bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies on the surface antigenicity and susceptibility to antibody-dependent killing of developing schistosomula using sera from chronically infected mice and mice vaccinated with irradiated cercariae.
Authors: Bickle Q D , Ford M J 
Published: December 2022

Abstract
Changes in the surface antigenicity and susceptibility to in vitro killing during development of schistosomula of Schistosoma mansoni were studied using serum from chronically infected mice (CIS) and from mice vaccinated with highly irradiated (20 krad) cercariae (VS). Binding of these sera was quantitated by counting the number of P388D1 cells (a transformed, macrophage-like cell of mouse origin, bearing Fc receptors for IgG) binding to the parasite surface. Compared with schistosomula derived in vitro by mechanical transformation (MS), schistosomula recovered 3 hr after skin penetration in vitro (SS) showed a significant loss in surface binding of CIS. Schistosomula recovered 3 hr after skin penetration in vivo (SRS) showed even less binding, and this trend continued such that parasites recovered from the lungs 5 days after infection (LS) showed only minimal binding, and 10-day-old worms from the portal system showed no significant binding. In contrast, VS, which bound significantly less well to MS than CIS, showed enhanced binding to SS, and in the face of their declining antigenicity with respect to CIS, 3- to 24-hr SRS maintained this raised level of antigenicity. Although there appeared to be a decline in binding of VS thereafter, LS remained antigenic, still binding as many cells as MS did despite the fact that they also expressed host antigens detected using antisera raised against mouse RBC. In spite of this persistence of VS binding up to the lung stage, resistance to eosinophil-mediated killing in vitro had developed by 48 hr post-infection, and LS were totally resistant to both eosinophil- and C-mediated killing.
Generation of cytotoxic lymphocytes by SV40-induced antigens.
Authors: Chang C , Chang R , Mora P T , Hu C P 
Published: December 2022

Abstract
In order to study the correlation of in vivo tumor transplantation immunity and in vitro immunologic assays, cell-mediated cytotoxicity against SV40-transformed cells was studied in AL/N strain mice by using 51Cr-release assay. Killing of SV40-transformed AL/N fibroblast cells was observed by spleen cells of AL/N mice immunized with syngeneic SV40-transformed cells. Immunization with the solubilized SV40 tumor-specific transplantation antigen (TSTA) that induced transplantation immunity in vivo did not elicit cytotoxic spleen cells in vitro. However, the spleen cells from mice immunized with solubilized TSTA and then sensitized in vitro with SV40-transformed cells became cytotoxic against SV40-transformed fibroblasts. Similarly, SV40 TSTA (T antigen) purified by immunoprecipitation was able to prime the lymphocytes in AL/N mice: the primed lymphocytes could differentiate into cytotoxic lymphocytes upon in vitro stimulation by SV40-transformed cells. These data indicate that SV40 TSTA (T antigen) plays a role in the induction of cytotoxic lymphocytes.
Lymphoepithelial interactions in the mouse thymus: phenotypic and kinetic studies on thymic nurse cells.
Authors: Kyewski B A , Kaplan H S 
Published: December 2022

Abstract
Thymic nurse cells (TNC), complexes between epithelial cells and thymocytes, are further characterized. Our results show that TNC are predominantly located in the subcapsular and outer cortical region of the mouse thymus. The enveloped thymocytes display the characteristics of cortical thymocytes. They are PNA+, Thy-1+, Lyt-123+, TL+, ThB+, H-2K+, IA+, and cortisone and radiation sensitive. In vitro cultivation of TNC in the presence of interleukin 2 induces a phenotype change to Lyt-1-, ThB-, Lyt-23+. The yield of TNC is highly dependent on the isolation conditions. Moreover, the thymocytes enveloped by an individual TNC do not constitute a single clone. The latter findings strongly suggest that complete envelopment is probably an isolation artifact. However, the cellular composition of the complexes is not random but rather the result of a preexisting in vivo association between an immature thymocyte subpopulation and outer cortical epithelial cells. TNC represent the in vitro correlate of this in vivo interaction. The implications of these results for intrathymic T cell differentiation are discussed.
Membrane attach complex of complement (MAC): three-dimensional analysis of MAC-phospholipid vesicle recombinants.
Authors: Podack E R , Müller-Eberhard H J , Horst H , Hoppe W 
Published: December 2022

