bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of lymphocyte responsiveness in early experimental syphilis. II. Nature of cellular infiltration and Treponema pallidum distribution in testicular lesions.
Authors: Lukehart S A , Baker-Zander S A , Lloyd R M , Sell S 
Published: December 2022

Abstract
The nature of the cellular infiltration and the distribution of Treponema pallidum during rabbit testicular infection were examined by immunofluorescence and light microscopy. Low numbers of treponemes are demonstrable in the perivascular regions on day 3 post-infection. On days 6, 10, and 13, large numbers of organisms are found in the interstitial spaces. The treponemes do not appear to invade the walls or lumina of the seminiferous tubules, although tubular atrophy is obvious. On days 17, 24 and 31, treponemes are no longer identifiable by immunofluorescence in infected testicles. The cellular infiltration, which is apparent on day 6, reaches its peak on day 13, corresponding to the amount of swelling observed grossly. The infiltrate is primarily lymphocytic, but macrophages are also observed during the peak cellular response. These cells are located, as are the treponemes, in the interstitial spaces. The lymphocytes are demonstrated by specific immunofluorescence to be predominantly T cells. The peak T cell infiltration in the infected testicle is followed rapidly by the disappearance of the organisms from that organ. Thus, it is postulated that infiltration by specifically sensitized T cells results in the clearance of large numbers of T. pallidum from infected tissues.
Hybridoma cell lines secreting monoclonal antibodies to mouse H-2 and Ia antigens.
Authors: Ozato K , Mayer N , Sachs D H 
Published: December 2022

Abstract
Hybridoma cell lines secreting antibodies to mouse H-2 or Ia antigens have been generated by fusing mouse immune lymphocytes with appropriate myeloma lines. Among the 11 established clones reported here, nine produce anti-H-2 antibodies and two produce anti-Ia antibodies. The specificities and cross-reactions of these monoclonal antibodies have been studied in detail. One hybridoma antibody reacted only to Kk antigens without any detectable cross-reactions, thus suggesting reaction to a private specificity of the Kk molecule. All other anti-H-2 hybridoma antibodies appeared to detect public specificities as defined either by reactions with products of more than one H-2 locus or with different alleles at one or more loci. The two anti-Ia antibodies both reacted with I-E/C products, but exhibited different cross-reactivity patterns. Strain distribution analyses so far indicate that the public specificities detected by these monoclonal antibodies are considerably different from those that had been established by traditional serology. Since public specificities defined by the hybridoma antibodies must by definition represent cross-reactions, these findings may have important implications relating to the structure and evolution of MHC gene products.
Contact hypersensitivity, humoral immunity, and specific unresponsiveness can be induced in Syrian hamsters with simple haptens.
Authors: Streilein J W , Sullivan S , Thompson S 
Published: December 2022

Abstract
Several inbred strains of Syrian hamsters have been immunized by skin painting with highly reactive haptens. Classical contact hypersensitivity has been assayed by the ear swelling response: the response is hapten-specific, exaggerated after re-immunization with the original hapten, and can be transferred adoptively to naive syngeneic hamsters with viable lymphoid cells, suggesting that contact hypersensitivity is mediated in hamsters by T lymphocytes. Moreover, skin painting with hapten induces significant serum titers of anti-hapten antibodies, indicating that antigen-specific B lymphocytes are also activated. Hamsters can be rendered unresponsive to these same haptens by conventional methods: 1) i.v. inoculation of the soluble hapten sulfonate or 2) inoculation of hapten-derivatized syngeneic lymphoid cells. Hamsters treated with these "tolerizing" maneuvers develop profound hapten-specific unresponsiveness that can be adoptively transferred to naive recipients with living lymphoid cells. "Unresponsive" animals, however, make strong anti-hapten antibody responses that rival the humoral immune responses found after skin sensitization. The data suggest that an active process is involved in the induction and maintenance of the unresponsive state, but responsibility can not be assigned firmly to putative suppressor T cells or to an antibody-mediated B suppressor modality.
The role of the spleen in tumor growth kinetics of the murine B cell leukemia (BCL1).
Authors: Slavin S , Morecki S , Weiss L 
Published: December 2022

