bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibodies that distinguish non-small cell from small cell lung cancer.
Authors: Mulshine J L , Cuttitta F , Bibro M , Fedorko J , Fargion S , Little C , Carney D N , Gazdar A F , Minna J D 
Published: December 2022

Abstract
Two murine IgG2Ak monoclonal antibodies (703D4, 704A 1) were produced and characterized after immunization with a human large cell lung cancer line (NCI-H 157). These antibodies detect different epitopes on 31 kilodalton [35S]methionine incorporating protein(s). Radiobinding and immunohistochemical studies show these antibodies bind to most (11/13) human non-small cell lung cancer (adenocarcinoma, epidermoid, and large cell), but not to small cell lung cancer (0/11) tumors tested. The epitopes these antibodies recognized are also expressed on human melanomas (7/8), two other tumors (osteogenic sarcoma, renal cell carcinoma), but not on many other human tumors (breast, colon, neuroblastoma, lymphoid), and not on a panel of normal adult human tissues. Because the antigen(s) are preserved after fixation and because of their ability to distinguish lung cancer types from each other and normal tissues, they should be of clinical, as well as of biologic interest.
Depression of natural killer cytotoxicity after in vivo administration of recombinant leukocyte interferon.
Authors: Maluish A E , Ortaldo J R , Conlon J C , Sherwin S A , Leavitt R , Strong D M , Weirnik P , Oldham R K , Herberman R B 
Published: December 2022

Abstract
One hundred thirty-four patients with a variety of malignancies were treated in two phase I clinical trials of recombinant leukocyte A interferon (IFL-rA) produced by recombinant DNA methodology. IFL-rA was given by intra-muscular injection either twice daily or three times weekly for 28 days. Extensive monitoring of natural killer (NK) cell cytotoxicity was done on these patients with rigorously standardized assays and determination of the inherent variability of NK function for each individual. Interferon, as used in these two treatment regimens, failed to produce an appreciable increase in NK activity; in the majority of patients, there was no significant change in NK activity from the pretreatment baseline levels. An unexpected finding was the depression of NK activity in 30% of the patients. The data have been analyzed in terms of their possible relationship to dose and schedules of IFL-rA administration and to antitumor response.
In vivo role of natural killer cells: involvement of large granular lymphocytes in the clearance of tumor cells in anti-asialo GM1-treated rats.
Authors: Barlozzari T , Reynolds C W , Herberman R B 
Published: December 2022

Abstract
The present study was performed to further evaluate the possible in vivo involvement of natural killer (NK) cells in host resistance against tumors. Selective depression of NK activity in Wistar Furth rats was induced by i.p. or i.v. injection of rabbit anti-asialo GM1. This antiserum has previously been shown to produce a decrease in NK activity and a parallel increase in tumor growth in mice. In the present study, rats treated with this antibody showed a parallel decrease in NK activity and in the frequency of large granular lymphocytes (LGL) in the spleen and peripheral blood, indicating that the antiserum-induced depression of NK activity in these sites was probably caused by an elimination of most effector cells. To further determine the possible role of rat LGL in tumor rejection in vivo, we studied LGL involvement in the rapid clearance of radiolabeled tumor cells from the lungs, an assay previously shown to correlate well with in vitro NK activity. Animals treated with anti-asialo GM1 antiserum were found to have a substantial decrease in the in vivo rate of clearance of tumor cells from the lungs. Furthermore, the adoptive transfer of a highly enriched population of LGL into NK-depressed animals 2 hr before tumor challenge, partially restored their cytotoxic activity against established cell lines in vitro and their ability to eliminate radiolabeled cells from the lungs. These results provide direct support for the hypothesis that NK cells are involved in in vivo resistance to tumors, particularly in the elimination of potentially metastatic tumor cells from the circulation and capillary beds.
Two classes of bystander B cell response: activation requirements reflect those of B cells in general.
Authors: Ratcliffe M J , Julius M H 
Published: December 2022

