bluuebunny/crossref_metadata_2025_split huggingface dataset:
How complement kills E. coli. II. The apparent two-hit nature of the lethal event.
Authors: Wright S D , Levine R P 
Published: December 2022

Abstract
We have studied the nature of complement (C) action on red blood cells and E. coli with respect to the number of "hits" required for membrane damage. Our method of analysis involves adding various amounts of purified C7 or C8 to serum preparations immunochemically depleted of C7 or C8, respectively, in order to construct dose-response curves for the action of C's terminal complex. The shape of the dose-response curves reflects the single or multiple-hit nature of C action. Our method confirms that C acts on red cells by a 1-hit mechanism, whether measured by lysis or by the permeation of a small molecule. In contrast, we find with E. coli that C-mediated outer membrane damage, inner membrane damage, and killing all appear to require more than 1 hit. We have also discovered a property of E. coli that displays a nonlethal 1-hit response to C that is particularly useful in the analysis of multiple-hit dose-response curves. Simultaneous measurements of this single-hit phenomenon and the multiple-hit killing of E. coli allow us to make direct comparisons of the amount of C needed for each response. On the basis of the midpoints of the single and multiple-hit curves, C-mediated membrane damage and killing of E. coli appear to be a 2-hit process.
Reciprocal transfer of abnormalities in clonable B lymphocytes and myeloid progenitors between NZB and DBA/2 mice.
Authors: Jyonouchi H , Kincade P W , Good R A , Fernandes G 
Published: December 2022

Abstract
Previous studies in this laboratory revealed that NZB mice have abnormalities of myeloid progenitor populations from an early age such that they are poorly responsive to a particular type of colony-stimulating activity (CSA). In addition, these mice develop abnormally high numbers of B cells that can be cloned in semisolid agar cultures and that are atypical in resisting inhibition by anti-mu antibodies. To investigate whether these abnormalities, like other autoimmune phenomena studied previously, are transferrable with hemopoietic cell grafts, we performed reciprocal bone marrow transplants between NZB and normal DBA/2 mice. Irradiated control mice given syngeneic marrow did not change with respect to any of the parameters that were measured. In contrast, DBA/2 recipients of NZB marrow were indistinguishable from NZB mice in terms of CSA responses and incidences of anti-mu resistant B cells. The proportions but not total numbers of clonable B cells ere elevated in these mice until at least 16 wk after grafting. Conversely, NZB mice given DBA/2 cells had all of the normal characteristics of DBA/2 mice. Transplantation did not cause significant changes in hematocrits, reticulocyte counts, or spleen weights. Therefore, all elements necessary for expression of these lymphoid and nonlymphoid abnormalities of NZB mice are intrinsic to radiosensitive hemopoietic cells.
Deactivation of human neutrophil chemotaxis by chemoattractants: effect on receptors for the chemotactic factor f-Met-Leu-Phe.
Authors: Donabedian H , Gallin J I 
Published: December 2022

Abstract
Normal human peripheral blood PMN were exposed to varying concentrations of partially purified chemotactic complement fragments (C5fr) and a chemotactic peptide N-formyl methionylleucylphenylalanine (f-Met-Leu-Phe). This exposure resulted in a decreased chemotactic response termed deactivation of chemotaxis. Deactivation was found to be nonpreferential for the deactivating stimulus when high concentrations of either f-Met-Leu-Phe (10(-6) M) or C5fr (20 micrograms/ml) were used. When PMN were incubated with lower concentrations of C5fr (10 micrograms/ml), there was preferential deactivation towards C5fr. Similarly, preferential deactivation of chemotaxis was observed when PMN were incubated with 10(-6) M f-Met-Leu-Phe, but this was transient and cells were nonpreferentially deactivated 60 min after the initial exposure to f-Met-Leu-Phe. The availability of receptors for tritiated f-Met-Leu-Phe was examined by Scatchard analyses and measurement of reversible f-Met-Leu-[3H]Phe binding to C5fr and f-Met-Leu-Phe-deactivated PMN. When PMN f-Met-Leu-Phe receptors were studied immediately after exposure to concentrations of C5fr causing either preferential or nonpreferential deactivation, there was increased receptor availability compared with control PMN. In contrast, PMN deactivated with high concentrations of f-Met-Leu-Phe 10(-6) M) had a transient decrease in the number of receptors followed 1 hr later by an increase in the number of receptors. This was similar to the functional correlate of preferential deactivation of chemotaxis immediately after incubation with f-Met-Leu-Phe followed by nonpreferential deactivation in these same PMN. The data indicate that preferential deactivation of chemotaxis may be associated with a preferential decrease (down-regulation) of chemoattractant receptors and that nonpreferential deactivation is associated with an increase in chemoattractant receptors.
Lipid metabolism during mediator release from mast cells: studies of the role of arachidonic acid metabolism in the control of phospholipid metabolism.
Authors: Marquardt D L , Nicolotti R A , Kennerly D A , Sullivan T J 
Published: December 2022

