bluuebunny/crossref_metadata_2025_split huggingface dataset:
Generation of a cloned NK cell line derived from the "null cell" fraction of human peripheral blood.
Authors: Hercend T , Meuer S , Reinherz E L , Schlossman S F , Ritz J 
Published: December 2022

Abstract
The present studies were designed to determine the conditions for generation of human NK clones. First the "null cell" (NC) fraction of human peripheral blood mononuclear cells, which contains the NK effectors, was purified using negative selection with anti-T3, anti-T8, anti-B1, and anti-Mo2 monoclonal antibodies. Subsequently, NC were cloned by limiting dilution using a combination of phytohemagglutinin (PHA) and lymphocyte-conditioned medium (LCM) as an initial stimulus. Colonies could be easily obtained with this procedure, but the maintenance of long-term growth of the cultures represented a major problem. A cloned cell line termed JT1 was generated and has been proliferating continuously in culture for more than 6 mo. The phenotype of JT1 cells was analyzed several times with a series of monoclonal antibodies. These cells did not express surface markers related to thymic (T3-, T4-, T8-, T11-), B cells (B1-, J5-), or myelomonocytic (Mo1-, Mo2-, MY7-) differentiation. In contrast, 95% of JT1 cells reacted with the anti-T10 monoclonal antibody. T9, Ia, and J2 antigens were also present on JT1 cells, but their expression appeared variable from one determination to another. This cloned cell line maintains a strong cytotoxicity against common NK targets, such as K562 and Molt 4 cell lines, and a moderate ADCC activity. In addition, after several months in culture, JT1 cells are still capable of being regulated by interferon, because this lymphokine rapidly enhances cytotoxicity against K562 cells.
Serologically detectable MHC and tumor-associated antigens on B16 melanoma variants and humoral immunity in mice bearing these tumors.
Authors: Baniyash M , Smorodinsky N I , Yaakubovicz M , Witz I P 
Published: December 2022

Abstract
We compared the expression of serologically detectable MHC and tumor-associated antigens on low and high metastasis variants of B16 melanoma tumor. Complement-dependent cytotoxicity, radioimmunobinding, and quantitative absorption assays showed that with respect to both types of antigens the low metastasis variant B16-F1 expressed a higher serologically detectable antigenicity than B16-F10, its high metastasis counterpart. A reverse situation existed in terms of in vivo immunogenicity of these metastasis variants. Sera from C57BL/6 mice bearing locally growing B16-F10 tumors had a higher binding activity to B16 cells than sera from B16-F1 bearers. Accordingly, in vivo propagating B16-F10 tumors had a higher content of tumor-associated Ig than B16-F1 tumors.
LPS-induced differentiation of a murine B cell leukemia (BCL1): changes in surface and secreted IgM.
Authors: Lafrenz D , Koretz S , Stratte P T , Ward R B , Strober S 
Published: December 2022

Abstract
We examined the effect of LPS-induced differentiation on surface and secreted IgM in a cloned BCL1 in vitro cell line. Incubation of this cell line with LPS resulted in a decrease in the amount of membrane IgM, measured by both immunofluorescence and immunoprecipitation, and an increase in IgM secretion, measured by plaque-forming cells (PFC). Activation to high rate secretion was independent of cell cycle in synchronized cells and was independent of DNA synthesis because PFC formation was not inhibited by hydroxyurea. Almost all cells in the in vitro line were shown to contain large quantities of intracytoplasmic IgM before LPS activation. Thus, it would appear that the in vitro cell line represents a partially activated stage of differentiation compared to normal resting B cells or to the in vivo line of BCL1. Analysis of the two forms of mRNA coding for membrane and secreted IgM showed that, at least for cells at the level of differentiation examined here, the control of membrane IgM expression is post-transcriptional. The differentiation of resting B cells to the plasma cell level appears to consist of multiple stages of differentiation. The present data suggest that LPS provides at least two signals of activation. One induces the resting cell to synthesize cytoplasmic IgM, increase surface IgM, and to begin cell division. The second induces the secretion of intracytoplasmic IgM associated with a decrease in surface IgM.
Local adoptive transfer of skin delayed-type hypersensitivity initiated by a single T lymphocyte.
Authors: Marchal G , Seman M , Milon G , Truffa-Bachi P , Zilberfarb V 
Published: December 2022

