bluuebunny/crossref_metadata_2025_split huggingface dataset:
Requirement for human red blood cells in inactivation of C3b in immune complexes and enhancement of binding to spleen cells.
Authors: Medof M E , Lam T , Prince G M , Mold C 
Published: December 2022

Abstract
We showed previously that soluble immune complexes (IC) added to normal human serum and unseparated autologous blood cells bind predominantly to red blood cells (RBC) bearing C3b receptors. RBC-associated IC are processed both by C3b/C4b inactivator (I) cleavage of C3b and by alternative pathway-dependent C3b generation, and are returned to the serum in a modified form. In the present study, soluble IC were prepared by using 125I-BSA and guinea pig anti-BSA, and were treated with diluted human serum to optimize sustained C3b-dependent binding to human RBC. This binding to RBC could not be abrogated by preincubation of IC with heat-inactivated human serum or purified serum regulatory proteins, I and beta 1H (H), but after binding, pretreated IC dissociated. When IC were prepared with serum containing 125I-C3, treatment with I + H did not release labeled C3 from the complexes. Analysis by polyacrylamide gel electrophoresis in sodium dodecyl sulfate (SDS-PAGE) of 125I-C3b in IC showed similar labeled peaks whether IC were pretreated with buffer or with I + H or were bound to RBC without pretreatment. In contrast, when IC containing 125I-C3b were exposed to I + RBC, nearly 70% of the label was released from the IC. The released material analyzed by SDS-PAGE showed major 125I-C3 peaks corresponding in m.w. to free beta-chain and alpha 1 cleavage products of 30,000 to 33,000 daltons. IC in undiluted serum after incubation with RBC gave less binding to human polymorphonuclear leukocytes than after incubation without RBC, but notably more binding to guinea pig spleen cells and human lymphoblastoid cells. These findings argue that exposure to serum regulatory proteins does not prevent subsequent binding of experimental IC to RBC, that RBC binding promotes degradation of C3b in IC which proceeds beyond iC3b, and that this I-mediated breakdown renders IC reactive with spleen cells.
Local activation of the killing mechanism in PU5 antibody-dependent cell-mediated cytotoxicity effector cells.
Authors: Wei W Z , Lindquist R R 
Published: December 2022

Abstract
This study was undertaken to determine whether ADCC effector cells expressed their killing mechanism globally throughout the entire cell surface or locally in a restricted area. Nonantibody-coated erythrocytes were bound to PU5 ADCC effector cells by either Con A or protein A-Ig bridges, and the effector cells with the adherent nonspecific erythrocyte target cells were mixed with specific antibody-coated erythrocytes. Our results indicated that the Con A or protein A-Ig-linked erythrocytes were not destroyed while the effector cell was in the process of killing specific antibody-coated erythrocytes. Therefore, the ADCC killing mechanisms of PU5 cells require activation by the interaction of Fc receptor with specific antibody-coated erythrocytes, and these killing mechanisms, once activated, are expressed in a locally restricted area of the effector cells rather than globally throughout the entire surfaces of the ADCC effector cell. Previously, we investigated the expression of the killing mechanism in cytolytic T lymphocytes (CTL) and found that alloimmune CTL in the process of killing specific target cells did not kill nonspecific targets linked to the CTL by either wheat germ agglutinin or immunoglobulin bridges. Thus, with respect to the surface membrane expression of lytic activity, CTL and the PU5 ADCC effector cells are similar. Our findings support the view that the various effector killing cells have a common cytolytic pathway and differ only by the recognition and triggering mechanisms.
The migration of activated murine T lymphocytes in vitro. II. Evidence for differential locomotion of T cell subsets.
Authors: Hoffman R A , Ascher N L , Hanto D W , Simmons R L 
Published: December 2022

