bluuebunny/crossref_metadata_2025_split huggingface dataset:
Growth of an interleukin 2/interleukin 4-dependent T cell line induced by granulocyte-macrophage colony-stimulating factor (GM-CSF).
Authors: Kupper T , Flood P , Coleman D , Horowitz M 
Published: December 2022

Abstract
Lymphokine activities in conditioned medium from activated helper T cell lines are most commonly defined by the proliferation of "specific" lymphokine-dependent cell lines. Various sublines of IL 2-dependent (and ostensibly specific) HT-2 and CTLL cells have now been shown to proliferate in response to BSF-1/IL 4 as well. After activation with antigen or mitogen, D10.G4.1, an antigen-specific cloned T helper cell that has recently been shown to produce IL 4 but not IL 2, secretes two distinct cytokines that induce the growth of HT-2 cells. These "T cell growth factors" (TCGF) can be separated by reversed phase high-performance liquid chromatography (RP-HPLC). The TCGF activity of one of these factors can be blocked by 11B11, an antibody specific for IL 4. The second TCGF activity is not affected by 11B11 or by antibodies specific for IL 2. This TCGF activity can be neutralized by a goat polyclonal antibody to granulocyte-macrophage colony-stimulating factor (GM-CSF), and has a RP-HPLC elution profile identical to that of recombinant GM-CSF. Recombinant GM-CSF induces both proliferation and long-term growth of HT-2 but not CTLL cells, and this activity can be neutralized by the same antibody to GM-CSF. GM-CSF is best known as a factor that induces the maturation and growth of granulocytes and macrophages from bone marrow-derived hematopoietic precursor cells. The ability of GM-CSF to induce the growth of certain T cell lines indicates that this molecule may play a role in T cell-mediated immune responses, either as an autocrine growth factor or a paracrine stimulus from both lymphoid and nonlymphoid tissues that produce this cytokine.
Comparison of the calcium requirement for the induction and maintenance of B cell class II molecule expression and for B cell proliferation stimulated by mitogens and purified growth factors.
Authors: Dennis G J , Mizuguchi J , McMillan V , Finkelman F D , Ohara J , Mond J J 
Published: December 2022

Abstract
As an important intracellular second-messenger, the concentration of calcium in the cytosol [Ca+2]i influences diverse cellular activities. To investigate the calcium requirement for distinct phases of B cell activation, we studied the effect of altering the quantity of extracellular calcium on the induction of increased B cell MHC class II molecule (Ia) expression and DNA synthesis by different B cell mitogens. During short-term cultures (less than 24 hr), the induction of class II molecules by anti-immunoglobulin (anti-Ig) and calcium ionophore were dependent on the presence of extracellular calcium, whereas activation induced by B cell stimulation factor-1 (BSF-1) was minimally dependent on extracellular calcium, and that induced by LPS was independent of it. During longer-term cultures (i.e., greater than 24 hr), the heightened class II molecule expression that was induced by all of the B cell mitogens used was significantly compromised by depletion of extracellular free calcium. Although the anti-Ig-stimulated increase in expression of Ia could be restored by the addition of calcium to the medium at 12 hr, it could not be restored when the addition of calcium was delayed to 24 hr after the onset of culture. This was in marked contrast to the finding that BSF-1-stimulated B cell responses which were suppressed after 24 hr of culture in the presence of EGTA could be restored by the addition of calcium. Activation of B cells along the pathway leading to DNA synthesis demonstrated a requirement for extracellular calcium which was greater than that required for induction of MHC class II molecule expression. Thus, LPS-stimulated size increases of B cells after 12 hr of culture was dependent on extracellular calcium while its induction of MHC class II molecule expression was independent of extracellular calcium at this early time point. These observations indicate that the extracellular calcium requirement for B cell activation is dependent both on the activation pathway utilized by the mitogenic signal and on the duration of cell activation. Furthermore, they demonstrate that B cell stimuli that can initiate B cell activation in the relative absence of extracellular calcium may require extracellular calcium for maintenance of this activational state.
Qc-1, a novel Q-region-controlled CTL determinant expressed on B lymphocytes.
Authors: Homer R J , Murphy D B 
Published: December 2022

