bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determination of IgG subclasses and Gm allotypes in culture supernatants of pokeweed mitogen-stimulated human blood lymphocytes.
Authors: Morell A , Van Loghem E , Nef M , Theilkaes L , Skvaril F 
Published: December 2022

Abstract
Concentrations of the 4 IgG subclasses, of IgM, and of IgA were determined in culture supernatants of pokeweed mitogen-stimulated mononuclear cells isolated from human peripheral blood. Time-course studies showed cumulative secretion of IgM, IgA, and the subclasses IgG1, IgG2, and IgG3 but not of IgG4. In supernatants of 7-day cultures of unseparated mononuclear cells, IgG1 was predominant, followed by IgG2 and IgG3. Removal of most monocytes from the mononuclear cells resulted in an overall decrease of immunoglobulin production but had no influence on the relative IgG subclass distribution. In supernatants of T cell-enriched cultures, the synthesized IgG was deficient in IgG1. Likewise, in supernatants of B cell-enriched cultures, IgG2 exceeded IgG1 concentration. Elimination of the T gamma cells suggested some influence of this subset on IgG2 production. Gm allotypes determined in supernatants corresponded to those in serum of the blood donors.
Serologic and biochemical identification of minor histocompatibility (H-4) antigens.
Authors: Long P M , Lafuse W P , David C S 
Published: December 2022

Abstract
Mouse alloantiserum capable of detecting minor histocompatibility antigens has been produced. Cytotoxic antibody to products of the H-4 locus was produced by reciprocal immunization of minor H loci congenic strains B10 (H-4a) and B10.129(21M) (H-4b), with mitogen-stimulated lymphocytes and epidermal cells. Absorption studies suggested antibodies to more than 1 specificity. The antibodies cross-react with products of other minor H loci. Alloantiserum to the H-4 gene product precipitates a glycoprotein with a m.w. of approximately 45,000 from radiolabeled Con A-stimulated lymph node cells.
The relationship between surface immunoglobulin isotype and the immune function of murine B lymphocytes. V. High affinity secondary antibody responses are transferred by both IgD-positive and IgD-negative memory B cells.
Authors: Lafrenz D , Strober S , Vitetta E 
Published: December 2022

Abstract
We examined the adoptive secondary anti-DNP responses restored by surface IgD+ and IgD- memory B cells. Several parameters that might affect the affinity and magnitude of the adoptive responses were studied: 1) time after priming of cell donors, 2) source of anti-IgD antibodies used for immunofluorescent cell staining, 3) adjuvant used for priming, 4) carrier protein used for priming, 5) amount of antigen used for the challenge of adoptive hosts, and 6) the strain of ice used as donors and recipients. In contrast to previous reports, the present results demonstrate that the selection of cells with high affinity antigen receptors can occur to the same extent in both the delta + and delta - memory cell pools. This suggests that the loss of surface IgD is not a necessary intermediate stage in the maturation of memory B cells.
Acquisition of syngeneic I-A determinants by T cells proliferating in response to poly (Glu60Ala30Tyr10).
Authors: Nepom J T , Benacerraf B , Germain R N 
Published: December 2022

Abstract
The T cell proliferative response in mice to the synthetic polymer GAT is under Ir gene control, mapping to the I-A subregion of the H-2 major histocompatibility complex (MHC). Antigen-dependent proliferation in vitro of in vivo GAT-primed lymph node cells can be inhibited by a monoclonal antibody to Ia-17, an I-A public determinant. Using this antibody for direct immunofluorescent analysis, T cells in GAT-stimulated proliferative culture are identified that express syngeneic I-A during culture. This expression is strictly antigen dependent, requires restimulation in vitro, and requires the presence of I-A-positive adherent antigen-presenting cells. T cells bearing I-A can be enriched by a simple affinity procedure, and I-A-positive cells separated on a FACS are shown to retain antigen-specific reactivity. The acquisition of I-A determinants by T cells under these culture conditions is not nonspecific. The Ia determinants borne by T cell blasts appear to be dictated by the I subregion to which the relevant Ir gene maps, and which codes for the Ia molecule involved in presentation of the antigen. Thus, (B6A)F1 (H-2b X H-2a)F1 LNC express I-Ak antigens when proliferating to GAT but not when stimulated by GLPhe, the response to which is under I-E subregion control. The relation of Ir gene function to Ia-restricted antigen presentation and self-Ia recognition is discussed.
Photobleaching recovery studies of antigen-specific mouse lymphocyte stimulation by DNP-conjugated polymerized flagellin.
Authors: Peacock J S , Barisas B G 
Published: December 2022