Abstract
Lymphocytes that were activated by various means (recovered from an in vivo allograft site, sensitized in mixed lymphocyte culture, or stimulated by Con A in vitro), were extremely motile in vitro when compared to unsensitized lymph node lymphocytes. Allosensitized lymphocytes generated in vitro and in vivo (harvested on days of peak cell-mediated cytotoxicity) were more motile than Con A-activated lymphocytes (harvested on the day of peak thymidine incorporation). Protein (bovine serum albumin, normal mouse serum, or alpha-casein) was chemokinetic for all of the lymphocyte preparations, especially those activated by alloantigen or Con A. When these bulk populations were used, no evidence was found to suggest these materials were chemotactic for activated lymphocytes; the various proteins promoted comparable chemokinetic effects. Treatment of allosensitized lymphocytes generated in vitro with Lyt-2 antisera and complement significantly reduced cell-mediated cytotoxicity, but had no effect on random motility. Conversely, treatment with anti-Lyt-1 antisera and complement impaired the motility of the residual cell population in response to chemokinetic normal mouse serum or alpha-casein. Within the bulk population of lymphocytes allosensitized in vitro, the cells that migrate most quickly are predominantly Thy-1.2, Lyt-1+2-, are not as cytotoxic, and do not incorporate thymidine as actively as the unseparated population. These experiments indicate that subpopulations of lymphocytes demonstrate locomotor heterogeneity. Studies designed to determine if a specific lymphocyte population can manifest directional motility (i.e., chemotaxis) will require the use of various antigen-sensitized lymphocyte clones at defined stages of the cell cycle.
Enhancement of natural cytotoxicity by beta-endorphin.
Authors: Mathews P M , Froelich C J , Sibbitt W L , Bankhurst A D 
Published: December 2022

Abstract
The role of enkephalins, beta-endorphin, or other neuropeptides produced by the nervous system in the alteration of immune responsiveness is generally unknown. The present studies were undertaken to investigate the role of these neuropeptides in the modulation of human spontaneous cytotoxicity induced by natural killer (NK) cells. Natural cytotoxicity was measured by using a standard 51Cr release assay with radiolabeled K562 cells. NK activity was significantly enhanced by both beta-endorphin (30.5 +/- 11.5%, M +/- SE, relative enhancement at 50:1, effector:target (E:T) ratio, 10(-14)M beta-endorphin) and methionine-enkephalin (met-enkephalin) (27.4 +/- 9.7% relative enhancement at 10(-9)M). The magnitude of relative enhancement significantly correlated with increasing concentrations of beta-endorphin. Leucine-enkephalin, alpha-endorphin, and morphine did not augment NK activity. The enhancement of NK activity with beta-endorphin increased at all E:T ratios tested. Naloxone inhibited the augmentation of NK activity produced by beta-endorphin and met-enkephalin. By using a combination of a standard 51Cr release and soft agarose single cell analysis assays, beta-endorphin increased both the number of E:T cell conjugates and the number of active killer cells among target-binding cells. The maximal effector cell recycling capacity was increased by 170%. These studies provide new insight into the mechanisms by which neuropeptides produced by the nervous system can alter immune responsiveness.
Spontaneous production of gamma-interferon in cultures of T lymphocytes obtained from patients with Behçet's disease.
Authors: Fujii N , Minagawa T , Nakane A , Kato F , Ohno S 
Published: December 2022

Abstract
The spontaneous production of interferon (IFN) in the cultures of peripheral blood mononuclear leukocytes (PBML) obtained from 30 patients with Behçet's disease was investigated. PBML obtained from each of 26 patients in the convalescent stage and four patients in the exacerbation stage were cultured at least twice without stimulation, and IFN activity in the culture fluid 2 to 7 days after the cultivation was assayed. Twenty PBML of normal healthy donors were also cultured simultaneously. PBML of all patients in the convalescent stage spontaneously produced high-titered IFN (60.0 +/- 9.5 IU/ml), but IFN activity produced in PBML cultures of four patients in the exacerbation stage was very low or was undetectable. Similarly, IFN was always detectable in the circulation of the patients whose PBML spontaneously produced IFN. All IFN activity detected both in the circulation and in the fluid of PBML culture from these patients was gamma-IFN, defined by virtue of its acid lability and antigenicity neutralized with antiserum for gamma-IFN and not with antisera for alpha- and beta-IFN. The cellular source of this gamma-IFN in the patients' PMBL was T lymphocytes and not non-T cells or macrophages. T lymphocytes did not require the help of macrophages. It is suggested that T lymphocytes of these patients may be stimulated by unknown causative agents in vivo and may produce gamma-IFN in vivo as well as in in vitro culture of T lymphocytes.
Immune capacity of the chicken bursectomized at 60 hr of incubation: surface immunoglobulin and B-L (La-like) antigen-bearing cells.
Authors: Jalkanen S , Granfors K , Jalkanen M , Toivanen P 
Published: December 2022

