bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differentiation of Lymphoid Cells: B Cell As a Direct Target and T Cell As a Regulator in Lipopolysaccharide-Enhanced Induction of Immunoglobulin Production
Authors: Shinohara Nobukata , Kern Milton 
Published: December 2022

Abstract
The cells involved in the stimulatory effect of bacterial lipopolysaccharide (LPS) on the induction of immunoglobulin (Ig) production by rabbit spleen cells cultured in the absence of antigen has been analyzed. Addition of LPS caused a several-fold enhancement of both DNA synthesis and Ig production. These enhanced activities were not significantly affected by depletion of adherent cells in the spleen cell population. Although inactivation of splenic T cells by anti-thymocyte serum (ATS) treatment did not affect the enhancement of DNA synthesis due to LPS, such treatment did adversely affect the enhancement of Ig production by LPS. Furthermore, the enhancement of Ig production of ATS-treated spleen cells by LPS was found to be dependent on the number of thymocytes added. In addition, the prior incubation of ATS-treated spleen cells with LPS resulted in effective enhancement of Ig production when such ATS-treated spleen cells and thymocytes were combined after removal of LPS. An identical experiment, except that thymocytes instead of ATS-treated spleen cells received the prior incubation with LPS, did not result in enhancement of Ig production. Finally, the enhanced Ig production due to LPS was inhibited by hydroxyurea, a known inhibitor of cellular DNA synthesis. The relationship between the mitogenic activity of LPS on B cells, the regulatory function of T cells, and the enhancement of Ig production by LPS is discussed in relation to the contrasting reports concerning the cellular target of LPS.
Specific Suppression of the Immune Response by Hgg Tolerant Spleen Cells
Authors: Doyle Michael V. , Parks D. Elliot , Weigle William O. 
Published: December 2022

Abstract
After adoptive transfer, the spleen cells from mice made tolerant to human γ-globulin (HGG) specifically suppress the immune response of normal spleen cells. However, this suppressive activity in the spleen cells of tolerant mice is only present for a brief period after treatment with tolerogen. Spleen cells from animals injected 10 days earlier with tolerogen reduce the immune response of an equal number of normal spleen cells by 75%. Spleen cells from mice made tolerant 40 days previously are, however, no longer suppressive, even though they remain completely unresponsive. These data suggest that active suppression of antigenreactive cells is not the mechanism responsible for maintaining tolerance to HGG, but rather is only transiently associated with the tolerant state. Further evidence in favor of the separation of the tolerant state from suppressive activity is that complete suppression of the normal spleen cell response requires either a high ratio of tolerant to immune competent cells or a delay in the antigenic challenge of the reconstituted recipients. By contrast, such manipulations are not required to demonstrate the complete unresponsiveness of the tolerant cells after adoptive transfer.
Influence of Colony Type on Susceptibility of Gonococci to Killing by Human Serum
Authors: McCutchan J. Allen , Levine Sharon , Braude Abraham I. 
Published: December 2022

Abstract
The virulence of gonococci is related to colony morphology and has been attributed to pili found only on the virulent types. Because complement-mediated serum killing is a major defense against other Gram-negative bacteria, we tested the resistance to normal human serum of virulent and avirulent types from two strains. Virulent types were more resistant than avirulent types. This stable, relative serum resistance of virulent colony types persisted during prolonged passage on agar. In addition, virulent types acquired complete resistance after exposure to serum which was rapidly lost during passage on agar. This acquired, complete resistance helps explain the observation that freshly isolated gonococci are resistant to their host's serum, but lose this resistance when passed on agar. The capacity to become resistant to the serum of newly infected patients may contribute to virulence of T1 and T2 gonococci.
Evidences for a “New” C1 Inhibitor, Factor S, Released from Leucocytes
Authors: Bernard A. , Boumsell L. , Good R. A. , Borsos T. , Day N. K. 
Published: December 2022