Abstract
Bystander anti-sheep red blood cell (SRBC) antibody responses were induced in cultures containing unprimed B cells, SRBC, particulate or soluble eliciting antigen, and helper T (Th) cells primed to the eliciting antigen. The use of long-term cultured Th cells, depleted of alloreactive cells, allowed direct assessment of the requirements for major histocompatibility complex- (MHC) restricted interactions in the cellular events leading to bystander B cell activation. H-2 restricted Th cell activation limited all bystander B cell responses; however, the requirement for H-2 restricted Th-B cell interactions varied with the state of activation of the responding B cell population before assay. Thus, we defined two classes of bystander B cell response. Activation of small (i.e., resting) SRBC-specific bystander B cells, purified by density gradient centrifugation, was completely restricted by B cell MHC. The requirement for high concentrations of eliciting antigen suggests that nonspecific binding of soluble or particulate antigen to the responding B cell surface plays a mandatory role leading to the activation of resting bystander B cells. The concomitant requirement for a restricted Th-B cell interaction suggests that this role is one of focusing antigen-specific, H-2 restricted T cell help to the resting B cell. In contrast, bystander responses, unrestricted by B cell MHC, were generated exclusively from large (i.e., blasted) B cells limited only by Th cell activation. This class of SRBC-specific bystander response correlated with an SRBC-dependent increase in the number of cells secreting antibodies that recognized degraded mouse RBC. Thus, we propose that the H-2 unrestricted anti-SRBC response is derived from the amplification of B cells activated in vivo to degraded homologous RBC. Both classes of anti-SRBC response were enhanced by the presence of the bystander antigen. This phenomenom is discussed in terms of a mitotic advantage provided by the interaction of antigen with surface immunoglobulin on specific bystander B cells.
Three different signals are required for the induction of cytolytic T lymphocytes from resting precursors.
Authors: Kanagawa O 
Published: December 2022

Abstract
The requirement for the signals in induction of cytolytic T lymphocytes (CTL) has been investigated. C57BL/6 X CBA/T6 F1 spleen cells stimulated with the lectin leukoagglutinin (L-A) failed to show CTL activity in a PHA-facilitated assay, although L-A-activated splenic T cells were able to respond to T cell growth factor (TCGF). Concanavalin A (Con A) on the other hand was able to induce cytolytic activity from CTL-P, as well as to render splenic T cells responsive to TCGF. Furthermore, L-A-activated splenic T cells could generate cytolytic activity upon subsequent culture in secondary mixed leukocyte culture supernatant (2 degrees MLC SN). In contrast, EL-4-derived SN (EL-4 SN) was unable to induce cytolytic activity from L-A-activated spleen cells. In addition, proliferation of L-A-activated spleen cells cultured in EL-4 SN was similar to those cultured in 2 degrees MLC SN. Nonactivated spleen cells were totally unresponsive to both SN in proliferation and generation of CTL. Analysis of T cell clones for the production of a factor necessary for induction of cytolytic activity revealed that both cytolytic and noncytolytic T cell clones were able to produce a factor(s) for the generation of cytolytic activity from L-A-activated T cells. On the other hand, SN from certain antigen-stimulated T cell clones produced factors capable of inducing cytocytic activity by L-A-activated T cells only in the presence of EL-4 SN. Neither EL-4 SN nor cloned T cell SN alone had such a capacity. The nature of the necessary lymphokines in the SN from the clone cells or from the EL-4 is unknown. In the case of the EL-4 SN, it is not known whether the presence of TCGF plays a role or whether that role is perhaps more differentiative than proliferative. This study provides evidence that the induction of CTL from CTL-P can be dissociated into activation, which is required to render T cells responsive to second signals, and differentiation, which is mediated by two different factors.
The nature of the interaction between suppressor and helper T cells in the response to LDHB.
Authors: Baxevanis C N , Nagy Z A , Klein J 
Published: December 2022

Abstract
Purified Lyt-1+2+ T cells were depleted of alloreactive cells by BUdR and light treatment, and then were primed in vitro against LDHB presented on allogeneic APC. Such cells could be restimulated by LDHB on the same allogeneic APC, but not by LDHB on APC syngeneic with the T cells. The restimulated T cells suppressed the proliferative response of Lyt-1+2- T cells primed and restimulated by the same antigen. The suppression, which was antigen specific, occurred after a 6-hr co-culture of the suppressor (Tse) and proliferating helper (Th) cells. The successful interaction (as measured by suppression) between allogeneic Th and Tse cells was found to be determined by the restriction specificity but not the MHC haplotype of Th cells, and the MHC haplotype but not the restriction specificity of Tse cells. Thus, suppression occurred only when the Tse cells carried genes controlling the MHC molecules that served as restriction elements for antigen recognition by the Th cells. No evidence could be obtained for the participation of APC in the Tse-Th interaction. The data suggest the interaction is based on the recognition by the Th cell of the antigen presented in the context of MHC molecules controlled by the Tse cell.
Natural killer (NK) cell activity during lymphatic regeneration: early appearance of Thy-1+ NK cells and highly interleukin 2-(IL 2) receptive, Thy-1- cells.
Authors: Hurme M , Sihvola M 
Published: December 2022

