bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies on the induction and expression of T cell-mediated immunity. XV. Role of non-MHC papain-sensitive target structures and Lyt-2 antigens in allogeneic and xenogeneic lectin-dependent cellular cytotoxicity (LDCC).
Authors: Bonavida B , Katz J 
Published: December 2022

Abstract
The present study examines the role of nonclass I MHC target membrane structures involved in lysis by cytotoxic lymphocytes in the lectin-dependent cellular cytotoxicity (LDCC) system. Cytotoxic cells of rodents and humans have been shown to nonspecifically lyse target cells of different origins and species. The mechanism by which such cytotoxicity takes place is not known, although several hypotheses have been put forth. This study examines the role of class I MHC expression on target cells and Lyt-2 antigens on the cytotoxic cells in both allogeneic and xenogeneic LDCC systems. Human peripheral blood lymphocytes, and murine-allosensitized cytotoxic T lymphocytes (CTL) are used as effector cells, and class I MHC-negative Daudi and class I MHC-positive Raji human target cells are used. The studies reveal that in LDCC, human lymphocytes lyse HLA-negative Daudi targets to the same extent as HLA-positive Raji targets. This was shown by the 51Cr-release assay as well as the single cell assay. Furthermore, allosensitized murine CTL lyse Daudi and Raji in LDCC, demonstrating that lysis of class I negative targets is achieved by xenogeneic CTL. Target cells treated with papain were found to be resistant to lysis in LDCC. However, incubation of papain-treated targets for 1 to 2 hr resulted in recovery of cytotoxicity. In the single cell assay, the papain treatment of targets slightly reduces the frequency of binders but significantly reduces the frequency of killers, revealing that the papain-sensitive structures are essential during the lethal hit stage of lysis. Monoclonal anti-Lyt-2 antibody inhibits lysis of both Daudi and Raji targets by murine CTL. The lack of discrimination between mouse and human targets by murine CTL suggests that the Lyt-2 molecule may have a different role than merely interacting with the target cell. In the LDCC system, we propose that class I MHC molecules are not essential for lysis. Several papain-sensitive and -insensitive target cell structures may participate in the cytolytic mechanism, and we propose that both the lectin and Lyt-2 molecules are involved in the perturbation of cell membrane conformation essential for lysis.
Reduced ecto-5'-nucleotidase activity and enhanced OKT10 and HLA-DR expression on CD8 (T suppressor/cytotoxic) lymphocytes in the acquired immune deficiency syndrome: evidence of CD8 cell immaturity.
Authors: Salazar-Gonzalez J F , Moody D J , Giorgi J V , Martinez-Maza O , Mitsuyasu R T , Fahey J L 
Published: December 2022