Abstract
We have used fluorescence photobleaching recovery (FPR) to study the lateral diffusion of antigen-receptor complexes during stimulation of DNP-specific mouse B cells by the T-independent antigens DNP-polymerized flagellin (DNP-POL). Depending on epitope density and dose, these antigens behave either as immunogens or tolerogens. Lymphocyte DNP receptors binding DNP0.5 flagellin monomer show a diffusion constant D of 2.2 X 10(-10) cm2 sec-1 and ca 50% fluorescence recovery after bleaching. For DNP-POL bound to DNP-specific lymphocytes, the observed diffusion constants decrease monotonically with increased antigen dose and epitope density. Under optimally immunogenic conditions of DNP2.3-POL at 1 micrograms/ml, D = 1.5 X 10(-11) cm2 sec-1, some 14-fold less than for a single DNP receptor. Under tolerogenic conditions lower diffusion constants approaching 0.8 X 10(-11) cm-2 sec1 are observed. The fraction of aggregates mobile on the time scale of the experiment remains constant at about 50 to 60% in all immunogenic situations, but falls abruptly to about 24 to 32% in precisely those situations where the antigen/dose combination is tolerogenic. This might support the hypotheses that there exist critical epitope densities above which antigens and receptors form rigidly cross-linked aggregates that bring about B cell tolerance. The mobility of DNP0.5 flagellin monomer bound to receptors left unoccupied after treatment with various doses and batches of DNP-POL is independent of DNP-POL presence. Receptor aggregate diffusion is unaffected by treatment with colchicine or cytochalasin B.
Structural studies of a human gamma 3 myeloma protein (Goe) that binds staph protein A.
Authors: Recht B , Frangione B , Franklin E , van Loghem E 
Published: December 2022

Abstract
The partial amino acid sequence of the Fc region of an unusual monoclonal immunoglobulin molecule (Goe), which had the allotypic markers Gm (b0, b3, b5, s, t, v), rarely encountered in Caucasians, was determined. Protein Goe was previously shown to belong to the gamma 3 subclass by antigenic typing, to possess a gamma 3-like hinge region and a gamma 1-like carboxy-terminal octadecapeptide, and to bind to staphylococcal protein A. The sequence of protein Goe resembled that of gamma 3 molecules except for the presence of tyrosine at position 296, alanine at position 339, and histidine and tyrosine at positions 435 and 436. It is of interest that histidine 435 appears to play an important role in binding to Staph protein A. Since tyrosine and phenylalanine at 296 and 300 are typical of G3m(g) molecules, whereas protein Goe is G3m(g-), this may correspond to the non-b1 allotypic marker. Of the numerous explanations to account for these findings, the most likely possibilities are that protein Goe is either a hybrid molecule or the product of a germ line gene representing the G3m s allotype, which is rare in Caucasians and common in Mongoloid populations. Support for the latter alternative is provided by the isolation from normal serum of a small amount of a protein having many of the properties of protein Goe.
Immune reactive measles virus polypeptides on the cell's surface: turnover and relationship of the glycoproteins to each other and to HLA determinants.
Authors: Fujinami R S , Sissons J G , Oldstone M B 
Published: December 2022

Abstract
To better understand the mechanism(s) whereby antibody and complement and cytotoxic lymphocytes lyse infected cells, we studied the structure, interrelationship and turnover of measles virus polypeptides expressed on the cell's surface. Of the 6 major viral structural polypeptides, L, HA, P, NC, F, and M, found in purified virions or infected cells, only 2, the HA and F, resided on the surface of infected cells. The HA was present primarily in the form of a 160k dimer, and F was identified as a 64k polypeptide migrating distinct from other viral polypeptides. With reduction, the HA migrated as a 80k monomer, and F0, after cleavage, was found to be composed of a 42k nonglycosylated polypeptide, F1, and a 24k glycosylated protein, F2. The relationship between F0 and F1 and between the HA dimer and monomer was verified by tryptic peptide mapping. The turnover of HA and F from the cell's surface was 10 and 9 hr, respectively. However, in the presence of specific antibody after a marked loss of viral antigen from the surface, the turnover for HA and F was 15 and 12 hr, respectively. Despite being independent molecules, HA and F were closely linked, as they moved together (co-capped) over the plasma membrane when incubated with monospecific or monoclonal antibody. In contrast, neither HA nor F co-capped with the major histocompatibility antigens or with other host cell proteins, which indicates a separation between these host cell proteins and measles viral glycoproteins on the cell's surface.
In vitro antigen-mediated clonal expansion of memory B lymphocytes.
Authors: Brooks K H , Feldbush T L 
Published: December 2022