Abstract
The three-dimensional structure of recombinants of the isolated membrane attack complex (MAC) of complement with single bilayer dioleoyllecithin (DOL) vesicles and with dimyristoyllecithin (DML) vesicles was determined. A total of four MAC-vesicle complexes were analyzed by imaging negatively stained specimens at various defined tilting angles under minimal dose conditions in the electron microscope and by computer-aided three-dimensional reconstruction. The information on electron micrographs obtained at 6 degrees angular increments from +60 degrees to -60 degrees was digitized by densitometric scanning, Fourier-transformed, corrected for imaging errors, cross-correlated, and synthesized to the three-dimensional image. All four MAC-vesicle recombinants showed stain penetration into the interior of the vesicle, indicating increased permeability of the bilayer to negative stain. The MAC appeared as a hollow structure of 16-nm height, 2.0-nm wall thickness, and a 3.0-nm torus at the free end with an outer and inner diameter of 20.0 nm and 10.0 nm. In MAC-DOL vesicles the hollow core of the MAC terminated at the membrane-binding site, and only small pores of up to 2.0-nm in diameter penetrated the bilayer. In one MAC-DML vesicle lipid discontinuities on the outer circumference of the MAC binding site mediated stain penetration. The second MAC-DML vesicle showed a channel of approximately 4.0 nm connecting the hollow core of the MAC across the bilayer with the vesicle interior. The results suggest the MAC may mediate increased membrane permeability by protein channel formation in addition to lipid reorientation.
Cell-mediated immunity in aged mice: an underlying lesion in IL 2 synthesis.
Authors: Thoman M L , Weigle W O 
Published: December 2022

Abstract
It is well established that immune potential declines with age and that aged animals are unable to mount vigorous cell-mediated immune responses. Production of the lymphokine, Interleukin 2 (IL 2) in response to the T cell mitogen concanavalin A or allogeneic stimulation is also diminished in aged individuals. This lesion in IL 2 synthesis in aged mice underlies their deficiency in cell-mediated responses. Mixed lymphocyte responses, cell-mediated lympholysis, and antigen-induced T cell proliferation are all markedly enhanced by supplementation with this lymphokine.
Spontaneous activation of the first component of human complement (C1) by an intramolecular autocatalytic mechanism.
Authors: Ziccardi R J 
Published: December 2022

Abstract
For biochemical characterization, the first component of human complement (C1) was reconstituted from physiologic concentrations of purified C1q, 125I C1r, and 131I C1s. Upon incubation at 37 degrees C, C1 spontaneously activated, as evidenced by the characteristic proteolysis of the C1r and C1s polypeptide chains as detected by SDS-PAGE analysis. This spontaneous C1 activation followed first-order kinetics (t 1/2 = 4 min and k = 0.173 min-1) with an activation energy of 19.1 kcal/mol. Spontaneous C1 activation was unaffected by the general protease inhibitor phenylmethylsulfonylfluoride (PMSF) but reversibly blocked by a known inhibitor of C1 activation, nitrophenylguanidinobenzoate (NPGB). Spontaneous C1 activation was measured at C1 concentrations ranging from 9 to 160 nM (i.e., 0.05 to 1.0 times physiologic concentrations). The data indicate that C1 spontaneously activates by an intramolecular autocatalytic mechanism, for first-order kinetics were observed over the entire concentration range with t 1/2 = 4 min at each concentration. However, the percentage of activable C1 decreased with dilution due to C1 dissociation (i.e., C1qr2s2 leads to C1q + C1r2s2). The observed concentration of C1 that spontaneously activated at each dilution equalled the concentration of C1 present as macromolecular C1. When reconstituted C1 was mixed with normal human serum (NHS) and then incubated at 37 degrees C, spontaneous C1 activation was completely inhibited. Pretreating NHS at 56 degrees C for 30 min destroyed its inhibitory activity. In conclusion, C1 spontaneously autoactivates at 37 degrees C by an intramolecular mechanism. This activation is suppressed in NHS.
Preferential idiotype-isotype associations in antibodies to dinitrophenyl antigens.
Authors: Scott M G , Fleischman J B 
Published: December 2022