Abstract
Recent studies indicate that both arachidonic acid (AA) metabolism and phospholipid (PL) metabolism are markedly stimulated during the release of mediators from mast cells. The relationship between stimulated AA metabolism and stimulated PL metabolism in isolated rat mast cells was investigated and then correlated with the secretory process. ETYA (5,8,11,14-eicosatetraynoic acid, a known inhibitor of cyclooxygenase and lipoxygenase pathways of AA metabolism) inhibited 32PO4 incorporation into phosphatidic acid (PA), phosphatidylinositol (PI), and phoshodidylcholine (PC) in both unstimulated mast cells and mast cells stimulated by cross-linking of surface IgE molecules. ID50 values for inhibition of mediator release and of basal and stimulated 32PO4 incorporation into PL were 50 to 60 microM ETYA. Indomethacin (1 to 10 microM) and aspirin (10 to 100 microM) had no significant effect on 32PO4 incorporation or on mediator release. AA (10 microM) inhibited PL labeling in resting mast cells and rendered the cells less responsive to secretory signals. Preincubation of the cells with indomethacin (1 microM) blocked both of these AA effects. When AA was added to stimulated mast cells, however, both PL labeling and mediator release were enhanced. Thus, each of the alterations in AA metabolism caused parallel changes in mast cell PL metabolism and in mediator release. Since both basal and stimulated PL metabolism were modified by ETYA and AA, some form of direct regulation of mast cell PL metabolism by AA metabolites seems likely. The close parallelism of effects on mediator release and on PL metabolism suggests that modulation of mast cell function by AA metabolites may be mediated at lest in part by effects on lipid metabolism.
A genetic locus responsible for salmonella susceptibility in BSVS mice is not responsible for the limited T-dependent immune responsiveness of BSVS mice.
Authors: Briles D E , Benjamin W H , Williams C A , Davie J M 
Published: December 2022

Abstract
BSVS mice are known to be highly susceptible to salmonella infection. We have shown that the bulk of the difference in susceptibility between BSVS and salmonella-resistant A/J mice is the result of a genetic difference at a single locus not closely linked to H-2, Igh-C, or Hbb, and not X-linked. We have backcrossed the A/J allele at this locus into BSVS mice for 8 successive generations and have demonstrated that the salmonella resistance afforded by this allele is not the result of a restoration of the generalized poor T-dependent responsiveness of BSVS mice. The salmonella resistance locus we have examined with these 2 strains is probably the same as the Ity locus described by others.
Analysis of Ir gene control of cytotoxic response to hapten-modified self: helper T cells specific for a sulfhydryl hapten can substitute for an anti-TNP-H-2b self helper cell defect.
Authors: Fujiwara H , Levy R B , Shearer G M 
Published: December 2022

Abstract
Helper T cells specific for N-iodoacetyl-N'-(5-sulfonic 1-naphthyl) ethylene diamine (I-AED) were generated in (C56BL/6 X C3H/He)F1 mice by immunization with I-AED-modified syngeneic cells (AED-self). The requirements for activation of hapten-induced helper cells were investigated. The results demonstrated that activation of AED and trinitrophenyl- (TNP) helper cells was strictly hapten specific. In addition, F1 AEd-helpers could be activated efficiently by either I-AED-modified H-2b or H-2k self components to enhance the anti-AED self-CTL responses. This contrasts with the previous findings demonstrating the failure of TNP-H-2b self to activate F1 TNP-helper cells. After AED-helpers were activated, they were capable of augmenting sensitization of cytotoxic T cells (CTL) against TNP-self. These results indicate that although the activation of hapten-reactive helper cells is antigen (hapten)-specific, the subsequent helper activity, as determined by augmentation of CTL responses against another hapten, is antigen nonspecific. Since helper function was antigen nonspecific, F1 AED-helper cells activated by AED-H-2b or AED-H-2k self were tested for their ability to augment the F1 and anti-TNP-H-2b CTL response. The results indicate that the Ir gene defect in the ability of F1 spleen cells to respond to TNP-H-2b self could not be corrected by these helper cells. These results are discussed in the light of Ir gene controlled differences in the activation of AED and TNP-helper cells and possible models for augmenting CTL responses against various antigens in strains that generate marginal helper activity to TNP-self.
Immunoglobulin-bearing cells are a target for the antigen-induced inhibition of pokeweed mitogen-stimulated antibody production.
Authors: Stevens R H 
Published: December 2022