Abstract
An in vitro model for the propagation and expansion of the memory B lymphocyte population is described. DNP-BGG immune cells were mixed with OVA immune cells and challenged immediately with DNP-OVA. After the 1st response had begun to wane, the cells were rechallenged with DNP-OVA (day 11 of culture). An average of 13-fold more PFC were observed after delayed challenge (day 11). This expansion in the PFC response was an antigen-dependent process and did not involve recruitment of new memory cells from the virgin lymphocyte pool. The level of expansion of the memory cell pool was also calculated using limiting dilution analysis and was found to fall in a range of 16- to 67-fold increase in precursor frequency. In addition to the expansion of the memory B cell population, we also observed the development of 2 immunoregulatory cycles previously observed only in vivo. First, in the presence of persistent antigen, a cyclical PFC response was seen. Second, after day 10 of culture, optimal PFC numbers were observed only when DNP-lysine was added to the plaque assay. Such hapten-augmentable PFC responses have been reported by other investigators as indicative of anti-idiotypic regulation. This possibility is examined more extensively in the following communication.
A monoclonal antibody inhibiting human neutrophil chemotaxis and degranulation.
Authors: Cotter T G , Spears P , Henson P M 
Published: December 2022

Abstract
The hybridoma technique of Kohler and Milstein was used to raise a monoclonal antibody against human neutrophils it has been found to inhibit neutrophil chemotaxis and degranulation. The antibody has been termed NCD 1. Incubation of 12 micrograms of NCD 1 with neutrophils (2 X 10(6)), followed by incubation with cytochalasin B and stimulation with either C5a, fMet-Leu-Phe, or soluble aggregated immunoglobulin, resulted in the inhibition of lysosomal enzyme release. The inhibition was not cytochalasin B dependent, since lysosomal enzyme release induced by opsonized zymosan or opsonized sheep erythrocytes was also inhibited, even in the absence of cytochalasin B. NCD 1 had no affect on enzyme release induced by the calcium ionophore A23138 or by phorbol myristate acetate. The antibody also inhibited neutrophil chemotaxis to zymosan-activated plasma and fMet-Leu-Phe. By contrast, superoxide production stimulated by phorbol myristate acetate, opsonized zymosan, or fMet-Leu-Phe was not affected by NCD 1. Similarly, uptake of 51Cr-labeled opsonized sheep erythrocytes into neutrophils was resistant to the effects of the antibody. NCD 1 Fab fragments did not inhibit lysosomal enzyme release or chemotaxis, althugh binding to the neutrophil surface was demonstrated by immunofluorescence. NCD 1 F(ab')2 fragments behaved analogously to the whole antibody. Binding of both fMet-Leu-[3H]Phe or 125I-soluble aggregated immunoglobulin to the cells was not inhibited by the antibody, which implied that NCD 1 was inhibiting some post-ligand binding event.
Phagocytosis and killing of the protozoan Leishmania donovani by human polymorphonuclear leukocytes.
Authors: Pearson R D , Steigbigel R T 
Published: December 2022