Abstract
Pretreatment of sheep erythrocytes (E) with supernatants of short-term cultures of mouse spleen or thymus cells induces the following interactions with guinea pig complement: 1) Supernatant pretreated EAlim (S.EAlim) are less susceptible to lysis by excess complement. S.EAC1̄4 yield a lower C2 titer, have an increased Tmax, but an unchanged C2 decay when compared with medium-pretreated EAC1̄4. Lysis of already formed EAC1̄4̄2̄is not inhibited. Therefore the inhibition affects C2 activation. 2) E, pretreated with supernatant (S.E), are able to fix C1̄, as detected by transfer to EAC4: In order to generate the same number of C1̄-fixing sites by using IgM hemolysins, five to six times the optimal amount is required. Yet S.EC1̄ cannot be lysed by the other components added in excess. S.EC1̄ can remove C4 from the fluid phase with the same efficiency as EIgMC1̄ but S.EC1̄ treated with C4 cannot remove C2. 3) Native C1̄ binds to S.E: S.E and EIgM remove C1 from the fluid phase with the same efficiency; fixation of 1̄ on S.E is decreased after incubation with native C1̄
Complement Lesions in Cell Membranes from Joint Effusions of Various Types of Arthritis
Authors: Dourmashkin R. R. , Patterson S. 
Published: December 2022

Abstract
Electron microscopy of differentially centrifuged synovial fluid from patients with differing types of arthritis revealed a few membranes bearing complement lesions. This finding occurred equally in patients with seronegative arthritis as well as in patients with rheumatoid arthritis and positive rheumatoid factor. By incubating effusion leukocytes in vitro with effusion fluid, and peripheral leukocytes with syngeneic serum complement, under conditions in which classical complement activation was inhibited, it could be shown that this finding was through activation of the alternative pathway, by means of lysosomal enzymes. It is not clear where, in inflammatory exudates, is the site of action; it may be on the internal membranes of already damaged cells, as no detectable cytotoxic effect could be found by using 86Rb as a marker for specific release in PMN leukocytes. By means of hemolysis of indicator cells, lysosomal enzyme was found to have the net effect of inhibiting the lysis of indicator cells in the presence of complement activated by the alternative pathway.
Stimulation of Murine B Lymphocytes by Isolated C3b
Authors: Hartmann K.-U. , Bokisch V. A. 
Published: December 2022

Abstract
Purified human C3b added to mouse lymphocyte suspensions triggers activation of B lymphocytes. Activation of up to 50% of the cells was detected by increased incorporation of 3H-thymidine, blast cell formation, and antibody secretion (polyclonal development of plaque-forming cells).
Activation was observed in suspensions of lymph node and spleen cells of all mouse strains tested, including DBA/2, BALB/c, C3H/HcJ and Nu/nu, the congenitally thymus deficient strain. Removal of the rapidly adhering or thymusderived cells did not reduce activation. Activation was dependent on the dose of added C3b, which was varied between 1 and 50 µg/0.5 ml culture, and was potentiated by the presence of fetal calf serum. Addition of soluble rabbit anti-C3 reduced the stimulatory activity of C3b, and Sepharose-bound anti-C3 removed the activity from the C3b solution. C3a or C3c did not activate the lymphoid cells, and addition of C3b inactivator (partially purified from human serum) strongly inhibited the stimulation.
Activation of Guinea Pig B Lymphocytes by Fragments of the Third Component of Complement
Authors: Koopman W. J. , Sandberg A. L. , Wahl S. M. , Mergenhagen S. E. 
Published: December 2022

Abstract
Recent evidence suggests that the third component of complement (C3) may play an important role in regulating immune function at the cellular level. Fragments of C3, derived by proteolysis of purified guinea pig C3, were tested for their capacity to induce mediator production and proliferation in guinea pig lymphocytes in vitro. Trypsin digestion of C3 yielded C3a and C3b (1% trypsin, 2 min, 20°C) or C3c and C3d (2% trypsin, 1 hr, 20°C). These fragments were separated either by Sephadex G-75 (C3a and C3b) or Bio-Gel P-100 (C3c and C3d) column chromatography and were characterized both immunoelectrophoretically and functionally by rosette inhibition. Guinea pig B lymphocytes produced a mononuclear chemotactic factor when stimulated with C3b and, to a lesser extent, with native C3, as demonstrated by the presence of chemotactic activity in supernatants assayed in modified Boyden chambers. These fragments did not induce cell proliferation.
Different Behaviour of Native and Purified C1q, a Subunit of the First Component of Complement
Authors: Loos M. , Hill H. U. 
Published: December 2022