Abstract
In vivo primed T cells injected in the footpad of naive recipients elicit a typical delayed-type hypersensitivity (DTH) reaction in the presence of their specific antigen. The values of the footpad swelling obtained after these transfers show a clear distinction between negative and positive responses. Serial dilutions of primed T cell populations allow the establishment of titration curves by limiting dilution analysis according to Poisson distribution. The single hit titration curve indicates that a unique cell type underlies the DTH reaction. Furthermore, by using cloned T cells it can be demonstrated that the transfer of a single cell is able to initiate a DTH reaction. The revelation of T cell activity at unit level needs an optimal dose of antigen mixed with the sampled cells.
Neonatal suppression with anti-Ia antibody. I. Suppression of murine B lymphocyte development.
Authors: Fultz M J , Scher I , Finkelman F D , Kincade P , Mond J J 
Published: December 2022

Abstract
To investigate the role of sIa in B lymphocyte development, mice were injected from birth with hybridoma anti-Ia antibody. There was on the average a 95% reduction in the number of sIgD+ cells, and 85% diminution in the number of sIgM+ cells, a small but significant increase in the number of sIgM+ sIgD- sla- B cells, as well as a dramatic increase in the number of sIgM- cells bearing a B lineage antigen. Exposure of cells to high doses of anti-Ia antibody in vitro or in vivo for 24 hr did not affect the number of sIg+ lymphocytes. Thus, it appears that chronic anti-Ia administration critically alters normal B lymphocyte development.
Regulation of rat B cell responses by T cell subsets and interleukin 2.
Authors: Rosenberg J S , Gilman S C , Feldman J D 
Published: December 2022

Abstract
T cell and interleukin 2 (IL 2) regulation of two phases of B cell activation, 3H-TdR uptake and differentiation to antibody-forming cells, were examined. Monoclonal antibody specific for rat kappa light chains (Mab alpha K) stimulated 3H-TdR uptake in vitro in B cell fractions of Lewis spleen cell populations in the presence of T cells and macrophages (M phi); IL 2 reconstituted the response in enriched B cell cultures depleted of T cells and M phi. When IL 2 was added to primary in vitro cultures, spleen cells yielded 100 to 400 anti-SRBC PFC/culture; no PFC were recorded in the absence of IL 2. These results suggested that IL 2 served as a " second signal" for activation in responsive B cell populations. When monoclonal antibody specific for the W3/25+ T cell subset (Mab W3/25) was incorporated into the assay system, both 3H-TdR uptake and PFC responses were inhibited. IL 2 enhancement of B cell responses or responses of reconstituted B cell and T cell fractions was eliminated in the presence of Mab W3/25, indicating that IL 2 mediation of B cell responses was due in part to participation of W3/25+ T cell helper function. In contrast, monoclonal antibody directed to the OX8-bearing T cells (Mab OX8) had no effect on B cell responses. W3/25+ T cells provided helper activity in the generation of a PFC response, whereas OX8+ cells suppressed the antibody response. W3/25+ T cells responded to antigenic stimuli in the presence of IL 2 by undergoing increased blast transformation. OX8+ cells did not exhibit any response. These data define a regulatory network by which T cells, IL 2, and B cells interact to produce in vitro DNA synthesis and antibody formation in activated rat B cells.
Evidence for covert cellular interaction sites expressed by activated T lymphocytes.
Authors: Thomas D W , Hoffman M D 
Published: December 2022

Abstract
In this report we examined the effects of trypsin treatment of immune guinea pig T lymphocytes on their binding to syngeneic macrophages. Immune T cells positively selected by culture for 1 wk with antigen and treated with trypsin showed dramatic binding to macrophages in the absence of additional antigen. This binding was rapid and greatest at 1 hr after the addition of trypsin-treated T cells to macrophages. Thereafter, the bound T cells dissociated from the macrophages and did not rebind. Dissociation of macrophage-bound T cells appeared to be an active process that could be inhibited by blocking T cell protein synthesis. Macrophage binding by trypsin-treated T cells was dependent on prior in vitro stimulation; similar treatment of immune T cells taken directly from the animal did not augment binding, and treatment of T cells cultured without antigen resulted in only modest binding. In addition, the trypsin-induced binding phenomenon showed elements of genetic restrictions. Trypsin treatment of immune T cells selected by culture for 1 wk with antigen resulted in preferential binding to syngeneic macrophages. In addition, immune F1 T cells selected by culture with antigen-pulsed parental macrophages preferentially bound to macrophages of the haplotype used for selection. Evidence is presented suggesting that the trypsin-induced binding was not simply due to antigen carry-over from the trypsinized lymphocytes and favoring the possibility that this binding may be antigen-independent. These results suggest that antigen-activated T cells express covert interaction sites for macrophages and that these sites are actively covered-up by other membrane components.
The antigens of pigeon breeder's disease. VII. Isoelectric focusing studies on unfractionated pigeon dropping extract.
Authors: McCormick D J , Fredricks W W , Tebo T H , Calvanico N J 
Published: December 2022