Abstract
BCL1 is a transplantable B cell leukemia resembling human chronic lymphocytic leukemia-lymphoma maintained by cell passage in BALB/c mice. After BCL1 inoculation (10(7) cells), all mice developed extreme B lymphocytosis in the blood (less than or equal to 440,000 lymphocytes/mm3) and marked splenomegaly (50 times normal nucleated cell numbers). BCL1 infiltrated the spleen before peripheral leukemia was overt (3 days vs 28 days, respectively). BCL1 development in splenectomized mice was characterized by a delayed onset of leukemia (greater than 20,000 cells/ mm3 at 59 vs 28 days in intact mice), doubled median survival (102 vs 53 days, respectively), and reduced peak level of leukemic counts in the blood (125,000 vs 440,000 cells/mm3). Early splenectomy at different time intervals, ranging between 1 hr to 3 days after BCL1 inoculation, significantly delayed onset of the disease and prolonged survival, indicating that homing to the spleen occurred as early as 1 hr after inoculation. Splenectomy at 7 days still delayed onset of leukemia but did not affect survival. No significant effect on BCL1 kinetics was noticed when splenectomy was done on day 21. All splenectomized mice showed significantly lower peripheral blood counts as compared to intact mice (98,000/mm3 vs 440,000/mm3, respectively). The data show that the spleen plays a major role in the pathogenesis and prognosis of BCL1.
Cellular events in tolerance. VIII. Analysis of the proliferative capacity of antigen-binding cells isolated from normal or tolerant spleens.
Authors: Venkataraman M , Scott D W 
Published: December 2022

Abstract
Previous studies in our laboratory have demonstrated that hapten-binding lymphocytes (ABC) can be isolated from the spleens of mice rendered tolerant to the hapten. These cells are reduced in PFC precursor frequency when stimulated with either specific antigen or mitogen (Reference 6). In the present studies, we have combined antigen-specific cell isolation and an analysis of thymidine uptake by purified B cells to determine whether hapten-binding B cells in tolerant mice can be stimulated to proliferate in response to specific antigen. Compared with normal ABC, "tolerant" ABC showed a significantly reduced thymidine incorporation responsiveness in vitro. This suggests that unresponsiveness in adult mice can result in an impairment of clonal proliferation. Hence, these "tolerant" ABC appear to be functionally though not physically, deleted.
Induction and suppression of immunoglobulin synthesis in cultures of human lymphocytes: effects of pokeweed mitogen and Staphylococcus aureus Cowan I.
Authors: Pryjma J , Muñoz J , Galbraith R M , Fudenberg H H , Virella G 
Published: December 2022

Abstract
The synthesis and secretion of immunoglobulins by human peripheral blood mononuclear cells in cultures stimulated with pokeweed mitogen or Staphylococcus aureus Cowan I were evaluated by enumeration of cells containing cytoplasmic immunoglobulins and cells actively secreting immunoglobulins, and by quantitation of immunoglobulins released into culture supernatants. The two mitogens caused comparable stimulation of immunoglobulin production; however, in contrast to pokeweed mitogen, S. aureus was active in cultures depleted of T lymphocytes, and its stimulatory effects were resistant to the influence of suppressor T cells generated by co-stimulation with concanavalin A or by preincubation without mitogenic stimulus. These results indicate distinct pathways of induction and suppression of immunoglobulin synthesis for these two polyclonal B cell activators, and suggest that stimulation by S. aureus is less thymus dependent than that induced by pokeweed mitogen.
The role of anti-H-2K and H-2D alloantibodies in enhancement and acute antibody-mediated rejection of mouse skin allografts.
Authors: de Waal R M , Capel P J , Koene R A 
Published: December 2022

Abstract
The enhancing and destructive effects of anti-H-2Kd and anti-H-2Dk antibodies were studied in B6AF1 recipients of B10.D2 or B10.BR skin allografts. The anti-H-2 antibodies were isolated from B6AF1 anti-B10.D2 and B6AF1 anti-B10.BR alloantiserum by adsorption to donor strain red blood cells and subsequent elution. Acute antibody-mediated rejection of B10.D2 or B10.BR skin grafts was readily induced by administration of anti-H-2K or H-2D antibodies, respectively, along with rabbit complement. Treatment of the B6AF1 recipients with the antibody eluates on day 0, 2, and 4 after transplantation resulted in specific and significant prolongation of graft survival. Both graft destruction and enhancement can therefore be mediated by antibodies directed against the same H-2 specificity.
Induction of anti-ssDNA antibodies in normal and preautoimmune mice in vivo.
Authors: Pancer L B , Bell D A , Singhal S K 
Published: December 2022