Abstract
In vivo immunization with tetanus toxoid causes the appearance of B cells in the circulation that can produce IgG-antitetanus toxoid antibody in vitro after stimulation by T cells and pokeweed mitogen. Addition of soluble tetanus toxoid to these cultures, however, causes a profound inhibition of the in vitro IgG, but not IgM, antitetanus toxoid antibody production. Treatment of the lymphocytes with 10 microgram of tetanus toxoid for as little as 1 hr at 37 degrees C was sufficient to promote this antigen-specific inhibition. The antigen could be added, however, as late as 3 days after the culture initiation for the inhibition to be observed. Cell separation studies indicated that the inhibitory activity could be found in both the E-rosette positive and E-rosette negative populations. Further studies on the non-E-rosetting cells showed that: 1) inhibition induced in antigen-treated cells could not be transferred to untreated cells; 2) adherent cells were not responsible for the inhibition; 3) treatment of the surface Ig+ cells with antigen was sufficient for the inhibitory effects; and 4) in vivo generated lymphoblastoid cells that produce IgG-antitetanus toxoid antibody in vitro but are surface Ig- were not inhibited by soluble antigen. The results in this study thus indicate that cells in both the E-rosette positive and negative subsets can be responsible for the antigen-induced inhibition of in vitro antibody production observed in the majority of immunized donors.
Lymphocyte recognition of lymph node high endothelium. III. Enhancement by a component of thoracic duct lymph.
Authors: Carey G D , Chin Y H , Woodruff J J 
Published: December 2022

Abstract
The first step in the entry of blood lymphocytes into lymph node is the binding of these cells to venules lined by high endothelium (HEV). This recognition event has been studied using a model system in which rat thoracic duct lymphocytes (TDL) adhere selectively to HEV when overlaid onto lymph node sections. We now report that this binding is increased by a lymph fraction designated adherence enhancing factor (AEF). Lymph depleted of cells and chylomicra was fractionated with (NH4)2SO4. Material that precipitated between 60 and 80% saturation was dissolved in buffer and extracted with chloroform/methanol; the aqueous phase was used as the source of AEF. The factor was nondialyzable, trypsin sensitive, and heat stable (70 degrees C, 30 min). Lymph node sections pretreated with AEF showed a 2- to 3-fold increase in the number of TDL bound to HEV and a 5 to 10-fold increase in the number of HEV with more than 5 adherent lymphocytes. The effect of AEF was specific: 1) No increase in lymphocyte binding to non-HEV areas of the tissue section occurred. 2) The binding of both TDL and spleen lymphoid cells to HEV was enhanced, but thymocyte attachment was not promoted. We conclude that AEF has biologic properties that might enable it to play a physiologic role in lymphocyte recirculation.
Detection and localization of a lectin on Actinomyces viscosus T14V by monoclonal antibodies.
Authors: Cisar J O , Barsumian E L , Curl S H , Vatter A E , Sandberg A L , Siraganian R P 
Published: December 2022

Abstract
A cell-associated lectin activity that mediates lactose-inhibitable adherence of Actinomyces viscosus T14V has been localized to a specific population of fimbriae by the use of monoclonal antibodies. Nine monoclonal antibodies were produced that reacted with only 1 of 2 immunoelectrophoretically distinct fimbrial components on T14V. The fibrillar morphology of this component was revealed by the immunoelectronmicroscopic examination of bacteria incubated with the monoclonal antibodies. The lectin activity associated with these structures was detected when isolated fimbriae were cross-linked with monoclonal antibodies to form immune complexes with agglutination activity for neuraminidase-treated human erythrocytes, a reaction that was inhibited by lactose. Although the 9 monoclonal antibodies differed in their fine specificities, they reacted only with strains of A. viscosus and A. naeslundii that exhibited lactose-inhibitable adherence. These findings indicate that the lectin activity common to these bacteria resides on fimbriae that are antigenically related to those of T14V.
The role of interleukin-2 (IL-2) in the differentiatin of cytotoxic T cells: the effect of monoclonal anti-IL-2 antibody and absorption with IL-2 dependent T cell lines.
Authors: Kern D E , Gillis S , Okada M , Henney C S 
Published: December 2022

