bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cell-Mediated Immunity to Friend Virus-Induced Leukemia
Authors: Ting Chou-Chik , Rodrigues Dennis , Bushar Grace Shiu , Herberman Ronald B. 
Published: December 2022

Abstract
The primary cell-mediated cytotoxic response to a Friend virus-induced leukemia, FBL-3, in C57BL/6 mice was measured by the 125IUdR release assay. Intraperitoneal (i.p.) inoculation of 1 × 101 FBL-3 cells produced progressive tumor growth (progressors); subcutaneous (s.c.) inoculation of as many as 5 × 106 FBL-3 cells produced only transient tumor growth (regressors), and these mice would subsequently resist i.p. challenge of FBL-3 cells at 3 days after s.c. inoculation. The kinetics of the primary cell-mediated cytotoxic response of regressors was biphasic. Significant cytotoxicity could be detected at 3 to 5 days after s.c. inoculation of 5 × 106 FBL-3 cells, peaked at days 10 to 14, declined to a very low level or became undetectable around days 20 to 30; then the reactivity reappeared and persisted at least up to 60 days. In progressors, the kinetics of the cell-mediated cytotoxic response was similar to the regressors, but the reactivity was much lower. The cytotoxic response was found to be T cell dependent, during both the first peak (days 10 to 14) and the second peak (days 40 to 60). In adoptive transfer experiments, lymphocytes from regressors gave 90% protection against i.p. challenge of FBL-3; lymphocytes from progressors only gave 40% protection.
Antigenic Determinants of Adenovirus Capsids
Authors: Willcox Nicholas , Mautner Vivien 
Published: December 2022

Abstract
We have tested the two principal theories which explain the previous finding that small amounts of type-specific antibody to the adenovirus hexon can neutralize infectivity, whereas even large amounts of cross-reactive antibody do not.
It has been suggested that the type-specific determinants are especially prominent in the virion. We have therefore measured the capacity of whole virus to bind appropriate antibodies, using a sensitive radioimmunoprecipitation (RIP) system. In fact, virions bound typespecific and cross-reactive antibodies impartially. Moreover, they bound both much less effectively than did free hexon or disrupted virus, suggesting that many of each kind of determinant are inaccessible in virions. It has been suggested that the type-specific determinants are confined to those hexons located next to the pentons, and that they are the targets for neutralizing antibody. We have therefore studied the antigenicity of peripentonal and nonamer hexons isolated from virions, and found that each possessed both kinds of determinants. Furthermore, these were present in the same proportions as in hexons purified from the soluble antigens in infected cells (“free hexons”).
We conclude that the mechanism of neutralization by antibody is complicated, and that the type-specific determinants exposed on the virion must play a crucial role.
Antibody-Mediated Cell Cytotoxicity in a Defined System: Regulation by Antigen, Antibody, and Complement
Authors: Lustig Hannah J. , Bianco Celso 
Published: December 2022

Abstract
The use of a serum-free environment and target cells carrying defined amounts of radiolabeled antigen allowed a quantitative study of the role of antigen, antibody, and complement on antibody-mediated cell cytotoxicity (AbMC).
For lysis to occur, a minimum number of antigen molecules must be present on the target cell. 51Cr release from target cells with lower antigen density requires larger concentrations of effector cells and antibodies.
Target cell-bound complement, itself unable to mediate cytotoxicity, reduces the number of IgG molecules required for lysis. The antibody and complement, however, have to be bound to the same target cell. Bystander complementcoated erythrocytes, present in the same reaction mixture with IgG-coated targets, are not lysed.
Blocking of AbMC is effected only by antigen, either soluble or in immune complexes prepared in antigen excess. Antigen competes at the level of the target cell. Blocking at the level of the effector cell, by use of immune complexes prepared at equivalence or in antibody excess, is difficult to achieve. The large number of cells with Fc receptors contained in mouse spleens may explain this finding. Arming of effector cells by passive binding of immune complexes is poorly effective as a means of obtaining lysis of the target cells.
In all situations, the outcome of the reaction is determined by the presence of free antibody-combining sites, alone, or in immune complexes, that are able to combine with the target cell membrane antigen. The requirements for lysis are rather stringent.
Kinetics of the Antibody Response to Type III Pneumococcal Polysaccharide
Authors: Jones Jeffrey M. , Amsbaugh Diana F. , Prescott Benjamin 
Published: December 2022