Abstract
Chickens were surgically bursectomized at 60 hr of incubation before the bursal anlage appears. Completeness of the bursectomy was confirmed at autopsy at 10 wk of age. These embryonically bursectomized (Bx) chickens are known to produce immunoglobulins of IgM, IgG, and IgA classes, but so far no specific antibodies have been observed even after heavy immunization. Regarding the appearance of surface immunoglobulin positive (s-Ig+) cells, the most striking effect of bursectomy was observed in the frequency of s-IgG+ cells, which were markedly decreased in the spleen, peripheral blood, and thymus of the Bx birds when compared with the age-matched controls. s-IgM+ cells were significantly decreased in the peripheral blood and s-IgA+ cells in the spleen of the Bx birds. In contrast to these findings, s-Ig+ cells of all three classes were present in normal frequency in the bone marrow. Bursectomy had no effect on the total lymphocyte and other white cell counts in the peripheral blood. Likewise, no effect on the frequency of B-L (Ia-like) antigen-positive cells in different organs was observed.
Lipopolysaccharide inhibits the binding of colony-stimulating factor (CSF-1) to murine peritoneal exudate macrophages.
Authors: Chen B D , Lin H S , Hsu S 
Published: December 2022

Abstract
These studies demonstrate the potent effect of bacterial endotoxin (LPS) on the inhibition of iodinated colony-stimulating factor- (125I-CSF-1) binding by murine peritoneal exudate macrophages (PEM) from C3H/An and C57BL/6 mice. As small an amount as 0.1 ng/ml LPS is sufficient to cause a significant inhibitory effect; this effect is temperature-, time- and concentration-dependent. LPS, however, causes minimal or no inhibition of 125I-CSF-1-binding by PEM from LPS-resistant C3H/HeJ mice. Inhibition of 125I-CSF-1-binding does not appear to be a result of a direct occupancy by LPS of CSF-1 receptors present on the cell membrane and is most likely due to a progressive loss of available CSF-1-binding sites. The effect can be neutralized by the addition of the antibiotic polymyxin B, which binds to the lipid A portion of LPS. The action of LPS on PEM is transient; treated cells recover their 125I-CSF-1-binding activity whether or not LPS is later removed. The restoration of 125I-CSF-1-binding activity can be blocked completely by the addition of cyclohexamide. These findings suggest the rapid, LPS-induced disappearance of CSF-1 receptors from the cell surface may be related to the activation of macrophages by LPS.
Monoclonal antibodies to hamster class II MHC molecules distinguish T and B cells.
Authors: Witte P L , Streilein J W 
Published: December 2022

Abstract
Monoclonal antibodies were prepared against cell surface antigens present on Syrian hamster lymphocytes and a hamster B cell lymphoma line, GD-36. One of these antibodies, S11, precipitated glycoproteins of 29,000 and 39,000 m.w. These glycoproteins were shown to be identical to or a subset of la-like glycoproteins precipitated by hamster alloantisera; however, molecules identified by S11 differed from the predominant hamster la homologues detected with a cross-reactive monoclonal antibody to murine la.7. The immunofluorescence pattern of both anti-la reagents, S11 and anti-la.7, on hamster lymphoid cells is similar by fluorescence-activated cell sorter analysis. A subpopulation of spleen and lymph node cells stains brightly with these antibodies. By two-color fluorescence, this peripheral lymphocyte subpopulation, identified with monoclonal anti-hamster la, also bears surface immunoglobulin (IgM). These data strongly suggest that hamster resting peripheral B cells, and not T cells, express la antigens and can be identified and isolated differentially by using this marker.
Striking paucity of HLA-A, B, C and beta 2-microglobulin on human neuroblastoma cell lines.
Authors: Lampson L A , Fisher C A , Whelan J P 
Published: December 2022