Abstract
The appearance of natural killer (NK) cells, i.e., cells that can lyse tumor-derived target cells without intentional immunization, was studied during regeneration after a sublethal dose (300 mg/kg) of cyclophosphamide (Cy). It was found that NK activity started to increase in parallel with the number of cells in the spleen, reaching normal levels 8 to 9 days after Cy injection. The early appearing NK cells differed, however, from the NK cells of the normal spleen; all the activity was abolished by treatment with a monoclonal anti-Thy-1 antibody plus complement (C). The early regenerating population contained cells that could given rise in vitro, in the presence of interleukin 2 (IL 2), to higher amounts of NK-active cells than cells of a normal spleen. Pretreatment with anti-Thy-1 (plus C) did not inhibit the formation of these in vitro NK-active cells, indicating that they were not derived from these Thy-1+ NK cells. The NK cells formed in vitro expressed both the asialo GM1 and the Thy-1 antigens. These data suggest that i) the expression of the Thy-1 antigen on NK cells is connected to their stage of maturation or to the rate of proliferation, and ii) the precursors for the in vitro activated NK cells are not NK-active cells themselves.
Binding of cyclosporine by human lymphocytes and phospholipid vesicles.
Authors: LeGrue S J , Friedman A W , Kahan B D 
Published: December 2022

Abstract
The purpose of this investigation was to identify and characterize a possible plasma membrane receptor for cyclosporine (CsA) on human lymphoid cells. Binding of 3H-CsA by normal human lymphocytes and purified lymphoid subpopulations was examined using ligand concentrations ranging from 5 X 10(-7) to 10(-10) M. Specificity was determined using a 500-fold excess of unlabeled drug. No differences were observed in the uptake of 3H-CsA by B cells or T cells using Cartesian or semilogarithmic analyses. Scatchard analysis of the specific binding of CsA by normal peripheral blood lymphocytes yielded two dissociation constants: a high affinity site with a KD of 2 to 6 X 10(-9) M and a low affinity site with a KD of about 10(-7) M CsA. Scatchard analysis of specific CsA uptake by purified splenic T cells and B cells showed both populations to exhibit a low affinity site (KD = 3 to 6 X 10(-7) M and 5 to 8 X 10(-7) M, respectively), whereas only B cells bore a high affinity site (KD = 2 X 10(-9) M). Analysis of specific CsA uptake by cultured human kidney cells and phospholipid vesicles (1:1 molar ratio of phosphatidylcholine:cholesterol) showed both these targets to display a single, low affinity binding site (KD = 1 X 10(-7) M and 2 X 10(-8) M, respectively). The relevance of the low affinity site to CsA-mediated in vitro immunosuppression was suggested by the need for 10(-7) M CsA to achieve 50% suppression of lymphoproliferation during mixed lymphocyte culture. Taken together, these data argue against the existence of a specific CsA receptor on the surface of human T cells. Although a role for the high affinity B cell receptor in some types of CsA-induced immunomodulation cannot be excluded, the present study suggests that immunosuppression is achieved by the partitioning of the hydrophobic CsA molecule into the membrane lipid bilayer, thereby perturbing homeostatic control of membrane function.
The instructor cell for the human procoagulant monocyte response to bacterial lipopolysaccharide is a Leu-3a+ T cell by fluorescence-activated cell sorting.
Authors: Helin H J , Fox R I , Edgington T S 
Published: December 2022