Abstract
The role of polymorphonuclear leukocytes (PMN) in host defense against Leishmania donovani, the protozoan that causes visceral leishmaniasis, is unknown. To assess the ability of PMN to ingest and kill the infecting promastigote stage of the organism, cytocentrifuge preparations were made from tumbled suspensions of 5 X 10(6) PMN, an equal number of promastigotes, and fresh human serum deficient in the 6th component of complement. 53 +/- 9% PMN were found to have 1 or more associated promastigotes, and 81 +/- 14 promastigotes were found per 100 PMN after 15 min at 37 degrees C. There was a corresponding decrease in extracellular promastigotes from 5 x 10(6) ml to 2.7 X 10(4)/ml. Superoxide anion was generated during phagocytosis. Ingetion was saturable with respect to promastigote concentration, required heat labile factors, and was minimal when suspensions were incubated in ice water. Intracellular killing of promastigotes was indicated by a decline in cell-associated organisms without a concomitant increase in extracellular promastigotes. Light and electron microscopy showed disintegration of intracellular promastigotes. Oxidative killing mechanisms appear to be required for PMN killing of this protozoan organism, since there was no decline in intracellular organisms in PMN from a donor with chronic granulomatous disease. Promastigotes studied in a phagocyte-free system were susceptible to H2O2 generated from glucose by glucose oxidase or added directly at greater than or equal to 10(-5) M. Killing was enhanced by the addition of lactoperoxidase (50 mU/ml) with KI (0.05 mM) and inhibited by fresh, but not boiled catalase in the glucose-glucose oxidase system. These studies demonstrate that human PMN can ingest and kill L. donovani by the H2O2-peroxidase-halide system and may be capable of providing host defense against the invading, promastigote stage of this pathogen.
Transmethylation reactions are required for initial morphologic and biochemical responses of human monocytes to chemoattractants.
Authors: Pike M C , Snyderman R 
Published: December 2022

Abstract
Transmethylation reactions mediated by S-adenosyl-L-methionine are required for the chemotaxis of mononuclear leukocytes. It is not yet known, however, whether methylation reactions participate in the initial transduction of the chemotactic signals that lead to the alterations in cellular morphology required for chemotaxis and/or whether they are necessary for the subsequent biochemical events needed for sustained directed migration. We therefore investigated the effects of inhibiting methylation on 2 early responses induced by chemoattractant-receptor occupancy in human monocytes; the rapid morphologic alteration from round to a triangular, motile cell configuration (polarization) and the release of [3H]-arachidonic acid from membrane phospholipids. Both of these initial responses to 3 types of chemoattractants were severely depressed in monocytes treated with the methylation inhibitors, erythro-9-[2-hydroxy-3-nonyl]adenine (EHNA) plus adenosine and L-homocysteine or by 3-deazaadenosine plus L-homocysteine. These findings indicate that methylation reactions are required for the transduction of signals after chemotactic factor receptor occupancy in monocytes, which lead to a motile cellular configuration and release of arachidonic acid from membrane phospholipids. Activation of phospholipases with destruction of cell-associated phosphatidylinositol appears to account for the major source of arachidonic acid released by monocytes exposed to chemoattractants. This pathway for arachidonic acid release requires a transmethylation reaction since it is blocked by inhibitors of methylation.
An 8th rabbit b allotype (b92) detected by a genetic study.
Authors: Benammar A , Cazenave P A 
Published: December 2022

Abstract
Genetic study of the progeny of a Spanish wild rabbit has revealed 2 unknown allotypic specificities that behave as encoded by alleles at the b locus. One of these A92 is described in this paper. This specificity is located on immunoglobulin light chains and cross-reacts with anti-b4 and presumably with anti-b9 sera. These data indicate that A92 is a "new" allotype of the b series and is thus designated b92.
Absorption of normal lymphocytes on allogeneic spleen monolayers: depletion of alloreactivity is due to inhibition of CTL induction by released monolayer cells.
Authors: Kelso A 
Published: December 2022

Abstract
A technique for the haplotype-specific depletion of precursors of alloreactive cytolytic T lymphocytes (CTL-P) by absorption of unprimed spleen cells on allogeneic lymphocyte monolayers has been examined. When H-2d spleen cells were incubated on monolayers of H-2b spleen cells and the nonadherent cells were cultured in mixed leukocyte culture (MLC), CTL activity generated against the monolayer haplotype was 30- to 1000-fold lower than the equivalent cultures of unabsorbed H-2d cells. Cytolytic reactvity to a 3rd-party haplotype, H-2k, was reduced no more than 6-fold. However, culture of the same cells at limiting dilution indicated that the frequency of CTL-P against the monolayer haplotype in monolayer-nonadherent H-2d populations was not significantly different from the frequency in normal H-2d spleen. It was noted that MLC of monolayer-nonadherent H-2d populations were highly cytolytic for H-2d target cells. This reaction was reduced and the ability to generate anti-H-2b CTL was restored when the nonadherent cells were treated with anti-H-2b antibody and complement to eliminate contaminating monolayer cells released during absorption, and when monolayers were prepared from spleen cells depleted of Lyt 2-bearing cells (and hence CTL-P). These data suggested that the reduction in anti-H-2b reactivity of monolayer-nonadherent cells in MLC was due to inhibition by the competing anti-H-2d reaction of contaminating, monolayer-derived CTL-P. Although fluorescent labeling of monolayer cells indicated that these cells represented only 10% of the nonadherent population, flow cytometry and further limiting dilution analysis demonstrated that cells that detached from H-2b monolayers during absorption were enriched 2-fold in T lymphocytes and CTL-P over normal spleen. The strength of the anti-H-2d reaction by a minority of monolayer cells can thus be attributed both to the higher frequency of H-2b anti-H-2d than H-2d anti-H-2b CTL-P in spleen populations and to the preferential detachment of monolayer T lymphocytes during absorption.
kappa/lambda Shifts do not occur during maturation of murine B cells.
Authors: McGuire K L , Vitetta E S 
Published: December 2022