Abstract
Splenic lymphoid cells of normal and preautoimmune mice escape normal regulatory mechanisms in vitro and spontaneously synthesize anti-ssDNA antibody in the absence of any exogenous antigen. In addition, both the cultured cells and their cell-free supernatants were capable of inducing specific anti-ssDNA responses in vivo upon their injection into syngeneic recipients. The response was host-derived, required the participation of B and T cells, and was not due to polyclonal activation. The immunogen responsible for this response appeared to be membrane-associated, was found predominantly on cultured T cells, and was sensitive to DNase and proteolysis.
Role of accessory cells in B cell activation. I. Macrophage presentation of TNP-Ficoll: evidence for macrophage-B cell interaction.
Authors: Boswell H S , Sharrow S O , Singer A 
Published: December 2022

Abstract
The importance of cell interaction for thymic independent antigen responses has not been widely appreciated. The present report demonstrates, however, that macrophage-B cell interaction may be an important feature of B ce-l activation for the response to at least one polysaccharide thymic independent antigen, TNP-Ficoll. Experiments were performed demonstrating that a strict accessory cell requirement exists for the thymic independent response to soluble TNP-Ficoll, and that such accessory cells are both adherent and phagocytic, that is, macrophages. It was further demonstrated that macrophages could be pulsed with TNP-Ficoll and that these pulsed macrophages could activate B cells to respond, but only if the pulsed macrophages were viable. Thus, one function that macrophages can fulfill in responses to TNP-Ficoll is the specific function of antigen presentation. Such presentation of TNP-Ficoll by macrophages to B cells suggests that the antigen may not be activating B cells directly, and raises the possibility that the interaction of B cells and macrophages might be genetically restricted.
Is experimental autoimmune myasthenia gravis induced only by acetylcholine receptors?
Authors: Claudio T R , Raftery M A 
Published: December 2022

Abstract
EAMG has been induced in a wide variety of animals by using AcChR purified from electric organ and muscle sources. Electrophoresis of SDS polyacrylamide gels heavily loaded with purified AcChR often reveals the presence of minor contaminants. To test whether these contaminants or any other components present in Torpedo californica AcChR preparations could induce EAMG, solubilized Torpedo membrane fragments were depleted of AcChR by passage over an alpha-BuTx-conjugated resin and then injected into Lewis rats in an attempt to induce EAMG. The results demonstrated that some of the minor contaminants present in purified AcChR preparations were antigenic, but EAMG could not be induced with preparations enriched in these contaminants or containing other Torpedo non-AcChR components and lacking AcChR. The conclusion drawn from this study was that the acetylcholine receptor was the only component present in Triton X-100-solubilized Torpedo californica membrane fragments that could induce EAMG.
H-2 antigen requirements in the in vitro induction of SV40-specific cytotoxic T lymphocytes.
Authors: Gooding L R , Edwards C B 
Published: December 2022

Abstract
T cytotoxic cells generated to syngeneic SV40 virus transformants lyse only SV40 target cells that are syngeneic at the H-2 locus. In contrast, SV40-specific tumor transplantation immunity shows no requirements for syngeneic H-2. Inoculation of allogeneic or even xenogeneic transformants will confer immunity to a challenge of syngeneic SV40 tumor cells. The experiments described here represent an attempt to reconcile these apparently conflicting observations. In our hands, generation of SV40-specific T cytotoxic cells in vitro requires both in vivo priming and secondary in vitro sensitization. We have found that priming for a secondary syngeneic-restricted response requires only that the cell employed be SV40 transformed. That is, priming may be accomplished with syngeneic, allogeneic, or xenogeneic SV40 transformants. Thus, the apparent lack of H-2 restriction in vivo immunity does not eliminate a role for the H-2-restricted cytotoxic T cell in tumor transplantation immunity.
Antigen-specific factors produced by carrier-primed New Zealand Black mice.
Authors: Sawada S , Dauphinée M J , Talal N 
Published: December 2022