Abstract
Markedly reduced ecto-5'-nucleotidase activity was found in peripheral blood lymphocytes from 27 out of 30 homosexual men with the acquired immune deficiency syndrome (AIDS) in association with Kaposi's sarcoma (AIDS-KS; 2.67 +/- 1.70 U/10(6) cells; n = 13), opportunistic infections (AIDS-OI; 9.29 +/- 7.32; n = 7), or the AIDS-related complex (ARC; 9.82 +/- 6.12; n = 10). These values were significantly different from healthy controls (22.70 +/- 4.58; p less than 0.001). In AIDS-KS patients, both T cells and non-T cells exhibited significantly reduced ecto-5'-NT activity (p less than 0.001). AIDS-KS CD8 cells contained 20% of the mean ecto-5'-NT activity (7.04 +/- 3.53) displayed by control CD8 cells (34.07 +/- 4.86; p less than 0.001). No significant difference in enzyme level was observed between control and AIDS-KS CD4 cells (11.93 +/- 4.98 vs 7.98 +/- 3.28, respectively). In AIDS patients, lymphocyte ecto-5'-NT activity was inversely related (r = -0.518; p less than 0.01) to the absolute number of OKT10+ cells, but no correlation was found with the number of HLA-DR+ cells (r =-0.224). Two-color analysis of lymphocytes from AIDS-KS patients revealed that 75 +/- 12% of circulating CD8 cells expressed the OKT10 antigen, whereas only 10 +/- 6% of control CD8 cells did. HLA-DR antigens, which are not normally found on circulating resting T cells, were expressed in AIDS-KS CD8 cells, although to a lesser extent than OKT10. These data demonstrate that most AIDS CD8 cells differ from control CD8 cells. Although it has been suggested that these cells are activated cytotoxic or suppressor cells, the data presented here support the hypothesis they are immature. Reduced T cell ecto-5'-NT activity and enhanced expression of OKT10 and HLA-DR antigens on circulating CD8 cells, in conjunction with lack of transferrin receptor-(OKT9) and IL 2 receptor-(Tac) bearing lymphocytes, sustain this latter hypothesis. The correlation of the numerical reduction of CD4 cells with the reduced levels of ecto-5'-NT (r = 0.606; p less than 0.01) suggests that the abnormal maturation of CD8 cells seen in AIDS might be a consequence of the CD4 deficiency characteristic of this syndrome.
Longitudinal assessment of immunologic abnormalities of mice with the autosomal recessive mutation, "wasted".
Authors: Goldowitz D , Shipman P M , Porter J F , Schmidt R R 
Published: December 2022

Abstract
Mice homozygous for the autosomal recessive mutation wasted (wst/wst) undergo a progressive wasting beginning at the third week of postnatal life, when body weight declines in the mutants. The wst/wst mice do not survive past 30 days of age. The present report describes histologic and functional abnormalities in a longitudinal analysis (17 to 29 days postpartum) of wst/wst mice. In addition to a marked age-dependent decline in wst/wst body weight as well as spleen and thymus wet weight to body weight ratios, we have observed a significant decline in spleen and thymus cell number in these organs, compared with phenotypically normal (+/+ or +/wst) littermates. Histologic analysis of the wst/wst thymus revealed marked cortical pyknosis at 23 days of age and significant cortical depletion by 26 days postpartum. The wst/wst spleen at 23 days of age and later was characterized by a marked reduction in the content of red pulp. Lymphoproliferative responsiveness to Con A was markedly altered in the wst/wst thymus and spleen, in an age-dependent fashion, compared with normal littermates. The wst/wst spleen LPS responsiveness was also markedly altered in an age-dependent fashion. Hypotheses are presented concerning the possible site(s) of gene action in the wst/wst mutant which may mediate the observed morphologic and functional abnormalities.
Interleukins 2 and 3 regulate the in vitro proliferation of two distinguishable populations of 20-alpha-hydroxysteroid dehydrogenase-positive cells.
Authors: Keller J R , Weinstein Y , Hursey M , Ihle J N 
Published: December 2022

Abstract
The ability of interleukin 2 (IL 2), interleukin 3 (IL 3), and granulocyte/macrophage colony-stimulating factor (GM-CSF) to induce the proliferation of cells from thymus, spleen, or bone marrow was examined and compared with their ability to induce expression of the enzyme 20-alpha-hydroxysteroid dehydrogenase (20 alpha SDH). In the thymus, the peanut agglutinin agglutinated cells (PNA+) lacked 20 alpha SDH and showed no detectable response to IL 2, IL 3, or GM-CSF in either proliferation or induction of 20 alpha SDH. In contrast, the PNA nonagglutinated (PNA-) subpopulation expressed 20 alpha SDH and proliferated in response to Con A and/or IL 2. The responding cells that could be expanded in vitro with IL 2 expressed high levels of 20 alpha SDH. Neither IL 3 nor GM-CSF in the presence or absence of Con A had a demonstrable effect on the PNA- population. In cultures of bone marrow cells, both IL 3 and GM-CSF induced proliferation, whereas IL 2 had no effect on proliferation in the presence or absence of Con A. Thy-1-depleted bone marrow cells, expanded in tissue culture with IL3, contained cells that co-expressed Thy-1 and 20 alpha SDH. In contrast, cells proliferating in vitro to GM-CSF did not expressed Thy-1 or 20 alpha SDH. In cultures of normal splenic lymphocytes, two populations of cells capable of expressing 20 alpha SDH were detected. One population could be expanded in vitro with IL 2 and Con A, whereas the second was responsive to IL 3. In spleens from athymic mice, only the latter cells were detected. These results demonstrate that IL 3 and IL 2 responsiveness distinguishes two populations of 20 alpha SDH cells. The relevance of these observations to the possible relationship of IL 3 and IL 2 in T cell differentiation is discussed.
Structural similarities in the kappa light chains of human rheumatoid factor paraproteins and serum immunoglobulins bearing a cross-reactive idiotype.
Authors: Fong S , Chen P P , Gilbertson T A , Fox R I , Vaughan J H , Carson D A 
Published: December 2022