Abstract
A variety of approaches, including the use of a monoclonal antibody, have indicated that the lymphokine Interleukin 2 is a necessary and sufficient mediator for initiating cytotoxic T cell differentiation in vitro. Mitogen (Con A, PHA) stimulation of spleen cells and K/D or I region stimulation in primary MLC all led to IL-2 production, as measured by the growth of an IL-2 dependent T cell clone, and to the production of a "helper" factor necessary for cytotoxic T lymphocyte (CTL) differentiation against metabolically inactivated stimulator spleen cells. Several lines of evidence suggested that the IL-2 activity and CTL "helper" activity were due to a single molecular entity. These included the observations that: i) There was a linear relationship (R = 0.99) between IL-2 activity and relative CTL "helper" activity regardless of the preparation used (purified IL-2; MLC, or mitogen-induced supernatants). ii) Absorption of MLC supernatants with T cell "blasts" or with IL-2 dependent T cell lines concomitantly removed both IL-2 and CTL "helper" activities. iii) IL-2 activity purified by isoelectric focusing, or by polyacrylamide gel electrophoresis, displayed CTL "helper" activity. iv) Both CTL "helper" and IL-2 activities were neutralized by a monoclonal antibody directed against IL-2.
Role of accessory cells in B cell activation. IV. Ia+ accessory cells are required for the in vitro generation of thymic independent type 2 antibody responses to polysaccharide antigens.
Authors: Morrissey P J , Boswell H S , Scher I , Singer A 
Published: December 2022

Abstract
It has been previously shown that the in vitro antibody response to TNP-Ficoll requires the presence of adherent accessory cells. In order to determine if this characteristic was unique to TNP-Ficoll or a general feature of the TI-2 antibody responses, responses to the polysaccharide antigens TNP-Levan and TNP-Dextran were studied. Also, it was determined if the functionally relevant accessory cell expresses Ia determinants. Passage of spleen cells over Sephadex G-10 abrogated the response to TNP-Levan and TNP-Dextran as well as to TNP-Ficoll. Addition of adherent accessory cells to the G-10 passed spleen cells reconstituted the response to all 3 antigens. Pretreatment of the adherent accessory cells with a specific anti-Ia serum plus complement abrogated the ability of these cells to provide accessory cell function in the responses to all 3 antigens. Thus, an Ia-positive adherent accessory cell is required for the generation of TI-2 antibody responses to these polysaccharide antigens. This raises the possibility that genetic restrictions may exist between the Ia-positive accessory cell and the lymphocytes involved in the responses to TNP-Ficoll, TNP-Dextran, and TNP-Levan.
A new possible regulatory system for protein phosphorylation in human peripheral lymphocytes. I. Characterization of a calcium-activated, phospholipid-dependent protein kinase.
Authors: Ogawa Y , Takai Y , Kawahara Y , Kimura S , Nishizuka Y 
Published: December 2022

Abstract
A new species of protein kinase (protein kinase C), found in human peripheral lymphocytes, is 20 times more active than adenosine 3',5'-monophosphate-dependent protein kinase (protein kinase A) with histone as phosphate acceptor. This enzyme is normally present as an inactive form in soluble fraction, but attaches to membrane to exhibit full catalytic activity. This activation process is reversible, and absolutely requires Ca++. No other divalent cations can substitute for Ca++. The enzyme is independent of cyclic nucleotides. The active factor associated with membrane is phospholipid. The protein kinase shows a m.w. of 7.7 X 10(4). The pH optimum is 7.5 to 8.5. GTP does not serve as phosphate donor. The enzyme appears to show relatively broad substrate specificity that is distinctly different from that of protein kinase A. Although both protein kinases C and A react with H1 histone, analysis of the N-bromosuccinimide-bisected fragments of this radioactive histone has revealed that protein kinase C greatly favors seryl and threonyl residues of the C-terminal portion, whereas protein kinase A reacts preferentially with seryl residues in the N-terminal portion of this histone. Protein kinase C is protentially multifunctional and may regulate various Ca++-dependent cellular processes. It is noted that protein kinase C may be alternatively activated in an irreversible manner by limited proteolysis with Ca++-dependent neutral protease. The enzyme activated in this way is independent of Ca++ and membrane.
Unresponsiveness in hapten-specific cytotoxic T lymphocytes. I. Characteristics of tolerance induction in adult mice.
Authors: Butler L D , Miller S D , Claman H N 
Published: December 2022