Abstract
Using cloned cytotoxic T lymphocytes (CTL), we have identified a Q region controlled determinant with a unique strain and tissue distribution. Several strains that express the classically defined Qa-2 determinant and other Q region controlled determinants do not express the CTL determinant. In addition, strain BALB/cByJ, which does not normally express any Q region controlled cell surface determinant, expresses this new determinant. Cross-reactivity between the Q region controlled CTL determinant and a Kk region controlled class I product (probably H-2Kk) was observed. Finally, among lymphocytes, the CTL determinant is expressed preferentially (if not exclusively) on B cells, thus distinguishing it from all previously described Q region controlled determinants, which are expressed predominantly on T cells. We provisionally designate this novel Q region controlled CTL determinant Qc-1. The possibility that Qc-1 is recognized together with a self antigen is discussed.
Forssman glycolipid, an antigenic marker for a major subpopulation of macrophages from murine spleen and peripheral lymph nodes.
Authors: Bethke U , Kniep B , Mühlradt P F 
Published: December 2022

Abstract
Three hybridoma clones were isolated after hybridization of a mouse myeloma line with splenocytes from rats immunized with Forssman glycosphingolipid (Fo). Two of these clones produced Fo-specific monoclonal antibodies (MAB) of the IgM class, one MAB of the IgG2c class. In complement-dependent depletion experiments and immunofluorescence studies on the nature of Fo-positive leukocytes in CBA/J mice the following results were obtained: whereas blood monocytes, polymorphonuclear leukocytes, and lymphocytes were Fo negative, 5 to 10% of suspended spleen cells were positive. The majority of these were macrophage-like, glass- and nylon-adherent, nonspecific esterase-positive phagocytizing cells carrying Ia and globoside markers. These cells participated as accessory cells in the mixed lymphocyte culture reaction. In cell suspensions from axillary and inguinal lymph nodes, 2% were Fo positive. They were enriched up to 70% in the glass-adherent, esterase-positive population from this source. In contrast, no Fo-positive cells were detected in mesenteric lymph nodes, and less than 0.1% of the resident peritoneal macrophages bore this marker. The percentage of Fo-positive cells increased to 1% in thioglycollate-elicited peritoneal cells. Immunostaining of cryosections of lung and liver tissue showed alveolar macrophages and Kupffer cells, respectively, to be Fo negative.
Arachidonic acid acts as an intracellular activator of NADPH-oxidase in Fc gamma receptor-mediated superoxide generation in macrophages.
Authors: Sakata A , Ida E , Tominaga M , Onoue K 
Published: December 2022

Abstract
A protein kinase C inhibitor, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), inhibited phorbol ester (12-o-tetradecanoylphorbol 13-acetate)-induced and Fc gamma receptor-mediated superoxide anion (O2-) generations in guinea pig macrophages, but the inhibitory effect on Fc gamma receptor-mediated O2- generation was only partial. Both O2- generations were inhibited extensively by a phospholipase A2 inhibitor, 4-p-bromophenacyl bromide (4-pBPB). It was confirmed in control experiments that H-7 and 4-pBPB had no direct inhibitory effect on NADPH-oxidase activity. Dose-dependent stimulation of O2- generation was induced by arachidonate in macrophages, and the arachidonate-induced O2- generation was not inhibited by H-7. Arachidonate could also induce NADPH-oxidase activation in a post-nuclear fraction obtained from unstimulated macrophages and this activation was not inhibited by H-7, indicating that protein kinase C activation was not involved in this cellfree system. These results support the hypothesis that the O2- generation induced by Fc gamma receptor stimulation is mainly mediated by arachidonic acid which is released by the action of phospholipase A2 activated by receptor stimulation. Arachidonic acid seems to be acting rather directly in activating the NADPH-oxidase system of macrophage membrane. Protein kinase C may have a significant role in Fc gamma receptor-mediated O2- generation but it is not obligatory, and protein kinase C seems to activate NADPH-oxidase rather indirectly, probably by inducing the arachidonic acid release.
Desensitization of macrophage oxygen metabolism on immobilized ligands: different effect of immunoglobulin G and complement.
Authors: Valletta E A , Berton G 
Published: December 2022