Abstract
Isoelectric focusing (IEF) studies on pigeon dropping extracts (PDE) revealed that it is a complex mixture of components that are acidic in nature. Chromatographically purified antigens PDEB, PDE1, and PDE3 showed multiple bands in IEF, indicating a microheterogeneity of these components, with peak concentrations focusing at pH 6.1, 4.6, and 3.8, respectively. The isoelectric points are compatible with the chromatographic behavior of these antigens on DEAE-cellulose. Crossed immunoelectrofocusing (CRIF) resolved PDE into seven precipitin lines with rabbit antiserum in a pH gradient from 3.5 to 9.5, and into nine precipitable components in a pH gradient from 2.5 to 7.0. The complexity of this antigen source appears to reside in the heterogeneity of immunologically related antigens. A comparison of pigeon breeder's sera by CRIF of PDE revealed a qualitative difference in precipitation patterns obtained with symptomatic and asymptomatic individuals. Sera from all (eight out of eight) of the symptomatic breeders tested precipitated an unidentified component of PDE, whereas none (zero out of four) of the sera from asymptomatic breeders detected this antigen. These results suggest that CRIF of PDE is useful as a diagnostic tool and that some specific component of PDE may be involved in the pathogenesis of the disease.
Regulation of T15 idiotype dominance. I. Mice expressing the xid immune defect provide normal help to T15+ B cell precursors.
Authors: Kenny J J , Wicker L S , Guelde G , Scher I 
Published: December 2022

Abstract
The immune response to phosphocholine (PC) in many strains of mice is dominated by the T15 idiotype family of anti-PC antibodies. By introducing the CBA/N X-linked immune defect (xid gene) into these mice, one profoundly alters their ability to make a T15-predominant, IgM anti-PC response. This loss of T15 dominance in mice expressing the xid gene is not due to the presence of suppressor T cells or the lack of T15 idiotype-specific helper cells in these mice. Thus, one can reconstitute a T15 idiotype-dominant response in immune defective mice with B cells from normal mice, and in adoptive transfer assays the primed T helper cells from immune-defective mice provide qualitatively the same help to normal B cells as the T helper cells from normal mice. T15 idiotype dominance appears to be controlled by the expression and activation of Lyb-5+ PC-specific B cells. Thus, the majority of T15+ B cell precursors are restricted to this B cell subset, whereas the Lyb-5- B cell subset contains predominantly T15-, anti-PC B cell precursors, which produce mainly IgG antibodies after activation by PC-containing antigens.
Immunologic memory to phosphorylcholine III. IgM includes a fine specificity population distinct from TEPC 15.
Authors: Chang S P , Brown M , Rittenberg M B 
Published: December 2022

Abstract
Group I and group II variable regions expressed in the PC-KLH memory response may originate from distinct germ-line genes or group II may arise by somatic mutation of group I (TEPC 15) germ-line genes. A current version of the somatic mutation hypothesis proposes that somatic mutation is activated by the class switch from IgM to IgG or IgA. If group II results from somatic mutation during class switching, group II IgM antibodies would not exist. This prediction was tested in the present experiments. Group I and group II antibodies were separated from whole serum by affinity chromatography on PC-Sepharose. An ELISA was used to characterize the fine specificity and idiotype of the isolated antibody populations. Group I antibodies were inhibited by both PC and NPPC haptens and were T15 idiotype-positive. Group II antibodies were inhibited appreciably only by NPPC and were negative for the T15 idiotype. The purified group II antibodies contained a significant IgM component, and high levels of group II IgM were detected during the early secondary response to PC-KLH. These observations are inconsistent with the hypothesis that group II originates by somatic mutation activated by the class switch. These results strongly suggest that one or more of the germ-line genes (V, D, or J) of groups I and II are different. Alternatively, if group II antibodies arise from group I by somatic mutation, this mutation must occur before class switching.
Amphotericin B alters the affinity and functional activity of the oligopeptide chemotactic factor receptor on human polymorphonuclear leukocytes.
Authors: Lohr K M , Snyderman R 
Published: December 2022