Abstract
When the number of PFC present in the spleen was measured at 24-hr intervals after immunizing with an optimally immunogenic dose of type III penumococcal polysaccharide (SSS-III), maximal numbers of PFC were attained 4 days after immunization; thereafter, the number of PFC decreased rapidly. By contrast, serum antibody levels, which were measured in the same mice using a Farr test, reached peak values 5 days after immunization and then declined much more sowly than did the number of PFC. Two factors were found to contribute to this disparity. First, experiments conduceted with splenectomized mice showed that extrasplenic antibody synthesis, which began between days 3 and 4 after immunization and peaked on days 6 to 7, accounted for nearly one-third of the total amount of serum antibody produced. Second, the average rate of antibody synthesis by PFC increased through day 6 after immunization and then declined.
Antigen-antibody dissociation tests showed that the avidity of the serum antibody obtained 4 to 7 days after immunization was the same. Moreover, during the same interval, all the antibody detected by the Farr test was of the IgM class. Thus, a change in avidity or class of immunoglobulin after day 5 did not account for the disparity observed. The clearance rate of antibody injected i.v. into nonimmune and immunized mice was studied. The data obtained indicated that accelerated clearance of antibody was occurring prior to day 3 after immunization; however, after day 3 the antibody clearance rate was constant and was the same as that found when antibody was injected into nonimmune mice. These findings affirmed the results of previous studies showing that treadmill neutralization was not important in determining the serum antibody levels present after immunization with an optimally immunogenic dose of SSS-III.
Antibody Responses of Mice to Alkaline Detoxified Lipopolysaccharide
Authors: Von Eschen Kenneth B. , Rudbach Jon A. 
Published: December 2022

Abstract
The antibody responses of outbred normal mice and nude mice injected with alkaline detoxified lipopolysaccharide (Alk-LPS) were measured. In some cases the antibody responses to Alk-LPS were compared to responses made against lipopolysaccharide (LPS) and native protoplasmic polysaccharide (NPP). The kinetics of the primary responses to Alk-LPS and NPP were similar, whereas LPS stimulated a more rapid appearance of antibodies in the primary responses. Alk-LPS stimulated only primary antibody responses in both types of mice and sensitized nude mice for secondary responses which could be triggered with LPS. However, secondary antibody responses could not be triggered in normal mice primed with Alk-LPS. These data suggested that, on a functional basis, Alk-LPS possessed the specific antigenic signal associated with LPS antigens but lacked the second nonspecific mitogenic signal dependent on the lipid A portion of LPS.
In Vitro Induction of Cytotoxicity against Syngeneic Mastocytoma and Its Suppression by Spleen and Thymus Cells from Tumor-Bearing Mice
Authors: Takei Fumio , Levy Julia G. , Kilburn Douglas G. 
Published: December 2022

Abstract
P815 × 2 mastocytoma cells, when injected subcutaneously into syngeneic DBA/2 mice, induced T lymphocyte-mediated cytotoxicity in the mice. During the course of tumor growth this cytotoxic activity decreased and ultimately the tumor killed the mice. When spleen cells from mice with tumors in the early stages of growth were incubated in vitro with mitomycin C-treated tumor cells, specific cytotoxicity mediated by T lymphocytes was developed. In contrast, spleen cells, taken from mice with tumors at a later stage in their growth, did not develop cytotoxic activity. The unresponsiveness of spleen cells from mice with tumors in the latter stages of growth seemed to be due to the presence of suppressor cells since in vitro development of cytotoxicity by spleen cells from early tumor-bearing mice were inhibited by the addition of spleen cells or thymocytes from mice with progressively growing tumors. Normal spleen cells or thymocytes did not affect the response.
Lymphocyte Transformation Induced by Autologous Cells
Authors: Weksler Marc E. 
Published: December 2022

Abstract
Human mitogen-induced and cell line B lymphoblasts stimulate the proliferation of allogeneic and autologous lymphocytes in culture. The role in this reaction of EB viral determinants on the stimulating cells and immunity of the lymphocyte donor to the EB virus has been studied. The stimulatory capacity of cultured cell line lymphoblasts is not inhibited by incubating lymphoblasts with antisera to EB viral determinants. Cultured cell line B lymphoblasts stimulate as much thymidine incorporation by lymphocytes from donors with or without immunity to the EB virus. Further, a B lymphoblast cell line (U-698) which lacks the EB viral genome stimulated as much lymphocyte proliferation as did B lymphoblasts with the EB genome. Cultured T lymphoblast cell lines do not stimulate allogeneic lymphocyte proliferation. These cells appear to lack the determinants which stimulate lymphocyte transformation. No evidence was found that cultured cell line T lymphoblasts suppressed allogeneic lymphocyte proliferation. Mitogen-induced lymphoblasts from EB-immune and non-immune subjects stimulated the proliferation of autologous lymphocytes comparably. It is concluded that neither immunity to the EB virus nor expression of EB viral antigens on mitogen-induced or cell line lymphoblasts is necessary for the stimulation of lymphocyte proliferation.
Immunopathogenesis of Autoimmune Tubulointerstitial Nephritis
Authors: Hyman Lawrence R. , Colvin Robert B. , Steinberg Alfred D. 
Published: December 2022

