. The apparent m.w. of the cytoplasmic factor(s) is 100,000 by gel filtration. Chromatofocusing analysis suggested that these factors may consist of two components with the same m.w.