Abstract
Murine IgG antibodies to DNP-protein are predominantly IgG1 and IgG2 whereas those against DNP-Ficoll (DNP-F) are mainly IgG3. Isotype restriction in this and other systems may mean that certain heavy chain variable regions (VH) are preferentially associated with particular constant regions (CH) in the immune response. We studied idiotypes of several monoclonal antibodies to DNP in an effort to identify VH regions that may be restricted in this way. Two idiotypes, 7-17 and 8-11, identified on IgG3 hybridomas raised against DNP-Ficoll, were expressed prominently both in immune sera and by IgG3-secreting plaque-forming cells (PFC) against DNP-F. By contrast, these idiotypes were barely detectable in antisera to DNP-proteins and were not expressed by IgG1- or IgG2-secreting PFC. Thus, the 7-17, and 8-11 idiotypes may be restricted to IgG3 and to responses to T-independent DNP antigens. Conversely, the 460 idiotype was expressed prominently in antisera to DNP-proteins but only weakly in antisera to DNP-F. The 460 idiotype was found on IgG1 and IgG2 PFC but not on PFC secreting IgG3. These results suggest that in heterogeneous immune responses to a single antigenic determinant, certain VH regions may be preferentially associated with particular CH isotypes.
A reevaluation of the putative association between the Fc gamma receptor and histocompatibility antigens on human mononuclear leukocytes.
Authors: Pulleyblank B M , Falk J A , Letarte M , Dorrington K J , Falk R E 
Published: December 2022

Abstract
The controversial question of an association between human Ia antigens and the FcR for immunoglobulin G has been examined. The experimental basis upon which such a relationship has been predicted was reevaluated. Human allosera with specificity for classical transplantation antigens, HLA-DR, and the related supertypic specificities MB and MT have been tested for their capacities to inhibit homologous EA rosette formation by PBM and B-CLL cells. Both immune and "nonimmune" sera inhibited rosette formation. Sera were normalized with respect to IgG concentration, and no significant quantitative differences in the observed inhibition were seen. Positive reactivity of the antisera with Ia, HLA-A, or HLA-B antigens did not influence EA binding to FcR. Furthermore, F(ab')2 of IgG from reactive sera did not inhibit rosette formation. These observations have been extended using murine reagents. A.TH anti-A.TL serum, which reacts with human Ia in binding and immunoprecipitation studies, and five monoclonal antibodies, which have been raised against human Ia and bind to monomorphic determinants, were tested for an effect on EA rosette formation. When these reagents were tested at concentrations at which they could be shown to bind to antigens on the target cell population, no inhibition of EA rosette formation by human PBM, MON or B-CLL cells could be demonstrated. The studies provide no evidence to suggest the existence of an association between Ia and the human FcR.
Selective suppression of human B lymphocyte differentiation into IgG-producing cells by soluble Fc gamma receptors.
Authors: Bich-Thuy L T , Revillard J P 
Published: December 2022

Abstract
Receptors for the Fc part of IgG were isolated by affinity chromatography from supernatants of unstimulated human lymphocytes or polymorphonuclear neutrophils. When added to cultures stimulated by polyclonal activators, these soluble receptors selectively depressed the maturation of B lymphocytes into IgG-producing cells, whereas the number of IgM-producing cells was either increased or unchanged. The number of IgA-containing cells was not changed. The data support the concept of class-specific control of Ig synthesis by Fc receptors.
Two loci in I-J subregion of the H-2 complex controlling molecules selectively expressed on suppressor and helper T cells.
Authors: Ochi A , Nonaka M , Hayakawa K , Okumura K , Tada T 
Published: December 2022

Abstract
Different batches of alloantiserum directed at the I-J subregion products of the H-2 major histocompatibility complex (anti-I-J) induced either suppression or augmentation of the in vitro secondary antibody response when added in a minute quantity to the culture of primed spleen cells. The suppressive or augmenting effect of the individual antiserum was found to be determined by its predominant specificity for either one of the two different molecules, both encoded in the I-J subregion, that were selectively expressed on functionally different subsets of T cells, i.e., suppressor (Ts) and helper (Th2) T cells. This was determined by the differential absorption of antiserum with Lyt-1+ and Lyt-2+ T cells as well as with suppressor hybridomas that express an I-Jk product. It was found that the absorption of an anti-I-J antiserum with Lyt-1+ T cells resulted in the loss of activity to eliminate a set of helper T cells (Th2) while leaving the ability to affect antigen-specific suppressor T cells (Ts). The absorption of the same antiserum with either Lyt-2+ T cells or suppressor hybridomas eliminated the activity to kill Ts but not Th2. Thus, the results indicate that the I-J subregion accommodates two or more loci that code for discrete molecules expressed on functionally different subsets of T cells. Because the simple addition of a minute quantity of antisera to the culture resulted in the modulation of antibody response presumably by affecting these two sets of T cells, it is suggested that I-J subregion products act as functional molecules in regulatory cell interactions.
The induction of alloreactive cytotoxic responses in vivo are inhibited by pretreatment with M is-disparate cells.
Authors: Hayes R L , Claman H N 
Published: December 2022