Abstract
Monoclonal antibodies to beta 2-microglobulin (beta 2m), and to the native two-chain molecule, were used to assess the expression of the HLA-A, B, C molecules on human neuroblastoma-derived cell lines. In radioimmuno-, cytotoxic, and microscopic assays, employing fresh and fixed cells, neuroblastoma cells show at best weak activity as compared to glial or lymphoid cells. In binding inhibition assays, neuroblastoma extracts were 200- to 1800-fold less efficient in inhibiting the antibodies than were glial or lymphoid extracts. Immunoprecipitation and SDS-PAGE analysis confirmed that a beta m-like chain is synthesized by the neuroblastoma cells, but the HLA chain could not be visualized by this technique. HLA-A, B, C and beta 2m levels are known to vary among tissues and cell lines. Yet the magnitude of the differences between the neuroblastoma and lymphoid lines is much greater than the reported differences in expression between some of these same lymphoid lines and many other nonlymphoid malignant or nonmalignant cell types. Metastatic neuroblastoma tumor in bone marrow also showed weak HLA-A, B, C activity, with the cells appearing negative in microscopic assays. Possible clinical implications are discussed.
The products of transferred H-2 genes express determinants that restrict hapten-specific cytotoxic T cells.
Authors: Levy R B , Richardson J C , Margulies D H , Evans G A , Seidman J G , Ozato K 
Published: December 2022

Abstract
Cell lines into which cloned H-2 genes had been introduced (i.e., transformants) were used to correlate the genes and their products that are capable of functioning as H-2 restriction elements for hapten-self-(AED and TNP) specific cytotoxic T cells (CTL). These transformants provided a unique system in which major histocompatibility restricted (MHC) T cell recognition could be examined by using cells that express only H-2Ld or only H-2Dd gene products. BALB/c (H-2d) anti AED-self CTL lysed both the H-2Ld and Dd transformants, but not parental, i.e., untransformed, cells. The AED-self lysis of the Ld and Dd transformants was shown to be specifically inhibited by anti-H-2Ld and anti H-2Dd monoclonal antibody, respectively. In contrast to these results, BALB/c anti TNP-self CTL were found to lyse readily the Dd but not Ld transformed lines, supporting reports indicating that H-2Ld-restricted TNP-self CTL could not be detected. The results of this study thus demonstrate that the cell surface products encoded by these transferred MHC class I genes contain self determinants recognized by CTL.
The "lazy" NK cells of Chediak-Higashi syndrome.
Authors: Targan S R , Oseas R 
Published: December 2022

Abstract
Natural killer (NK) function, measured in a short-term (4-hr) 51Cr-release assay, is profoundly depressed in circulating PBL of donors with Chediak-Higashi syndrome (CHS). In this study, we demonstrate that CHS NK cells can express relatively normal lytic function after prolonged exposure in vitro to high levels of activating as well as cytotoxic stimuli. After activation with the human cloned interferon (B1) for 24 hr, CHS NK cells have lytic activity comparable to unactivated normals in a 4-hr 51Cr-release assay. In addition, after 5 days of activation with mitomycin C-treated B cell lines, CHS NK cells have levels of activity similar to those of activated normals but are defective in generating cytotoxic cells capable of lysing the stimulator B cell. Even though CHS NK cells are defective in a 4-hr 51Cr-release assay, after 16 hr they enhance their killing capability 200 to 400-fold. In fact, after 16 hr of interaction with K562 target cells, CHS NK cells are capable of releasing NK soluble cytotoxic factors. These results are consistent with the hypothesis that CHS NK cells have all the necessary cellular structures and molecules required for them to function as lytic effector cells, but their lack of cytotoxic function is due to a relative refractoriness in initiating the post-binding lytic mechanism.
Hapten-specific murine colony-forming B cells. III. Delineation of functional B cell subpopulations grown under different conditions.
Authors: Piper M , Pillai P S , Scott D W 
Published: December 2022