Abstract
During adhesion and spreading to immobilized immune complexes, casein-elicited mouse peritoneal macrophages produced superoxide anion. This production was time-dependent, ceased after a couple of hours, and was due to interaction with immunoglobulins G (IgG) because neither immobilized antigen alone nor immunoglobulins M with or without complement-derived fragments were efficient stimuli. Cultivation of macrophages on immobilized IgG for 24 hr caused desensitization of the response to an unrelated stimulus like zymosan. Desensitization was due neither to inhibition of binding and uptake of zymosan nor to alterations of NADPH oxidase. In fact, macrophages cultivated on immobilized IgG bound and internalized zymosan and responded to PMA with production of superoxide anion normally. Desensitization was not specific for casein-elicited macrophages because both resident peritoneal and Corynebacterium parvum-activated macrophages underwent desensitization if cultivated for 24 hr on immobilized immune complexes. Desensitization on immobilized IgG was maximal after 24 hr, lasted up to 3 days in culture, and was reversed by detaching macrophages from the IgG surface and further cultivating them in normal tissue culture plastic. Scavengers of products of the oxygen metabolism such as superoxide dismutase and catalase and inhibitors of arachidonic acid metabolism such as indomethacin and nordihydroguaiaretic acid did not prevent desensitization. In addition, the zymosan-stimulated release of arachidonic acid was suppressed after cultivation on immobilized IgG for 24 hr; also in this case, the response to PMA was conserved. Contrary to cultivation on immobilized IgG, cultivation of macrophages on fragments derived from C3 was not accompanied by desensitization of the response to zymosan. These results indicate that although the interaction of Fc receptors with their ligands does not impair binding and uptake of zymosan, alterations in the sequence of signals which leads to the activation of the oxygen metabolism can occur, causing a complete dissociation between phagocytosis and stimulation of the oxygen metabolism.
Role of a guanine nucleotide regulatory protein in the activation of phospholipase C by different chemoattractants.
Authors: Verghese M W , Charles L , Jakoi L , Dillon S B , Snyderman R 
Published: December 2022

Abstract
It is well established that formyl peptide chemoattractants can activate a phospholipase C in leukocytes via a pertussis toxin (PT)-sensitive guanine nucleotide regulatory (G) protein. Whether this pathway is similarly used by chemoattractant receptors as a class has been unclear. We now report that lipid and peptide chemoattractants in direct comparative studies induced similar amounts of initial (less than or equal to 15 sec) inositol trisphosphate (IP3) release in human polymorphonuclear leukocytes, but the response to lipid chemoattractants was more transient. Production of IP3 by all chemotactic factors was inhibited by treatment of the cells with PT, indicating that chemotactic factor receptors as a class are coupled to phospholipase C via a G protein that is a substrate for ADP ribosylation by PT. The peptide and lipid factors had comparable chemotactic activity, which was also inhibitable by PT. However, transient activation of phospholipase C is apparently an insufficient signal for full cellular activation, since the lipid chemotactic factor leukotriene B4 and platelet-activating factor were poor stimuli for O2- production and lysosomal enzyme secretion compared with N-formyl-methionyl-leucyl-phenylalanine (fMet-Leu-Phe). Nonetheless, treatment with PT inhibited O2- production and enzyme secretion in response to all chemoattractants, but as previously noted, did not affect Ca2+ ionophores, lectins, or phorbol myristate acetate. Formyl peptide and lipid chemotactic factors induced similar levels of Ca2+ mobilization when monitored by Quin 2 or chlortetracycline (CTC) fluorescence. Although these responses to fMet-Leu-Phe were blocked by PT, the Quin 2 and initial CTC response to the lipid factors were only partially susceptible. Thus, the lipid factors apparently utilize an additional PT-resistant mechanism for redistributing intracellular Ca2+. This latter process requires extracellular Ca2+ and may be independent of the PT-sensitive G protein.
Induction of platelet cytotoxic functions by lymphokines: role of interferon-gamma.
Authors: Pancre V , Joseph M , Mazingue C , Wietzerbin J , Capron A , Auriault C 
Published: December 2022