Abstract
Autoimmune tubulointerstitial nephritis (TN) was induced in strain XIII and Hartley but not strain II guinea pigs after immunization with rabbit tubular basement membranes (TBM) in CFA. Strain XIII guinea pigs developed extensive autoimmune TN associated with high anti-TBM (aTBM) antibody titers and linear deposits of IgG along renal cortical TBM after immunization with 10 µg to 10 mg of TBM. In addition, autoimmune TN was passively transferred to strain XIII animals by the i.p. injection of aTBM sera obtained from actively immunized Hartley guinea pigs. In contrast, strain II guinea pigs did not develop autoimmune TN after active immunization (10 µg to 10 mg) with rabbit TBM in CFA, and only produced high aTBM antibody titers with the highest immunizing antigen dose. At this dose (10 mg) the strain II animals demonstrated linear deposits of IgG along renal cortical TBM but did not develop autoimmune TN. Further, recipient strain II guinea pigs did not develop autoimmune TN after passive transfer of aTBM antisera despite renal cortical tubular deposition of aTBM antibodies. Both inbred guinea pig strains produced antibodies reactive with rabbit and rat renal basement membranes. No evidence for differences in nephritogenic TBM antigens could be demonstrated between strain XIII and strain II TBM. These observations indicate that 1) genetic factor(s) influence the production of antibodies reactive to autologous TBM, 2) after the deposition of antibodies on the TBM, additional or related genetic factor(s) determine the full expression of this autoimmune renal disease, and 3) aTBM antibody deposition on renal TBM is not sufficient to elicit autoimmune TN.
The Distribution of Ia Antigens on the Surfaces of Lymphocytes
Authors: Abbas Abul K. , Dorf Martin E. , Karnovsky Morris J. , Unanue Emil R. 
Published: December 2022

Abstract
The distribution of Ia antigens was studied on murine spleen lymphocytes by an ultrastructural technique employing deep freeze-etched replicas. Ia antigens were labeled on cells from appropriate congenic and recombinant strains of mice by incubating the cells with FITC-conjugated anti-Iak antibody, followed by ferritin-coupled Fab anti-FITC. Ia antigens were detected predominantly on immunoglobulin (Ig)-bearing B lymphocytes. Antigens coded for by the entire Ik region were present on the surfaces of 95% of the positive cells (from B10.BR mice) in densely packed microclusters. Ia specificities coded for by the I-A and I-C subregions (on 4R and B10.HTT mice) exhibited a more variable pattern, with 30 to 35% of the labeled cells having sparsely distributed Ia antigens in relatively discrete microclusters. Binding of anti-Iak antibody at 37°C led to patch formation but not to capping. Modulation of surface Ig left Ia antigens diffusely distributed on the cell surface, indicating that these two membrane proteins are independent molecules.
The in Vitro Suppression of Antigen- or Mitogen-Induced DNA Synthesis by Murine Spleen Cells after the Addition of Freshly Prepared Syngeneic Cells
Authors: Ficho Thomas W. , Baram Peter 
Published: December 2022

Abstract
The suppression of antigen- and mitogen-induced DNA synthesis by murine spleen cells in vitro was investigated. It appears that cultures receiving two signals exhibit marked suppression of DNA synthesis. The addition of KLH, PPD, Con A, PHA, or LPS to 72-hr-old cultures of KLH-stimulated murine spleen cells resulted in the suppression of DNA synthesis assayed at 144 hr. When small numbers of freshly prepared KLH-PPD SC or NSC were added to these cultures at 72 hr the suppression of DNA synthesis was abrogated. However, the addition of larger numbers of KLH-PPD SC or NSC resulted in increased suppression of DNA synthesis. Large numbers of KLH-PPD SC or NSC could substitute for the second stimulant (KLH, PPD, Con A, PHA, or LPS) in suppressing DNA synthesis. The addition of fresh cells obtained from KLH-PPD-immunized mice. Cells obtained 30 to 75 days post immunization were most effective in suppressing DNA synthesis.
Partial Characterization of the Rat Anti-Encephalitogenic Protein (RSCP)
Authors: MacPherson Catherine F. C. , Armstrong Holly 
Published: December 2022