Abstract
The first component of complement (C1) consists of three distinct subunits, C1q, C1r, and C1s. Two different forms of C1r and C1s were described, a proesterolytic (native) and esterolytic (active) form. Our experiments suggest that C1q also exists in two different forms. After centrifugation of undiluted human serum on a sucrose gradient (5% to 30%, pH 7.35, µ = 0.06, 16 hr, 4°C, 39,000 rpm) C1 activity was found in the 19S region. After centrifugation of diluted human serum (1:50 in 5% sucrose buffer, pH 7.35, µ = 0.06) no C1 activity was found. The loss of C1 activity was due to the loss of C1q activity, whereas the activity of the subunits C1r and C1s was detected in the 7S and 4S region, respectively. Under similar conditions the hemolytic activity of purified C1q was not affected. Addition of purified C1q to diluted human serum led to a reassociation of purified C1q with C1r and C1s in serum as tested hemolytically as well as by ultracentrifugation.
Techniques of Fractionating Complement in-Vivo by the Use of Activated Complement Components to Trigger the C3b Feedback Cycle
Authors: Mak L. W. , Lachmann P. J. , Majewski J. 
Published: December 2022

Abstract
Cobra venom factor is a highly effective complement-activating agent in vivo by virtue of its ability to trigger the C3b feedback cycle. An investigation has been made to see whether triggering of the C3b feedback cycle by activated autologous complement components could similarly provide a mechanism for in vivo complement activation.
It has been found that C4oxy2 added to serum triggers the C3b feedback cycle, effectively in vitro. Similar C3b, Bb can be used as the triggering enzyme.
Experiments have been performed in vivo in rats showing that significant complement activation accompanied by the leukocyte changes characteristic of CVF treatment can be produced with the altered complement components. Such techniques promise to be applicable to complement (in)activation in vivo in man.
Participation of the Alternative Pathway in Complement Metabolism in Systemic Lupus Erythematosus
Authors: Wilson M. R. , Arroyave C. M. , Tan E. M. 
Published: December 2022

Abstract
In order to determine if in vivo activation of the alternative pathway of complement was present in systemic lupus erythematosus (SLE), highly-purified Factor B was labeled with radioactive iodine (125I), and its metabolism studied in 11 patients with SLE and 6 control subjects. Serum factors, which could activate the alternative pathway of complement in in vitro assays were demonstrated in 6 of 11 patients with SLE. These serum factors were detected by lysis of glutathione-sensitized human erythrocytes and by C3 and Factor B conversion in the presence of EGTA (10 mM) and MgCl2 (0.3 mM) conditions which block activation of the classical pathway but permit activation of the alternative pathway. All 6 patients with serum factors capable of activating the alternative pathway in vitro, had in vivo evidence of alternative pathway activation as measured by an increased fractional catabolic rate (FCR) of Factor B.
Absence of demonstrable effects of thymocytotoxic antibodies on serum thymic hormone level in NZB mice
Authors: Gershwin M. Eric , Steinberg Alfred D. 
Published: December 2022

Abstract
Sir: We are pleased to read the new data provided by Bach, Dardenne, and Bach on the critical question: Is a decrease in thymic hormone(s) levels responsible for the development of autoimmunity in New Zealand mice? There is no question that these workers have provided the world with important ideas and information regarding autoimmunity and thymic factor(s). We believe, however, that Drs. Bach and co-workers have misinterpreted the thrust of our paper. Contrary to their assertion above, we do not conclude that the decrease in “thymic hormone levels” is due to NTA. Rather, we conclude that insufficient information is available to implicate decreased thymic hormone(s) levels as the cause of autoimmune disease in New Zealand mice. Most difficult to explain are the immunologic abnormalities in NZB and especially in NZB/NZW mice before the fall in thymic hormone(s) as measured by the mouse rosette assay.
Immunologic Characteristics in Relation to High and Low Leukemogenic Activity of Radiation Leukemia Virus Variants
Authors: Haran-Ghera Nechama , Rubio Nazario 
Published: December 2022

Abstract
Comparative analysis of immune responses induced by two variants of the radiation leukemia virus having high (A-RadLV) or low (D-RadLV) leukemogenic potential was performed. Effective immunization could be induced only with RadLV variants having low leukemogenic potential when injected into adult mice of specific strains, (D-RadLV in C57BL/6 mice and A-RadLV in (BALB/c × C57BL/6)F1 mice). Immunologic cross-reactivity among the RadLV variants and the leukemic cells induced by them was demonstrated in several systems. Transplantation resistance could be induced in certain strains against challenge of leukemic cells induced by both RadLV variants. Isoantisera, raised in the suitable strains, could neutralize effectively the leukemogenic activity of both A-RadLV and D-RadLV. Leukemic cells induced by each of the variants shared cell-surface antigens. Circulating anti-tumor antibodies, induced by both variants in the appropriate strains, lysed efficiently the target leukemic cells.
Activation of the Classical Complement Pathway by Fc Fragment of Human IgA
Authors: Burritt Mary F. , Calvanico Nickolas J. , Mehta Satish , Tomasi Thomas B. 
Published: December 2022