Abstract
Antigen- or mitogen-stimulated CD4+/CD- lymphocytes produced factors able to induce normal human platelets into cytotoxic effectors toward the young larvae of Schistosoma mansoni. The neutralization by monoclonal anti-IFN-gamma antibody of the induction of the platelet killer effect, the presence of IFN-gamma in the CD4+/CD8- lymphocyte supernatant, and, finally, the direct inducer effect of recombinant IFN-gamma clearly demonstrated that IFN-gamma was one of the factors responsible for the induction of platelet cytotoxic functions.
Depletion of natural killer cells in mice by monoclonal antibody to NK-1.1. Reduction in host defense against malignancy without loss of cellular or humoral immunity.
Authors: Seaman W E , Sleisenger M , Eriksson E , Koo G C 
Published: December 2022

Abstract
Weekly injections of a monoclonal antibody (MAb) to the antigen NK-1.1 were used to sustain depletion of NK cells from the spleens of adult C57BL/6 mice for up to 8 wk. Mice depleted of NK cells in this manner had no lasting alteration in the distribution of other lymphocyte subsets in the spleen and did not demonstrate reduced cellular or humoral immunity. Depletion of NK cells, however, markedly increased the localization and growth of B16 melanoma cells or CT 38 colon carcinoma cells in the lung after i.v. administration of tumor cells. Moreover, mice given B16 tumors and treated with anti-NK-1.1 had reduced survival. NK cells were important in host resistance to sublines of B16 that had been passaged either in vivo or in vitro, which express, respectively, high and low levels of class I major histocompatibility antigens. These findings support a role for NK cells in host defense against malignancy. The ability to selectively remove NK cells in vivo by MAb will permit a better understanding of their physiologic role.
Phenotype and localization of thymocytes expressing the homing receptor-associated antigen MEL-14: arguments for the view that most mature thymocytes are located in the medulla.
Authors: Shortman K , Wilson A , Van Ewijk W , Scollay R 
Published: December 2022

Abstract
The monoclonal antibody MEL-14 recognizes a lymphocyte surface structure (the MEL-14 antigen) involved in migration of lymphocytes into lymph nodes. Its use as a maturation marker for T cells within the thymus led to the view that a small population (1 to 2%) of MEL-14high thymocytes located in the inner cortex represented fully mature cells about to exit as thymus emigrants. The medulla, in this view, contained only the phenotypically mature but MEL-14low cells, and was not the source of thymus emigrants. The data we present, derived from flow-cytometric analysis of suspension-stained CBA mouse thymocytes, is not in accordance with this view. A high proportion (approximately 20%) of thymocytes express relatively high levels of MEL-14; these include some immature Ly-2- L3T4- and nonmature Ly-2+ L3T4+ thymocytes. Among the 12 to 14% thymocytes of mature phenotype (PNAlow or H-2Khigh or Ly-2+ L3T4- and Ly-2- L3T4+), more than half express relatively high levels of MEL-14. The mature phenotype and MEL-14moderate-to-high cells (8% of thymocytes) appear too numerous to account for the few percent MEL-14high cells seen in the cortex in frozen sections, and the mature phenotype but MEL-14low cells (2 to 3% of thymocytes) too few to fill the medulla; however, both together account numerically for the medullary population. By section staining, the medulla contains Ly-2- L3T4+ and Ly-2+ L3T4- cells in a characteristic 2:1 ratio; by suspension staining this ratio agrees with that of the total mature phenotype population, but not with that of the MEL-14low subset previously claimed to represent medullary cells. Another paradox is apparent when suspension staining and section staining are compared: suspension staining reveals that many mature phenotype cells coexpress high levels of both MEL-14 and H-2K, yet section staining reveals H-2Khigh cells in the medulla but not in the inner cortex, and reveals scattered MEL-14high cells throughout the cortex but not in the medulla. We suggest that section staining for MEL-14 fails to locate the mature cells that stain for MEL-14 in suspension; the few MEL-14high cells localized in both the inner and the outer cortex on section staining are predominantly immature Ly-2- L3T4- and nonmature Ly-2+ L3T4+ thymocytes; the majority of thymocytes of mature phenotype, whether MEL-14high or MEL-14low on suspension staining, are of medullary location; the medulla is the most likely immediate source of thymic emigrants.
The effects of phorbol ester on alloantigen presentation.
Authors: Minami M , Ebner S A , Stadecker M J , Dorf M E 
Published: December 2022