Abstract
A protein antigenically similar to the anti-encephalitogenic bovine spinal cord protein (BSCP) was detected in saline extracts of rat nervous tissues by immunodiffusion analyses using a rabbit anti-BSCP serum. Rat SCP (RSCP) appears to be evenly distributed throughout all parts of the rat nervous system and occurs also in the thymus, thyroid, and adrenal glands. Although immunodiffusion analyses indicated that RSCP shares some antigenic sites with BSCP, anti-RSCP sera reacted only with RSCP, indicating that the major immunogenic determinants of the RSCP are peculiar to the rat and differ from the immunogenic determinants of human, monkey, rabbit, guinea pig, or bovine SCP. Immunoelectrophoretic analyses of concentrated pastes of rat brain (RB) or rat spinal cord (RSC) in agar at pH 8.6 revealed that RSCP occurs in two molecular forms having the electrophoretic mobilities of a serum β-globulin and a serum γ-globulin, respectively. However, γ-RSCP is the predominant component of extracts of brain or spinal cord. γ-RSCP was isolated from RB and RSC by a procedure which involved: a) extraction with 0.05 M ammonium acetate buffer, pH 4.0; b) batch absorption of impurities on CM-52 cellulose; c) batch absorption of RSCP on SP-Sephadex, pH 3.5; d) elution of RSCP from SP-Sephadex, pH 5.5; and finally, e) gel filtration on Sephadex G-50 superfine. Purified γ-RSCP formed one band when analyzed by polyacrylamide electrophoresis in acid gels containing 8 M urea. In contrast, two bands were always present when γ-RSCP from brain or spinal cord were subjected to SDS-polyacrylamide electrophoresis in 15% gels. The larger of the two components of brain γ-RSCP had a m.w. of 12,400 daltons, whereas the two components of spinal cord γ-RSCP were smaller. The molecular sizes of brain RSCP and spinal cord RSCP was estimated by gel filtration chromatography to be 12,400 daltons. The amino acid compositions of γ-RSCP prepared from RB or RSC were similar except that γ-RSCP from RSC contained twice as much half-cystine and a slightly higher proportion of basic amino acid than γ-RSCP from RB.
Pathogenetic Mechanisms in Immune Polioencephalomyelitis: Induction of Disease in Immunosuppressed Mice
Authors: Duffey Paul S. , Martinez Douglas , Abrams Gerald D. , Murphy William H. 
Published: December 2022

Abstract
Immune polioencephalomyelitis (IPE) was induced by the i.p. injection of x-irradiated (10,000 R) syngeneic line Ib malignant lymphocytes into C58 mice that were 7 or more months old and in young mice immunosuppressed by x-ray or drugs. The occurrence of IPE in young immunosuppressed C58 mice was systematically analyzed. When mice less than 2 weeks old were x-irradiated with 600 R, IPE could not be induced. The incidence in 1-month-old mice was approximately 50% and increased progressively with the age except for a drop in incidence at 3 months. An analysis of the dose effects of x-irradiation on the occurrence of IPE in mice of different ages revealed a marked increase in the incidence in 3- and 5-month-old mice beginning at dose levels of 450 R and 300 R, respectively. Considered together, these data indicated that two subpopulations of immunocytes differing in x-ray sensitivity interacted to protect mice from IPE. It appears that under natural conditions an x-ray sensitive cell population, possibly having suppressor function, decreased with age and made mice susceptible to induction of IPE. Five-month-old mice were immunosuppressed with an LD10 of cyclophosphamide, prednisolone, or methotrexate to determine whether mice immunosuppressed with drugs also were susceptible to the induction of IPE. The incidence was 89%, 13%, and 5%, respectively. The mouse strain specificity of IPE induction also was studied. In 6- to 8-month-old mice suppressed with 600 R, IPE could not be induced in non-H-2k strains: BALB, C57BL/6, NZB. Of the H-2k strains tested (CBA/J, C3H/He, AKR/J, C58), the disease could be induced only in the C58 and AKR/J strains. Histopathologic studies showed that CNS lesions in immunosuppressed C58 and AKR/J mice did not differ significantly from those in old C58 mice with IPE. Taken together, the results of these studies indicate that IPE can be used as a model for analyzing age-dependent diseases of suspected immunopathologic etiology.
Delayed Hypersensitivity and Granulomatous Response After Immunization with Protein Antigens Associated with a Mycobacterial Glycolipid and Oil Droplets
Authors: Granger Donald L. , Yamamoto Ken-Ichi , Ribi Edgar 
Published: December 2022