Abstract
The monoclonal antibody (MoAb) 17.109 recognizes a cross-reactive idiotype (CRI) associated with the light chains of Waldenstrom's macroglobulins with rheumatoid factor (RF) activity. The MoAb also reacts with a proportion of IgM-RF molecules from the sera of rheumatoid arthritis and primary Sjogren's syndrome patients, and from the sera of seropositive normal human subjects. In the present experiments, we used affinity chromatography to purify the 17.109 CRI-positive immunoglobulin from serum and have analyzed the isolated material by Western blotting. The purified 17.109 CRI-positive material from the sera of rheumatoid arthritis patients, Sjogren's syndrome patients, and normal subjects contained exclusively kappa light chains, and had demonstrated RF activity. In every case the 17.109 CRI-positive isolates reacted with antibodies against synthetic peptides corresponding to both the conserved second and third complementarity-determining regions (CDR) of the monoclonal kappa IgM-RF paraprotein Sie. The binding was inhibited specifically by the free peptides in solution. The antipeptide antibodies did not react appreciably with unfractionated human immunoglobulin. The data establish that the 17.109 CRI-positive immunoglobulin from diverse human sera have similar or identical second and third light chain CDR. These results suggest i) that the MoAb 17.109 identifies the protein product of a single or a very few V kappa genes, ii) that the ability to make kappa light chains with the 17.109-associated variable region is widespread in the human population, and iii) that the 17.109-defined kappa variable region segment is associated with IgM-RF autoantibodies.
A third immunoglobulin class in amphibians.
Authors: Hsu E , Flajnik M F , Du Pasquier L 
Published: December 2022

Abstract
A new class of immunoglobulin (IgX) has been found in the South African frog, Xenopus laevis, and other related species. IgX can be immunoprecipitated by monoclonal antibodies directed against determinants found on Xenopus light chain, or on variable regions of heavy chains. Reagents specific for the heavy chain of IgM or the amphibian IgG equivalent, IgY, failed to react with IgX. IgX, which exists in serum as a polymer, is composed of subunits of disulfide-bonded heavy chains of 80,000 daltons and light chains of 25,000 to 29,000 daltons. Like mu, the heavy chain of IgX carries a large amount of asparagine-linked carbohydrate, but the partial peptide maps of the two are different. Although the concentration of IgX varies greatly in the serum of individual frogs, it is always secreted in cultures of cells from the spleen and intestinal mucosae.
A histamine-releasing factor from activated human mononuclear cells.
Authors: Kaplan A P , Haak-Frendscho M , Fauci A , Dinarello C , Halbert E 
Published: December 2022