Abstract
The influence of anti-immunoglobulin M (IgM) and anti-IgD on the ability of fluorescein (FL)-specific B cells to proliferate in a colony-forming assay, and of their progeny to further differentiate in response to different FL-antigens was studied. Splenic FL-specific B cells were purified on FL-gelatin plates and were then cultured in semisolid agar in the presence or absence of anti-mu, and anti-delta, or both. Experiments were performed under conditions of either sheep red blood cell (SRBC)-potentiated or SRBC + lipopolysaccharide (LPS)-potentiated colony growth. The resulting colonies were then tested in secondary filler cell-dependent microcultures for the ability to be triggered by different classes of FL-antigens to yield plaque-forming cells (PFC). Anti-delta inhibited 47% of colony growth under both agar culture conditions. Anti-mu inhibited 55% of colony growth in SRBC + LPS-potentiated agar cultures, and inhibited 72% if only SRBC was present. If anti-delta and anti-mu were added together, inhibition was nearly additive. When anti-Ig-treated colonies were tested for PFC responses against FL-polymerized flagellin (POL), both normal and anti-delta resistant colonies, grown under both agar culture conditions, responded well. Anti-mu resistant colonies were refractory to FL-POL challenge. Only normal or anti-delta resistant colonies grown in SRBC + LPS agar cultures were able to respond well to FL-Ficoll, whereas even normal SRBC-potentiated colonies responded poorly. All except SRBC-potentiated, anti-mu treated colonies were able to respond to nonspecific signals present in cultures containing FL-KLH and activated T cell help. These data suggest that addition of specific anti-Ig antibodies, and variation of agar culture conditions, can select for B cell subpopulations responsive only to certain types of antigens.
An analysis of the sensitivity of somatic cell hybrids to natural killer cell- and natural cytotoxic cell-mediated lysis.
Authors: Lin Y , Collins J L , Patek P Q , Cohn M 
Published: December 2022

Abstract
The analysis of the NK and NC sensitivity of somatic cell hybrids formed between parental cell lines that differ in their NK and NC sensitivity has shown the following. 1) The dominant expression of both NK and NC recognition determinants on target cells; 2) the dominant expression of two post-recognitive NC resistance mechanisms, one requiring protein synthesis and one being protein synthesis independent; and 3) the dominant expression of a post-recognitive NK resistance mechanism, which is protein synthesis independent. The post-recognitive protein synthesis-independent NC resistance mechanism confers no NK resistance and the post-recognitive NK resistance mechanism confers no NC resistance. Whether the post-recognitive protein synthesis-dependent NC resistance mechanism confers NK resistance remains open to question. The analysis of the hybrids indicates that transformed cells become sensitive to either NK- or NC-mediated lysis by losing their resistance to the lytic activity of these effector cells, and it appears that differentiation plays a role in determining whether NK or NC resistance will be lost upon transformation. A model is proposed in which the differentiation into a fibroblast associates the loss of NC resistance with transformation, whereas the differentiation into a lymphocyte associates the loss of NK resistance with transformation. Because the loss of NK resistance is not associated with the transformation of fibroblasts, they remain NK resistant, and because the transformation of lymphocytes is not associated with the loss of NC resistance, they remain NC resistant. This provides the basis for the target specificity exhibited by NK and NC effectors.
Requirements for the binding of human plasma fibronectin to the C1q subunit of the first component of complement.
Authors: Sorvillo J , Gigli I , Pearlstein E 
Published: December 2022

Abstract
We have shown previously that [125I]fibronectin (Fn) binds to solid-phase C1q in a dose-dependent manner. When C1r and C1s were added, the binding of Fn to C1q was abolished; removal of C1r and C1s restored Fn binding to C1q. In this report, we have systematically examined the optimal conditions that favor the Fn-C1q interaction. Our studies show that purified native 125I-Fn binds to C1q in a specific, saturable manner. Maximal 125I-Fn binding to C1q and gelatin occurs at low ionic strength (mu = 0.05) and drops sharply as the ionic strength is increased. At mu = 0.20, the binding to C1q is inhibited by 95%, whereas the binding to gelatin is inhibited by 50%. Optimal binding of Fn to C1q and gelatin occurs between pH 5.5 and 7.5, is decreased by 45% at 4 degrees C, and increases with incubation time; saturation of binding occurs in 60 min at 37 degrees C. Scatchard analysis of binding at mu = 0.05 indicates a single class of high affinity binding sites (Kd = 3.7 X 10(-8) M +/- 0.36 SD). The Kd of the reaction when C1q is bound to either plastic or immune complexes is essentially the same, and, in both cases, increases as the ionic strength of the medium is increased. Finally, significant binding of Fn to C1q can be demonstrated at physiologic ionic strength employing either insoluble immune complexes containing C1q or chemically cross-linked C1q.