Abstract
Alloreactive cytotoxic cells (CTL) are subject to regulation. These experiments were designed to study the in vivo down-regulation of CTL. Mice injected with allogeneic lymphoid cells (responders) develop CTL that are assayed in vitro by their ability to lyse 51Cr-labeled target cells of an appropriate H-2 haplotype. However, if CBA/J responder mice (H-2k, mls d) are pretreated with spleen cells from C3H/HeN mice, which are H-2 compatible (H-2k) but Mis- and minor antigen-disparate (mis c), there is virtually complete inhibition of the ability to develop CTL against A/J cells (H-2a, mls c) in vivo. In a similar manner, pretreatment of CBA/J responders with B10.BR (H-2k, mls b) cells resulted in the inhibition of the CTL response against B10.A(4R) (H-2h4, mls b). The state of CTL responsiveness appears to be H-2 restricted and requires that the allogeneic cells used for immunization share minor histocompatibility antigens with the strain of mouse selected for pretreatment.
Immunity to herpes simplex virus type 2. IV. Impaired lymphokine production during recrudescence correlates with an imbalance in T lymphocyte subsets.
Authors: Sheridan J F , Donnenberg A D , Aurelian L , Elpern D J 
Published: December 2022

Abstract
Cell-mediated immunity (CMI) to herpes simplex virus type 2 (HSV-2) was studied in patients with recurrent disease. Peripheral blood lymphocytes (PBL) obtained during recrudescence (0 to 3 days post-onset of lesion), convalescence (4 to 14 days), and quiescence (greater than 14 days), which were cultured in vitro in the presence of UV-inactivated HSV-2 (G) antigen, demonstrated similar, virus-specific lymphoproliferative responses. However, the production of the lymphokine, leukocyte migration-inhibition factor (LIF), was completely suppressed during recrudescence. During convalescence, LIF production returned to levels similar to those of PBL from seropositive controls (without a history of recurrent subsets revealed a significant increase in the proportion of T8+ and Ia+ cells during recrudescence and at prodrome (24 to 48 hr before onset of lesions). Glass adherence reduced the proportion of both T8+ and Ia+ cells and restored early (1 day) LIF activity, and recrudescent PBL suppressed the proliferation of autologous T cells in presence of UV-HSV-2 (G) antigen. The expression of both phenotypes and LIF production returned to control levels during convalescence.
Potentiation of the primary humoral immune response in vitro by C5a anaphylatoxin.
Authors: Goodman M G , Chenoweth D E , Weigle W O 
Published: December 2022

Abstract
The effect of the anaphylatoxin C5a on the primary humoral immune response to SRBC was studied in culture of spleen cells from C3H mice. The addition of human C5a to antigen-stimulated cultures resulted in a significant, dose-dependent augmentation of the primary PFC response to antigen. The specificity of this effect was affirmed by the ability of C5ades Arg, but not of the structurally analogous C3a anaphylatoxin, to act in a parallel fashion. Enhancement could be observed over a range of doses of antigen. Brief preincubation of macrophages, but not of lymphoid cells, with C5a was sufficient to cause subsequent enhancement of the primary humoral immune responses. The duration of preincubation required for this effect closely paralleled that for binding of C5a to peritoneal cells. Immunopotentiation by C5a appears to involve the function of C5a receptor-bearing, Ia- accessory cells as well as Ia+ antigen-presenting cells. Immunopotentiation could be observed when the addition of C5a was delayed for up to 24 hr after initiation of culture. Additionally, augmentation of tritiated thymidine uptake in mixed lymphocyte reactions was enhanced by the addition of C5a in a fashion parallel to that for the primary response to SRBC. These observations support a role for C5a as a modulator of cellular immunity in addition to its role in acute inflammation. Possible cellular mechanisms and implications for immunomodulation of immune responses are discussed.
Inhibition of antibody synthesis by histamine in concanavalin A-treated mice: the possible role of glucocorticosteroids.
Authors: Badger A M , Griswold D E , DiMartino M J , Poste G 
Published: December 2022