Abstract
A variety of responses of cells of the lymphoid system are associated with acquisition of the capacity to initiate the coagulation protease pathways. The initiating or procoagulant molecules are produced by the monocyte; however, a number of studies have indicated that lymphocyte collaboration is required. The induction of human monocyte procoagulant activity (PCA) by the model stimulus bacterial lipopolysaccharide (LPS) was examined in the present study by using relatively highly purified monocyte and lymphocyte populations in reconstitution experiments. Consistent with prior studies, the PCA response could not be generated by highly purified monocytes alone after exposure to LPS. The ability to generate PCA was restored to these monocyte populations by the addition of fibronectin-gelatin nonadherent lymphocytes, nylon wool effluent T cells, or Leu-3a+ inducer/helper T cells selected by fluorescence-activated cell sorting. T cells added to monocytes at a ratio of 8:1 or higher, and Leu-3a+ cells added at a ratio of 6:1 or higher, provided a maximal collaboration for monocyte PCA induction by LPS. These results substantiate further previous suggestions of an absolute requirement for collaborating T cells and demonstrate that these instructor cells carry a marker for the inducer/helper subset.
Analysis of the defects responsible for the impaired regulation of EBV-induced B cell proliferation by rheumatoid arthritis lymphocytes. II. Role of monocytes and the increased sensitivity of rheumatoid arthritis lymphocytes to prostaglandin E.
Authors: Hasler F , Bluestein H G , Zvaifler N J , Epstein L B 
Published: December 2022

Abstract
Diminished regulation of EBV-induced B cell proliferation by T cells from patients with rheumatoid arthritis (RA) is paralleled by diminished production of gamma-interferon in response to autologous but not allogeneic stimulation. We have shown that the adherent cell subpopulation within the autologous RA stimulators plays a major role in the RA defect. In analyzing the mechanisms responsible for the adherent cell effect in RA, we examined the contribution of prostaglandin production. Indomethacin treatment (1 microgram/ml) of the RA auto-MLR led to increased production of supernatant inhibitory activity (8% +/- 4 without, 57% +/- 4 with indomethacin), but had no significant effect on the inhibition of EBV-induced B cell proliferation by normal auto-MLR supernatants. Adding excess autologous adherent cells to the normal auto-MLR, however, led to an indomethacin-reversible decline in the production of the inhibitory factor without suppressing the auto-MLR proliferative response. The adherent cell effect could be reproduced by adding PGE1 or PGE2 (10(-8) to 10(-6) M) to the normal auto-MLR. PGE2 levels in 72-hr auto-MLR supernatants were similar in RA (4.2 +/- 1 ng) and normal control (3.6 +/- 0.5 ng/ml) supernatants. Because we could not detect differences in PGE production, we assessed the sensitivity of adherent cell-depleted normal and RA auto-MLR to exogenous PGE. Concentrations of 10(-7) to 10(-6) M PGE were needed to block production of the inhibitory factor by to normal cells, whereas only 10(-13) to 10(-12) M PGE1 completely blocked it in RA cell cultures. Thus, the defective production of gamma-interferon in the RA auto-MLR is, at least in part, due to enhanced sensitivity of the RA lymphocytes to adherent cell-produced prostaglandins.
Chemotactic properties of partially purified human epidermal cell-derived thymocyte-activating factor (ETAF) for polymorphonuclear and mononuclear cells.
Authors: Luger T A , Charon J A , Colot M , Micksche M , Oppenheim J J 
Published: December 2022

Abstract
Human epidermal cell thymocyte-activating factor (ETAF) derived from either normal epidermal cells or a squamous cell carcinoma cell line has recently been shown to be a low m.w. protein that is indistinguishable from human macrophage-derived interleukin 1 (IL 1). As with human IL 1, human ETAF elutes from Sephadex S-200 gel in two major peaks at m.w. 70,000 to 40,000 and m.w. 25,000 to 12,000. Rechromatography of the higher m.w. fraction of ETAF yielded some of the lower m.w. activity, and chromatofocusing of high m.w. ETAF yielded the same three isoelectric points as the lower m.w. ETAF. Partially purified human ETAF as well as IL 1 were chemotactic for polymorphonuclear and mononuclear leukocytes. In addition, exposure of PMN to ETAF stimulated increased metabolic activity as demonstrated by greater reduction of intracellular nitroblue tetrazolium. Therefore, this study lends further support for an important role of ETAF in the pathogenesis of inflammatory skin diseases.
The thymic differentiation markers T6 and M241 are two unusual MHC class I antigens.
Authors: van de Rijn M , Lerch P G , Knowles R W , Terhorst C 
Published: December 2022