Summary
Intact Fcα fragments from five human IgA myeloma proteins were produced by two different methods, high temperature trypsinolysis and IgA protease digestion. Three of the Fcα fragments activated the classical pathway as determined by the titers of the individual complement components. Two other fragments did not fix complement by either pathway.
Physicochemical Characterization of Complement-Interacting Factors from Taenia taeniaeformis
Authors: Hammerberg Bruce , Williams Jeffrey F. 
Published: December 2022

Abstract
Complement-fixing activity was washed from the surface of metacestodes of Taenia taeniaeformis and characterized physicochemically by enzymatic digestion, gel filtration, anion exchange chromatography, ultracentrifugation, and gel electrophoresis. The results provided evidence of an association between antihemolytic activity and macromolecules containing carbohydrate, protein, sulphate, and hexosamine, heterogeneous in net negative charge but resistant to proteolysis and β-elimination reactions, and free of sialic and uronic acids. The most active fraction was eluted from DEAE-cellulose with 0.3 M NaCl in 0.01 M Tris-HCl, pH 8.0, and when parasites were incubated with a source of 35SO4--, radioactivity was incorporated into molecules eluting under identical conditions. Active chromatographic fractions precipitated with protamine sulphate, suggesting that they were polyanionic in nature. There was some evidence of dissociation of the active substance on polyacrylamide gels where fast moving sulphate-containing bands were observed which no longer reacted with protamine or C.
The results are consistent with the possibility that the active substance is a polysulfated proteoglycan. Molecules of this nature have been detected on the surface of a variety of infectious organisms, and are known to interact with C nonimmunologically. Their location at host-parasite interfaces may have strategic significance in evasion of immune rejection and this possibility is discussed in relation to current understanding of immunity to T. taeniaeformis.
T Cell Tolerance in the Chicken
Authors: Grebenau Mark D. , Thorbecke G. Jeanette 
Published: December 2022

Abstract
T cell-mediated delayed hypersensitivity (DH) to human γ-globulin (HGG) can be induced in chickens by subcutaneous injection of the antigen in complete Freund's adjuvant (CFA). In the present work, it has been demonstrated that specific tolerance of the cells mediating this DH can readily be induced in both normal and bursectomized (BX) FP strain chickens by simple i.v. injection of soluble antigen, regardless of the presence of antibody production to the tolerogen. A significant degree of tolerance at the DH and helper T cell levels could be generated in BX birds by injection of as little as 0.5 mg of HGG; such a dose only induced tolerance in normal birds when it had been previously deaggregated by ultracentrifugation. Regular, nondeaggregated antigen could produce tolerance in normal animals, but only at doses of &gt;5 mg. The tolerizing injection induced a primary antibody response in normal birds in all cases, but a secondary response could not be obtained in animals rendered tolerant at the T cell level.
Establishment of tolerance appeared to be very rapid, and animals remained refractory to induction of DH for at least 3 weeks after the tolerizing injection. The mode in which the antigen was presented to the animals appeared to be crucial in determining whether tolerance or sensitivity would be established.
Leukocyte Complement: Assembly of the Membrane Attack Complex of Complement by Human Peripheral Blood Leukocytes in the Presence and Absence of Serum
Authors: Sundsmo John S. , Curd John G. , Kolb William P. , Müller-Eberhard Hans J. 
Published: December 2022

Abstract
The specific neoantigenic determinants (neoAg) that are indicative of the assembled C5b-9 C complex are generated on the surface of peripheral blood leukocytes (PBL) during collection and processing of blood. Formation of neoAg on PBL could be prevented by collecting blood directly into 20 mM EDTA and, could be induced in vitro by adding autologous serum to isolated PBL that lacked neoAg. When neoAg was induced by the addition of serum containing 125I-labeled C8, the C8 was incorporated into a 23S complex which could be eluted from PBL.
A mechanism for neoAg formation on PBL independent of exogenous serum factors was detected when PBL were placed into culture in serum-free medium. Results with metabolic inhibitors and 14C-leucine suggest that PBL can synthesize C5 and assemble the C5b-9 complex. The possible relevance of these findings to the understanding of mechanisms of cell-mediated cytotoxicity is discussed.
Aging and the Immune Response
Authors: Gardner Ian D. , Remington Jack S. 
Published: December 2022