Abstract
Administration of histamine (50 mg/kg) to BALB/C mice injected with concanavalin A (Con A) (100 micrograms, i.v.) 24 hr previously, results in a marked decrease in antibody synthesis to sheep red blood cells (SRBC) injected 2 hr later. This phenomenon occurs with nonimmunosuppressive doses of Con A and is strain-specific. It does not take place in the response to the T-independent antigen polyvinylpyrrolidone (PVP) or if histamine is administered after the antigen. Adoptive transfer of normal syngeneic cells at the same time as antigen does not reverse this effect. Excess suppressor cell generation was excluded by co-cultivation of treated spleen cells with normal cells in vitro and by determining their antibody response to SRBC 5 days later. 2-Methylhistamine, a histamine type 1 (H1) receptor agonist, mimicks the effect of histamine whereas dimaprit, a histamine type 2 (H2) receptor agonist, does not. Because histamine interaction with H1 receptors causes the release of adrenocorticotropic hormone (ACTH), we examined the effects of ACTH and corticosterone in this system and found that both could mimick the effect of histamine. These results suggest that the interaction of histamine with H1 receptors causes the release of glucocorticosteroids that may interfere with either Con A-activated T helper cell function or macrophage processing of T-dependent antigen.
Monocyte receptors for the Fc portion of IgG studies with monomeric human IgG1: normal in vitro expression of Fc gamma receptors in HLA-B8/Drw3 subjects with defective Fc gamma-mediated in vivo clearance.
Authors: Fries L F , Hall R P , Lawley T J , Crabtree G R , Frank M M 
Published: December 2022

Abstract
The Fc gamma receptors of reticuloendothelial cells are presumed to play an important role in the clearance of circulating particles opsonized with IgG. In order to quantify these receptors and assess their contribution to the clearance phenomenon in man, Scatchard analysis has been applied to 125I-IgG1 myeloma protein binding by a model mononuclear phagocyte, the peripheral blood monocyte. Close compliance to the criteria for linear Scatchard plots has been obtained. The kinetics of binding at 37 degrees C were consistent with a simple, reversible, bimolecular reaction. A saturable, single class of high-affinity binding sites was discerned with a Ka of 2.61 +/- 0.13 x 10(8) M-1 and a mean of 35,500 +/- 1700 receptors per monocyte. These receptors expressed approximately equal affinities for IgG subclasses 1 and 3, with progressively lower affinities for IgG subclasses 4 and 2, respectively. Parameters of IgG1 binding to monocytes of patients with dermatitis herpetiformis and normal individuals of HLA-B8/Drw3 haplotype were not significantly different from controls, despite the previous demonstration of retarded IgG-mediated clearance in one-half of such subjects. Receptor number and affinity failed to correlate with T 1/2 for sensitized erythrocyte clearance in vivo. Functional defects in in vivo clearance, even in the absence of circulating immune complexes, are not necessarily related to abnormal expression of Fc gamma receptors by phagocytes.
Proliferative responses of normal human B lymphocytes. Development of an assay system for human B cell growth factor (BCGF).
Authors: Muraguchi A , Fauci A S 
Published: December 2022

Abstract
A simple and reproducible system for inducing and measuring proliferation of normal human peripheral blood B lymphocytes was developed and employed as an assay for BCGF activity contained in supernatants of cultured human mononuclear cells. SAC was used to activate human peripheral blood B cells to develop into blasts with low levels of proliferation, and a marked synergistic effect on the proliferation of these activated B cell blasts was demonstrated when various culture-derived supernatants containing exogenous growth factors were added to the system. Substantial BCGF activity was obtained from culture supernatants of co-cultures of pooled allogeneic mononuclear cells from two donors, who were also stimulated with PHA. Kinetic studies demonstrated that maximal BCGF activity was produced in cultures carried for 72 hr or longer. A linear relationship was observed between the logarithm of dilution of added factor and incorporation of 3H-thymidine in the responding SAC-stimulated B cell blasts, suggesting the applicability of this system in screening and quantitating BCGF activity in supernatants of various sources, such as T cell clones, T cell neoplasms, and functional human T-T hybridomas. Furthermore, the system could potentially be adopted to the long-term culture of proliferating normal human B cells.