Abstract
The human beta 2-microglobulin (beta-2m)-associated human thymocyte differentiation antigens T6 and M241 were compared using biochemical techniques. T6 and M241 antigens reside on different molecules with apparent m.w. of 49,000 and 43,000, respectively. Here we show that both proteins have a protein backbone m.w. of 33,000. In addition, T6 and M241 have a large portion of their peptides in common. When we compared the protein backbone m.w. of T6 and M241 with the murine beta-2m-associated thymus leukemia (TL) antigens, we found a considerable difference in size, suggesting that T6 and M241 may not be human homologues of TL antigens and constitute a novel type of major histocompatibility (MHC) class I antigens.
Diverse specificities of five monoclonal antibodies reactive with glycophorin A of human erythrocytes.
Authors: Ochiai Y , Furthmayr H , Marcus D M 
Published: December 2022

Abstract
Glycophorin A (GPA), the major sialoglycoprotein of human red cells, bears blood group MN determinants, and is a useful marker of the erythroid lineage in differentiating cells. Five monoclonal antibodies that react with GPA and possess a spectrum of serologic properties and fine specificities were obtained by immunization of mice with umbilical cord erythrocytes. Three antibodies, B22A, D22 and E11B, did not agglutinate En(a-) erythrocytes, genetic variants that lack GPA, and F11 and J11A agglutinated these cells very weakly. Antibodies B22A, E11B, and F11 agglutinated protease-treated cells more strongly than untreated erythrocytes, and they appeared to react with a peptide determinant located on the C-terminal side of the site at which trypsin cleaves GPA in the intact erythrocyte. In contrast to B22A and E11B, the hemagglutinating activity of F11 was not inhibited by purified GPA, nor did it bind to GPA in a solid phase immunoassay, but it immunoprecipitated GPA. Antibodies D22 and J11A appeared to be directed against carbohydrate determinants, or conformational determinants created by hydrogen bonding or electrostatic interactions between carbohydrate and protein. A preferential reaction of antibody J11A with MM over NN GPA was demonstrated by its reactions with enzyme-treated erythrocytes, its inhibition by purified GPA or its tryptic fragments, and by an ELISA assay.
The relationship between immune interferon production and proliferation in antigen-specific, MHC-restricted T cell lines and clones.
Authors: Hecht T T , Longo D L , Matis L A 
Published: December 2022

Abstract
The release of immune or gamma interferon (IFN-gamma) by major histocompatibility complex (MHC)-restricted pigeon cytochrome c-specific Lyt 1+2-, interleukin 2 (IL 2)-producing proliferative T cell clones when cultured with antigen and antigen-presenting cells (APC) is a sensitive measure of the state of activation of the cell. In general, the fine specificity of T cell activation was similar when activation was measured either by IFN-gamma production or by proliferation. In response to antigen and the correct Ia molecule, the T cell clones produced both high titered IFN-gamma and a strong proliferative response. However, IFN-gamma production and the degree of proliferation of the T cell clones differed at high antigen concentrations. As antigen concentration increased, the magnitude of proliferation became submaximal whereas the IFN-gamma response became maximal suggesting that IFN-gamma produced by the cells might act as an autoregulatory molecule inhibiting the proliferative response. Stimulating the T cell to divide via its IL 2 receptor by adding exogenous IL 2 produced high levels of proliferation but only low titers of IFN-gamma activity. In addition, irradiation of the clone eliminated the IFN-gamma release induced by IL 2 but did not affect the IFN-gamma release induced by antigen and Ia. Thus proliferation is not essential for IFN-gamma production and unlike antigen and Ia, IL 2 functions predominantly as a proliferative signal and not as a signal for factor release. Two T cell clones showed a dissociation of IFN-gamma production and proliferation. In one case, a clone that proliferated in response to both allogeneic and antigenic stimuli released IFN-gamma in response to antigen but failed to produce IFN-gamma in response to the allogeneic stimulus. A second clone that showed a strong proliferative response to pigeon cytochrome c but no proliferative response to a species variant of cytochrome c, tobacco hornworm moth (THWM) cytochrome c, produced IFN-gamma when stimulated with either of these antigens. Thus, the sensitivity of detecting activation of T cell clones as measured by the release of an individual lymphokine varies from one clone to another.