Abstract
These experiments concern the regulation of cytotoxic T lymphocytes (CTL). Here we describe the induction of unresponsiveness in TNP-specific cytotoxic cells generated in vitro. Previous work has shown that i.v. injection of water-soluble TNP (TNBS) prevents in vivo generation of TNP-specific CTL in C3H/HeN mice. In contrast, this report shows that the in vitro generation of TNP-specific CTL from similarly treated C3H/HeN mice is not inhibited. Nevertheless, unresponsiveness in CTL can be induced with TNBS. This unresponsiveness appears to be H-2 linked, since 3 strains of H-2d mice (BALB/c, DBA/2J, and B10.D2) were rendered unresponsive after a single injection of TNBS, whereas 3 strains of H-2k mice (C58/J, C3H/HeN, and CBA/J) were not. This CTL unresponsiveness is antigen specific in both induction and expression. The unresponsiveness is reversed by pretreatment with cyclophosphamide but not by adult thymectomy. Furthermore, the addition of supernatants from Con A-stimulated spleen cells to cultures containing the unresponsive responder cells enhanced the generation of cytotoxic activity. These results suggest that a) the ability to induce TNP-specific CTL unresponsiveness is linked to H-2 loci, b) a regulatory network is involved in the unresponsiveness, which is sensitive to cyclophosphamide but resistant to adult thymectomy, and c) at least 1 level of regulation involves amplifying T cells.
Lymphocyte surface receptors and albumin.
Authors: Sidman C L 
Published: December 2022

Abstract
Albumin was shown to be hidden component of mouse B and T lymphocyte plasma membranes. It was readily radiolabeled from within the plasma membrane by a lipophilic, photoactivated reagent (125I-iodonaphthylazide) but not from the cell exterior by lactoperoxidase-catalyzed iodination; it was not detected by immunofluorescence on intact cells. The function of this cryptic lymphocyte membrane albumin is unknown at present. This cryptic albumin component was discovered during immunoprecipitation experiments using anti-Ig reagents. It is considered of general methodologic significance that many antisera, both native and rigorously Ig-absorbed (both positively and negatively), contained such contaminating activity. The possibility is raised that such contaminating activity may be involved in some reported findings of albumin-size "Ig-like heavy chains" in both the B and T lymphocyte lineages.
Regulatory effect of H2-D region antigens in the graft-vs-host response: F1 hybrid resistance to alloreactive T cells.
Authors: Elkins W L , Quant M M 
Published: December 2022

Abstract
The role of donor and host H2D alleles in the graft-vs-host response was evaluated by measurement of DNA synthetic response of donor lymph node cells in lethally irradiated hosts and by a mortality assay in sublethally irradiated F1 hosts. Comparison of the potency of graded doses of B10.A, B10.A(2R), and (B10.A X B10.A(2R))F1 cells in (B10 vs B10.A)F1 and other hosts expressing foreign KbIb revealed a deficient response of 10(6) B10.A(2R) cells, but only when the host was heterozygous d/b at H2-D. Studies with TI congenic donors failed to implicate T region antigens in this effect. These results are interpreted to suggest that under the conditions of these experiments there is F1 hybrid resistance to alloaggressive T lymphocytes that are homozygous in the Db region.
Spontaneous autoimmune thyroiditis in chickens. I. Effects of bursal reconstitution.
Authors: Polley C R , Bacon L D , Rose N R 
Published: December 2022

Abstract
Chicks from strains genetically susceptible or resistant to spontaneous autoimmune thyroiditis were neonatally treated with cyclophosphamide to induce lymphocytic depletion of the bursa of Fabricius. The subsequent bursal repopulation with B cells from donors matched at the major histocompatibility locus showed B cells to be intricately associated with the pathogenesis of spontaneous autoimmune thyroiditis, although they themselves did not carry the potential for initiation of the disease.
Primary in vitro antibody responses by purified murine B lymphocytes in serum-free defined medium.
Authors: Mosier D E 
Published: December 2022

Abstract
A serum-free medium formulation that allows a primary in vitro antibody response to the nonmitogenic thymic independent antigen TNP-AECM-Ficoll is described. Purified murine B lymphocytes and adherent accessory cells are required for optimal specific responses as well as for optimal B cell survival. The medium is based on Iscove's modification of Dulbecco's modified Eagle's medium and Ham's F-12 nutrient mixture. The serum-replacing components are insulin, transferrin, and progesterone. The survival of unstimulated murine T cells in this Iscove/F12 medium is poor, but B cells survive for relatively long periods of time. This medium should prove useful in defining the molecular requirements for B lymphocyte activation by antigen.