Abstract
Leukocyte chemotaxis is initiated by the binding of chemotactic factors to specific, high-affinity receptors. Amphotericin B, a polyene antibiotic that binds to membrane cholesterol, inhibits human neutrophil (PMN) chemotaxis. We examined the effects of this drug on PMN functions mediated by the oligopeptide chemotactic factor receptor. The antibiotic irreversibly inhibited chemotaxis and depressed the binding of the radiolabeled chemoattractant, fMet-Leu-[3H]Phe, to its receptor without affecting the receptor's specificity. The drug lowered the binding affinity of the receptor by up to fivefold and slightly increased its number. Doses of amphotericin B that depressed receptor affinity and inhibited chemotaxis did not diminish lysosomal enzyme secretion or superoxide anion production. Nystatin, a less potent polyene antibiotic, also diminished chemotactic factor binding, but to a lesser degree than amphotericin B did. A chemically unrelated antifungal agent had no effect on either binding or chemotaxis. Thus, pharmacologic manipulation can alter the affinity of the chemotactic factor receptor on human PMN; this alteration is associated with a change in receptor function. The data suggest that receptor affinity regulates or at least reflects its functional state, and that the transduction mechanisms for various biologic responses mediated by the chemoattractant receptor are heterogeneous. By pharmacologic alterations of receptor affinity, one may be able to modulate specific biologic responses elicited by chemoattractant receptor-ligand interactions.
The formylpeptide chemotactic receptor on rabbit peritoneal neutrophils. I. Evidence for two binding sites with different affinities.
Authors: Mackin W M , Huang C K , Becker E L 
Published: December 2022

Abstract
F Met-Leu-[3H]Phe and f Nle-Leu-[3H]Phe binding to rabbit peritoneal neutrophils and purified membranes were measured at 4 degrees C silicone oil centrifugation assays, and the results were analyzed by the LIGAND computer program, which permits analysis of ligand binding to multiple classes of binding sites. LIGAND analysis of peptide binding to intact neutrophil indicated that both f Met-Leu-[3H]Phe and f Nle-Leu-[3H]Phe detected two population of binding sites. The apparent Kd values for f Met-Leu-[3H]Phe binding were 1.6 +/- 1.0 X 10(-9) M and 2.2 +/- 0.9 X 10(-8) M, respectively, and 3.1 +/- 0.2 X 10(-9) M and 1.2 +/- 0.6 X 10(-7) M for f Nle-Leu-[3H]Phe. Furthermore, the higher affinity sites detected on whole cells comprised approximately 15 to 30% of the total sites. Two populations of binding sites were also detected on purified neutrophil plasma membranes by both radiolabeled chemotactic peptides. LIGAND analysis of peptide binding to purified membranes yielded apparent Kd values of 5.0 +/- 2.5 X 10(-10) M and 4.8 +/- 0.6 X 10(-8) M for f Met-Leu-[3H]Phe binding, and 4.7 +/- 4.2 X 10(-10) M and 3.0 +/- 1.3 X 10(-8) M for f Nle-Leu-[3H]Phe. The percentage of higher affinity sites detected by f Met-Leu-[3H]Phe and f Nle-Leu-[3H]Phe on purified membranes were 1 to 5% of the total sites detected. These data are consistent either with the existence of two independent binding sites for formylpeptides on rabbit neutrophils or receptor negative cooperativity.
Specific binding of phospholipid platelet-activating factor by human platelets.
Authors: Valone F H , Coles E , Reinhold V R , Goetzl E J 
Published: December 2022

Abstract
The binding of the phospholipid platelet-activating factor 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphorylcholine (AGEPC) to washed human platelets was more than 80% complete within 2 min, which coincided with the time of initiation of platelet aggregation by AGEPC. Scatchard plot analysis of the binding of [3H]AGEPC to platelets without and with an excess of unlabeled AGEPC revealed two distinct types of binding sites. One platelet site for AGEPC exhibited a high affinity (KD = 37 +/- 13 nM, mean +/- SD), was saturable, and had a low maximal capacity of 1399 +/- 498 (mean +/- SD) molecules of AGEPC/platelet. The other platelet site demonstrated a nearly infinite binding capacity, consistent with nonreceptor uptake of AGEPC into cellular structures. The specificity of the high-affinity binding site for AGEPC was assessed by comparing the capacity of several analogues of AGEPC to inhibit the binding of [3H]AGEPC to platelets and to induce platelet aggregation. An ether linkage in position 1, a short-chain fatty acid in position 2, and a choline moiety in the polar head group proved to be critical both for the binding of [3H]AGEPC to platelets and for the initiation of platelet aggregation. Exposure of platelets to AGEPC for 5 min at 37 degrees C functionally deactivated the exposed platelets to subsequent stimulation by AGEPC, as assessed by diminished aggregation, and concomitantly reduced the specific binding of [3H]AGEPC. Evaluation of the time course of the events of deactivation revealed the loss of an aggregation response to AGEPC after 90 sec at 37 degrees C, despite the retention of up to 50% of the specific binding sites for AGEPC.
Macrophages in resistance to rickettsial infections: genetic analysis of susceptibility to lethal effects of Rickettsia akari infection and development of activated, cytotoxic macrophages in A and B10.a mice.
Authors: Meltzer M S , Nacy C A , Stevenson M M , Skamene E 
Published: December 2022