Abstract
We have used highly specific affinity-purified antibodies against mouse kappa- and lambda chains in conjunction with both immunofluorescence analysis on the FACS and enzymatic radioiodination of murine splenocytes and bone marrow cells. Our results indicate that the kappa/lambda ratio of cell surface immunoglobulin is constant during the ontogenetic development of B cells, i.e., a shift in the kappa/lambda ratio does not occur during B cell maturation. Our results suggest that the events controlling kappa and lambda expression on murine B cells are decided very early in ontogeny, before significant antigenic selection.
Host modification of Sindbis virus sialic acid content influences alternative complement pathway activation and virus clearance.
Authors: Hirsch R L , Griffin D E , Winkelstein J A 
Published: December 2022

Abstract
Previous studies have shown that Sindbis virus, an enveloped alphavirus of the togavirus group, activates the alternative complement pathway in the absence of detectable antiviral immunoglobulin. The present studies examined the role of the host-determined sialic acid content of Sindbis virus on activation of the alternative complement pathway. Purified Sindbis virus grown in baby hamster kidney (BHK-SV) and in mosquito (MOSQ-SV) cells yielded virus with 10.2 and less than 2.0 nmol sialic acid/mg viral protein, respectively. Sindbis virus deficient in sialic acid (2.0 nmol sialic/mg) was also produced by treating the BHK-SV with neuraminidase (NANase-SV). When MOSQ-SV or NANase-SV was incubated in either C4DGPS or C2DHS, each consumed significantly more C3 than did BHK-SV, indicating that the ability of Sindbis virus to activate the alternative pathway is inversely related to its sialic acid content. Studies in vivo showed that virus deficient in sialic acid (MOSQ-SV) was cleared from the blood of mice much more efficiently than was virus rich in sialic acid (BHK-SV), after i.v. inoculation. Furthermore, when animals were depleted of C3 through C9 by cobra venom factor (CoVF) treatment, no differences in the clearance of high and low sialic acid-containing viruses were observed. Thus both the activation in vitro and complement-dependent clearance in vivo are significantly affected by the host-determined sialic acid content of Sindbis virus.
The binding of BCG-activated macrophages to tumor targets stimulates secretion of cytolytic factor.
Authors: Johnson W J , Whisnant C C , Adams D O 
Published: December 2022

Abstract
The binding of neoplastic targets and the secretion of a potent cytolytic protease (CF) by BCG-activated macrophages have previously been shown to be independent functions, both of which are necessary for completion of macrophage-mediated cytolysis. The present studies demonstrate that secretion of CF is triggered by the binding of neoplastic targets to BCG-activated macrophages. The binding of tumor targets, but not of normal lymphocytes, resulted in enhanced secretion of CF from BCG-activated macrophages, although not from macrophages elicited by thioglycolate broth. Dead or metabolically inactive tumor targets, as well as membrane preparations of tumor targets, induced secretion of CF from BCG-activated macrophages. The blocking of macrophage-target binding with a porous filter prevented augmented secretion of CF. Appreciable secretion of CF occurred in as little as 30 min after addition of tumor targets to BCG macrophages. Binding did not induce a generalized increase in secretion of neutral proteases by BCG macrophages, since secretion of plasminogen activator was actually decreased after the binding of P815 targets. The data suggest the selective binding of BCG-activated murine macrophages to neoplastic targets triggers the secretion of a potent CF.