Abstract
We studied antigen-specific suppression in NZB and B/W mice to investigate immunoregulatory circuits associated with autoimmune disease. Young NZB and B/W mice produced ample suppressor factor, and acceptor cells were present even in older mice. A low m.w. antigen-specific enhancing factor capable of augmenting the secondary in vitro IgG antibody response to DNP was found. These results indicate the complexity of immunoregulation in these autoimmune-susceptible mice.
Polyclonal activation of murine B lymphocytes by Fc fragments. I. The requirement for two signals in the generation of the polyclonal antibody response induced by Fc fragments.
Authors: Morgan E L , Weigle W O 
Published: December 2022

Abstract
Fc fragments derived from human IgG1 induce murine splenic B lymphocytes to undergo proliferation and differentiation to antibody-secreting cells. The polyclonal antibody response was found to require both the presence of macrophages and T cells. Spleen cell cultures from nude mice or T cell-depleted normal mice proliferate to the level of untreated control mice but do not produce polyclonal antibody unless T cells are added. Regulation of the Fc fragment induced B cell differentiation to antibody synthesis apparently occurs through two distinct signals. One signal is provided by Fc fragments for proliferation and the other by T cells for differentiation. This suggestion is supported by the observation that spleen cell preparations, devoid of T cells, are capable of proliferation to the level of normal spleen cell cultures in response to Fc fragments, but are incapable of making a polyclonal antibody response. The cell population that responds to the differentiation signal also responds to the proliferative signal. "Hot pulse" experiments demonstrated that proliferation precedes polyclonal activation.
Relationship between enhanced macrophage phagocytic activity and the induction of interferon by Newcastle disease virus in mice.
Authors: Hamburg S I , Cassell G H , Rabinovitch M 
Published: December 2022

Abstract
The relationship between phagocytic activity of peritoneal macrophages and serum interferon (IF) titers was evaluated in mice challenged with Newcastle disease virus (NDV). Time course studies indicated peak serum IF titers between 6 and 12 hr, whereas Fc receptor-mediated macrophage phagocytosis was maximal 18 hr after viral administration. Both responses decreased in parallel as the inoculated dose of the virus was reduced. Splenectomy, shown by others to decrease the NDV-induced serum IF titers, significantly decreased the stimulation of phagocytosis. The role of T cells in the response to the virus was studied with nude mice raised under germfree conditions. NDV-induced serum IF titers and macrophage phagocytosis were both diminished in BALB/c nudes compared with their heterozygous littermates. Both responses could be partially restored by transfer of thymocytes obtained from heterozygous mice. The results provide further evidence that in vivo macrophage stimulation by NDV is mediated by induced IF. The experiments with nude mice also indicate that the IF response to NDV is regulated by T lymphocytes.
Participation of lymphocyte activating factor (Interleukin 1) in the induction of cytotoxic T cell responses.
Authors: Farrar W L , Mizel S B , Farrar J J 
Published: December 2022

Abstract
The initiation of murine alloantigen-specific cytotoxic T cell responses is macrophage dependent. The requirement for macrophages can be replaced in macrophage-depleted cytotoxic T lymphocyte assay by a soluble factor released from phorbol myristic acetate-stimulated mouse peritoneal adherent cells or P388D1 macrophage tumor cells. On the basis of the cell of origin, m.w. (15,000), and elution profiles on DEAE cellulose and polyacrylamide gels, this macrophage-replacing factor for T cell-mediated cytotoxicity was identical to lymphocyte activating factor (LAF). The stimulatory effect of LAF was totally dependent on the presence of the priming alloantigen. The results presented in this report support the hypothesis that macrophage-mediated antigen-induced T cell activation is dependent on two signals, antigen and LAF.
The role in vivo of C3 and the C3b receptor in babesial infection in the rat.
Authors: Jack R M , Ward P A 
Published: December 2022