Abstract
A mycobacterial glycolipid (P3) mixed with protein antigens in oil-in-water emulsion induced lasting delayed hypersensitivity (DH) and granulomatous inflammation after intradermal injection into guinea pigs. This did not occur when P3 and bovine serum albumin (BSA) were given in Freund's incomplete adjuvant. The oil-in-water emulsions consisted of microscopic oil droplets suspended in aqueous medium. By separating oil and aqueous phases from BSA + P3 emulsion it was shown that antigen retained with oil droplets led to DH and granuloma formation. The association of antigen with oil droplets was P3 dependent and was quantitated with 125I-labeled BSA. The same phenomenon occurred with 125I-labeled rabbit γ-globulin (RGG) + P3 emulsion. Fluorescein-conjugated RGG was observed in a particulate state within or on oil droplets in emulsion containing P3. These physical characteristics of antigen + P3 emulsion appeared to be important for immunogenicity.
Physicochemical and Functional Characterization of the C1r Subunit of the First Complement Component
Authors: Ziccardi Robert J. , Cooper Neil R. 
Published: December 2022

Abstract
C1r was isolated from serum by an improved method and found to be a glycoprotein with a sedimentation coefficient of 7.0S. Under conditions of physiologic ionic strength and pH, C1r consists of two apparently identical noncovalently linked 95,000 dalton polypeptide chains.
Antisera to C1r detected a protein of γ-mobility on electrophoresis of serum in agarose in the presence of calcium, and a β-mobility protein when the electrophoretic separation was carried out in EDTA. On sucrose gradient ultracentrifugation of normal human serum in the presence of calcium, C1r antigenicity was found in the 19 S region of the gradient. On the other hand, when the gradient contained EDTA, C1r antigenicity was found in the 7 S region. No reaction of anti-C1r with C1r-deficient sera was observed. C1r had a high affinity for active or proenzyme C1s in the presence of calcium and was able to activate C1s and to form C1 in conjunction with C1q and C1s. Activation of C1s by C1r was inhibited by calcium, C1 inactivator, polyanethol sulfonate, and DFP. Activation of C1s by C1r occurred only after a preliminary incubation of C1r for a brief time at 37°C before addition of C1s. The ability of C1r to form C1 in conjunction with C1q and C1s was, however, progressively lost on incubation at 37°C. Trypsin, although potentiating the activity of crude C1r, did not modify the activity of purified C1r. Its action was on a trypsin-sensitive inhibitor separated from C1r in the final step of the isolation procedure.
The binding of 125I-C1r to sensitized sheep erythrocytes required the presence of C1q and calcium but not C1s, whereas the binding of 125I-C1s required C1q, C1r and calcium. Thus, C1r functions as not only the activator of C1s, but also serves as the physical link between C1q and C1s in macromolecular C1.
The Structure and Function of Immunoglobulin Domains
Authors: Yasmeen D. , Ellerson J. R. , Dorrington K. J. , Painter R. H. 
Published: December 2022

Abstract
The fragments related to the Cγ2 and Cγ3 homology regions of human IgG, described in the preceding paper by Ellerson, et al. were assayed for their ability to interact with complement, engage in cytophilic activity toward macrophages, and to play a role in controlling the catabolism of the whole IgG. The Cγ2-fragment retained about 3% of the activity of intact IgG in a whole complement-fixing assay in which the test proteins were adsorbed as monolayers onto polystyrene latex beads. However, in a fluid-phase C1-binding assay this fragment showed the same activity as IgG and Fc-fragment, when compared on a molar basis. Since the Cγ2-fragment represented only one intact domain, full expression of complement-fixing activity appeared to be independent of quaternary interactions. Thus IgG possesses two C1-binding sites. The Cγ3-fragment was inactive in both of the complement assays. The ability of IgG to interact with the Fc-receptor on guinea-pig macrophages was shown to be entirely a function of the Cγ3 region. This was demonstrated both in a direct assay in which tanned red cells coated with Cγ3-fragment formed rosettes with macrophages and in an indirect assay in which this fragment was able to inhibit rosette formation between IgG-coated red cells and macrophages. The rate of clearance of radiolabeled Cγ2-, Cγ3-, Fab, Fc fragments, and IgG from the circulation was measured in rabbits. The Cγ2 fragment was cleared with a half-time similar to that shown by intact IgG and Fc (about 70 hr) whereas Cγ3- and Fab fragments were cleared more rapidly (half-time, about 15 hr). The rate of clearance was not related to the presence of sialic acid or exposed galactosyl residues at the termini of the carbohydrate prosthetic groups. These data clearly show that at least three of the biologic functions of IgG are mediated fully and independently by one or other of the Fc domains.