Abstract
In studies to determine the effect of aging on the cell-mediated immune response to Toxoplasma gondii, aged mice showed a delayed onset of macrophage activation during acute infection with T. gondii when compared with young mice of the same strain. Activation appeared to be biphasic, with a peak occurring during the acute infection, followed by a transient decline and then a return to the high levels which are characteristic of the chronic infection. Macrophage activation decreased after approximately 11 weeks of infection in young mice; the decrease was less with increasing age except in the very oldest mice which also exhibited a marked decrease in activation. Specific lymphocyte transformation to Toxoplasma antigen did not reveal any age-related decline during the acute infection. With increasing age during chronic infection, antigen-specific lymphocyte transformation was enhanced except in very old mice. These results suggest that the increased “antigenic load” in older mice (see accompanying paper) with the chronic infection may result in enhanced cell-mediated immunity, but that at the extreme of old age there is a major decline in the inductive mechanism which overrides this stimulation.
Generation of Low-Dose Paralysis in the Absence of the Ability to Secrete Antibody
Authors: Markham Richard B. , Stashak Philip W. , Prescott Benjamin , Amsbaugh Diana F. , Baker Phillip J. 
Published: December 2022

Abstract
(CBA/N ♀ × BALB/c ♂) F1 male mice carry an X-linked defect, originating from CBA/N mice, which renders them unable to generate an antibody response to SSS-III. Histocompatible (BALB/c ♀ × CBA/N ♂) reciprocal F1 male hybrids do not carry the X-linked defect and therefore generate a readily detectable PFC response to SSS-III, which can be adoptively transferred into nonresponding reciprocal F1 male mice. In the present work, we shown that this adoptive response could be inhibited in recipient (CBA/N ♀ × BALB/c ♂) F1 male nonresponding mice in which low dose paralysis had been induced. Evidence is presented which indicates that such suppression is of host rather than donor cell origin.
The capacity to develop low-dose paralysis, a phenomenon that is antigen specific and has been attributed to the action of suppressor T cells, indicates that nonresponding (CBA/N ♀ × BALB/c ♂) F1 males (and presumably the CBA/N progenitor strain) have the ability to recognize this antigen. Furthermore, since these animals fail to make a serum antibody response to SSS-III, the signal that activates suppressor T cells cannot be circulating antibody or antigen-antibody complexes. These findings are most consistent with the view that low-dose paralysis of the response to SSS-III is not dependent on antibody-mediated feedback inhibition; rather, it is an active process mediated by suppressor T cells.
B Lymphocyte Precursors
Authors: Fairchild Sally S. , Cohen J. John 
Published: December 2022

Abstract
After surface immunoglobulin-bearing (sIg+) cells are removed from mouse bone marrow on an anti-Ig immunoadsorbent column, precursors of bone marrow-derived (B) lymphocytes can be observed to differentiate in vitro. Expression of sIg occurs spontaneously on approximately 50% of the small lymphocytes during 3 days in culture. The rate of expression is accelerated by lipopolysaccharide (LPS), cyclic AMP, or the cyclic AMP phosphodiesterase inhibitor R020-1724; after 20 hr in culture approximately 35% of the small lymphocytes are sIg+ in induced cultures compared to 11% in controls. Acquisition of the ability to respond by proliferation to the mitogen LPS does not occur spontaneously in vitro but can be induced. Mitogen responsiveness in unfractionated bone marrow cells is increased by a 2-day preincubation with any of the inducing agents (cAMP, R020-1724, or LPS itself). However, anti-Ig column-passed marrow can be induced only with LPS or another mitogen, dextran sulfate, and this induction is prevented by BUdR and light. We propose that immature B cells express sIg, and then must undergo further differentiation, possibly linked to cell division, before becoming responsive to LPS. Agents that raise intracellular cAMP accelerate expression of sIg and mitogen responsiveness in two distinct cell populations, and may do so by accelerating new genetic programs after determination events.