Abstract
The critical role of complement (C3) and the C3b receptor in facilitating the in vivo development of parasitemia with Babesia rodhaini in rats is documented. Depletion of serum C3 to less than 5% of normal levels by treatment of rats with the C3 inactivator isolated from cobra venom markedly delays the onset of parasitemia. Treatment of rats with trypan blue, an inhibitor of the C3b receptor, delays the development of parasitemia. Conversely, treatment of rats with suramin, a drug that blocks the C3b inactivator, markedly accelerates the progression of parasitemia and, correspondingly, the mortality rate. These observations suggest that the in vivo production of C3b and its interaction with C3b receptors on red cells and/or on parasites is a critical feature in babesial injection of rats. In support of the concept that B. rodhaini organisms contain C3b receptors, we have shown in vitro that parasites will activate the alternate complement pathway, resulting in uptake of radiolabeled C3, and that this uptake is blocked in the presence of trypan blue. Before and during the development of parasitemia, red cells become Coombs-positive for C3, but not for IgG. Taken together, the data support the vital role of C3 activation products (presumably C3b) and the C3b receptor in the facilitation of babesial infection in the rat.
Selective removal of T cell function from mouse lymphocyte suspensions by treatment with normal guinea pig serum.
Authors: Kierszenbaum F , Budzko D B , Miller H C 
Published: December 2022

Abstract
Treatment of murine spleen cells with normal guinea pig serum selectively abrogated responsiveness of these cells to the T cell mitogens PHA or Con A, but failed to affect responses to LPS, i.e., a B cell-specific mitogen. Although pretreatment with GPS inhibited the in vitro immune response of mouse splenocytes to SRBC, responses were normal after restoration with T cells only, indicating that B cells had been spared by GPS. Consistent with these results, incubation with GPS resulted in the loss of reactivity of mouse lymphoid cells in MLC as well as CML systems, both of which test for T cell activities. Furthermore, parental spleen cells treated with GPS were no longer capable of inducing a GVH reaction in F1 hybrids. When compared, the effects of GPS and anti-Thy-1.2 antibodies plus C were found to be comparable. These results indicate that GPS can selectively remove a number of T cell functions from heterogeneous murine lymphoid cell suspensions. Since spleen macrophages were insensitive to GPS cytotoxicity, lack of T cell function is not likely to be due to depletion of these accessory cells.
Resistance to fatal central nervous system disease by mouse hepatitis virus, strain JHM. II. Adherent cell-mediated protection.
Authors: Stohlman S A , Frelinger J A , Weiner L P 
Published: December 2022

Abstract
Resistance of SJL/J mice to intracranial inoculation with the JHM strain of mouse hepatitis, a coronavirus, is dependent upon the age of the animals at inoculation. Animals 12 weeks of age or older are resistant, whereas those 6 weeks or younger are uniformly susceptible to viral infection. Spleen cells or thioglycolate elicited peritoneal exudate cells can transfer resistance from 12-week-old to 6-week-old recipients. Removal of the adherent cells from either spleen or peritoneal cells ablated protection. Adherent cells from 12-week-old mice were protective even after depletion of Ia- and Thy-1-bearing cells. Antiviral antibody, thioglycolate injection into 6-week-old animals, and nylon wool-purified T cells were ineffective in mediating resistance. Adherent cells transferred 4 days before virus challenge, but not after challenge, were protective. Thus, there is an age-related change in SJL mice that protects from acute central nervous system disease, which may be due to maturation of a specialized adherent cell population.
In vivo responses to inhaled proteins. III. Inhibition of experimental immune complex pneumonitis after suppression of peripheral blood lymphocytes.
Authors: Shenker B J , Willoughby W F , Hollingdale M R , Mann T N 
Published: December 2022

Abstract
We have previously shown that inhaled Con A has a powerful enhancing effect on the formation of immune complexes between an inhaled antigen and circulating antibody. Immunohistochemical staining has demonstrated such complexes, together with host complement, in close association with foci of necrotizing destruction of the pulmonary parenchyma. We have postulated that Con A promotes immune complex formation indirectly through polyclonal activation of lymphocytes in the lung. In this paper we test this hypothesis in animals rendered unresponsive to Con A stimulation in vivo by i.v. administration of cholera toxin (CT). Such treatment raised the levels of cAMP in peripheral blood lymphocytes and inhibited their proliferative response to Con A in vitro. CT administration further blocked the local inflammatory response to intradermal injections of Con A, as well as the cell-mediated immune response to intradermal injections of BSA. Although CT failed to block the immune complex-mediated Arthus vasculitis in the skin, it did block production of immune complex pulmonary injury by antigen/mitogen aerosols, as did decomplementation with purified cobra venom factor. These findings support the hypothesis that polyclonal activation of pulmonary lymphocytes promotes immune complex-type alveolitis, possibly by facilitating interactions between humoral antibody and intra-alveolar antigen.