Abstract
B cells and Ia+ thyroid cells fail to stimulate alloreactive T cells in a primary mixed leukocyte reaction (MLR) and fail to activate some allo-class II (I-A) reactive T cell hybridomas. We now demonstrate that B cells can specifically stimulate a primary MLR in combination with the phorbol ester, PMA, but not with interleukin 1 (IL 1) or calcium ionophore. The primary MLR induced with B cells plus PMA can be blocked by either monoclonal anti-I-A or anti-L3T4 antibodies. In contrast, thyroid cells that can be induced to express Ia antigens after incubation with interferon-gamma fail to stimulate a primary MLR even in the presence of PMA or IL 1. We confirmed these observations by using the alloreactive T cell hybridoma, HTB-9.3, which does not react to stimulator B cells. In the presence of PMA, however, this I-Ab-specific hybridoma line was able to respond to relevant but not to control stimulator B cells. Furthermore, the response of HTB-9.3 to B cells plus PMA was also blocked by anti-I-A or anti-L3T4 antibody. In contrast to B cells, Ia+ thyroid cells could not activate HTB-9.3 even in the presence of PMA or IL 1. The data indicate that for primary class II restricted allo-responses, B cells provide signals that can be complemented with the phorbol ester PMA, whereas Ia+ thyroid cells do not, suggesting the existence of additional requirements for T cell activation.
Analysis of immune complexes in rheumatoid arthritis for Epstein-Barr virus antigens reveals cross-reactivity of viral capsid antigen and human IgG.
Authors: Inman R D , Chiu B , Hamilton N C 
Published: December 2022

Abstract
We recently defined the immunochemical characteristics of immune complexes (IC) isolated from synovial fluid (SF) of patients with rheumatoid arthritis with the use of Western blot analysis. In the present study, we probe for exogenous antigens in the IC by examining the specificity of antisera raised against the IC. Anti-IC antisera demonstrated strong reactivity against the viral capsid antigen (VCA) of Epstein Barr virus (EBV), which was not explained by preimmune reactivity, polyclonal B cell activation, or Fc-mediated binding in the immunofluorescence or ELISA systems used to measure antibody titers. However, comparable anti-VCA reactivity was detected in antisera raised against non-rheumatoid SF. This phenomenon was not due to antigen since monoclonal anti-VCA antibody probing the IC by Western blot detected only IgG, nor to idiotype/anti-idiotype interaction since normal IgG absorbed out the anti-VCA reactivity. A monoclonal anti-VCA antibody competitively inhibited the binding of anti-IgG to IgG, and Fc fragment of IgG competitively inhibited the monoclonal antibody binding to VCA. No relationship between IgG anti-VCA antibody and IgG rheumatoid factor could be demonstrated. These data demonstrate an unexpected cross-reactivity of Fc fragment of IgG and VCA of EBV through the analysis of SF IC.
Idiotypy of human anti-Candida albicans antibodies: recurrence, presence of a cross-reactive autoanti-idiotypic-like activity, and role in the induction of specific in vitro antibody response.
Authors: de Saint Basile G , Durandy A , Somme G , Griscelli C 
Published: December 2022

Abstract
Rabbit anti-idiotypic antibodies (L12) were raised against human anti-mannan of Candida albicans (CA) antibodies isolated from the serum of a normal donor. The absorbed anti-idiotypic antiserum bound to donor anti-CA mannan antibodies but not to control immunoglobulins. Binding was inhibited by CA mannan but not by other polysaccharide antigens. L12 was shown to cross-react with anti-CA mannan-isolated antibodies or with anti-CA antibody-containing sera from individuals unrelated to the donor. IgG fraction isolated from the donor serum was repeatedly absorbed on CA mannan Sepharose to remove anti-mannan antibodies. This IgG fraction (named autoanti-idiotypic fraction) blocked, in a dose-dependent fashion, the binding of rabbit anti-idiotype to donor anti-CA mannan antibodies. Moreover, this CP-depleted IgG fraction cross-reacted with public idiotypic determinants of unrelated anti-CA mannan antibodies. Finally, L12 induced sensitized lymphocytes to produce anti-CA mannan antibodies in vitro in the absence of antigen.