Abstract
Susceptibility to lethal effects of Rickettsia akari varies among mouse strains. Although most strains are resistant, A/J mice are extremely sensitive (10,000-fold difference in LD50 between resistant and sensitive strains). In contrast to most strains of mice, A/J mice also fail to develop activated, tumoricidal macrophages after any of several in vivo or in vitro treatments. Are susceptibility to R. akari and inability to develop activated, cytotoxic macrophages in the A/J strain causally related traits? Genetic analysis of macrophage tumoricidal activity in responsive B10.A and nonresponsive A mice suggested this trait was controlled by a single, autosomal, dominant gene. Among (F1 X A) backcross mice, the traits for defective macrophage cytotoxicity and abnormal accumulation of macrophages during inflammation (a response controlled by a single, autosomal, dominant gene) segregated independently. Genetic analysis of resistance to R. akari in sensitive A and resistant B10.A mice suggested this trait was also controlled by a single, autosomal, dominant gene. Among (F1 X A) backcross mice, however, traits for defective macrophage cytotoxicity and R. akari resistance segregated independently. Thus, development of activated tumoricidal macrophages, accumulation of macrophages at sites of inflammation, and resistance to the lethal effects of R. akari in A and B10.A mice were each controlled by single, autosomal, dominant, non-H-2-linked genes. However, genes for control of macrophage activation for tumoricidal activity and for resistance to lethal effects of R. akari infection are distinct.
B cell expression of endogenous retroviral envelope antigen: biochemical and immunofluorescence characterization.
Authors: Ewert D L , Halpern M S 
Published: December 2022

Abstract
Plasma cells of line 15I5 chickens have been shown to express antigen that is cross-reactive with endogenous retroviral envelope glycoprotein. In the present study, we isolated this antigen and showed that it is structurally homologous to envelope glycoprotein. As assayed by immunofluorescence, most, if not all, of the plasma cell-associated envelope glycoprotein is present on the cell surface although it is not bound to surface Ig or Ia antigen. Although envelope antigen was not detectable by immunofluorescence on the surface of 15I5 bursal cells or peripheral B lymphocytes, immunochemical assays established that retroviral envelope glycoprotein is present on the surface of the bursal cells but at much lower levels than on the surface of the plasma cells. Both bursal and plasma cells synthesize envelope glycoprotein. These findings indicate that an increased level of expression of endogenous retroviral envelope glycoprotein is a concomitant of the differentiation of B lymphocytes to plasma cells in 15I5 chickens.
MLR-specific suppressor T lymphocytes in man. II. Functional and membrane characteristics of a specific MLR suppressor subpopulation.
Authors: Fabio G , Scorza-Smeraldi R , Bonara P , Sabbadini Villa M G , Vanoli M , Calabi F , Zanussi C 
Published: December 2022

Abstract
Human MLR-specific suppressor T lymphocytes were induced by in vitro cultivation of human peripheral T lymphocytes in the presence of soluble HLA-DR alloantigens isolated from normal serum. The suppression is specific in that responder cells autologous to the suppressor cells respond to allogeneic stimulating cells that express the same HLA-DR specificity as that recovered from serum and used to induce the suppressor cells. This antigen-specific suppressor T cell population could be divided into suppressor and non-suppressor subpopulations as a function of adherence to a 6MB Sepharose immunoadsorbent coated with the inducing HLA-DR soluble antigen. As a consequence of activation by soluble DR antigen, the suppressor T lymphocyte population as well as the column-enriched suppressor subpopulation express new membrane specificities that can be recognized by antisera from pluriparous women. The specificities that are recognized are not found on autologous, unstimulated B and T cells, nor do they appear to recognize conventional HLA-A,B,C or DR determinants.