Abstract
Human mononuclear cells activated by streptokinase-streptodornase have been shown to elaborate a factor capable of releasing histamine from human basophils. We have developed reproducible methods for its production in large quantities by using cells obtained from leukapheresis packs, by detection utilizing donor basophils known to release well with anti IgE, and by quantitation of histamine by the radioenzyme method. Human histamine-releasing factor (HRF) gave a single peak upon gel filtration with an estimated m.w. of 32,000; SDS gel electrophoresis revealed a single major band as seen at m.w. 30,000. HRF can be resolved into at least two forms separable by ion-exchange chromatography on QAE Sephadex, and two peaks of activity were obtained by chromatofocusing or isoelectric focusing in gels at pH 6.9 and between 7.4 and 8.3. This factor represents an important potential link between cellular immunity and immediate hypersensitivity.
Activation of human polymorphonuclear neutrophil functions by interferon-gamma and tumor necrosis factors.
Authors: Shalaby M R , Aggarwal B B , Rinderknecht E , Svedersky L P , Finkle B S , Palladino M A 
Published: December 2022

Abstract
Recombinant human interferon-gamma (rHuIFN-gamma) and natural human tumor necrosis factor beta (nHuTNF-beta) (previously called lymphotoxin), purified to homogeneity, were used to assess their effects on certain functions of human polymorphonuclear neutrophils (PMN) in vitro. The treatment of PMN with 100 U of either rHuIFN-gamma or nHuTNF-beta for 20 min significantly increased their ability to phagocytize 1.5-microns latex beads as detected by flow cytometry. Preparations of recombinant human TNF-beta (rHuTNF-beta) showed activities similar to those of its natural counterpart in activating phagocytosis. In addition, a significant enhancement in PMN-mediated antibody-dependent cellular cytotoxicity was observed after treatment for 2 hr with IFN gamma and both TNF-alpha and TNF-beta. The enhancement by treatment with a combination of rHuIFN-gamma and nHuTNF-beta exceeded the enhancement caused by either agent alone. We also show that although lipopolysaccharide (LPS) is a potent stimulator of PMN function, polymyxin B can block LPS-induced but not lymphokine-induced activation. These data demonstrate new activities for both TNF-alpha and TNF-beta in augmenting the phagocytic and cytotoxic activities of PMN.
The mechanism of tumor growth inhibition by tumor-specific Lyt-1+2-T cells. I. Antitumor effect of Lyt-1+2-T cells depends on the existence of adherent cells.
Authors: Fujiwara H , Takai Y , Sakamoto K , Hamaoka T 
Published: December 2022

Abstract
In the present study we establish an assay system of tumor growth inhibition with the use of a diffusion chamber and investigate the mechanism by which tumor-specific Lyt-1+2-T cells exhibit their inhibiting effect on tumor cell growth. When a diffusion chamber containing X5563 plasmacytoma cells together with normal syngeneic C3H/HeN spleen cells was implanted in the peritoneal cavity of C3H/HeN mice, these tumor cells continued to proliferate at least 7 to 9 days. In contrast, spleen cells from C3H/HeN mice that had acquired X5563-specific immunity by intradermal (i.d.) inoculation of viable tumor cells, followed by surgical resection of the tumor, exhibited an appreciable inhibitory effect on the growth of X5563 tumor cells admixed in the chamber. This antitumor effect was mediated by Lyt-1+2-T cells and was tumor-specific, because the growth of X5563 or another syngeneic MH134 hepatoma cells was inhibited by spleen cells from C3H/HeN mice immunized to the respective tumor cell types. Most important, these tumor-specific Lyt-1+2-T cells lost their antitumor activity by depleting an adherent cell population contained in spleen cells, indicating that adherent cells are required for the Lyt-1+2-T cell-mediated antitumor effect. This was substantiated by the fact that immune spleen cells depleted of adherent cells could regain their tumor-inhibiting effect when normal spleen cells were added back as an adherent cell source, or more directly by adding back a splenic or peritoneal resident adherent cell population. These results indicate that tumor-specific Lyt-1+2-T cells mediate the tumor growth inhibition and that their antitumor effect depends on the coexistence of an adherent cell population.
Activation requirements of cloned inducer T cells. I. Differential inhibition by anti-L3T4 or anti-I-A is determined by the accessory cell population.
Authors: DeKruyff R , Clayberger C , Cantor H , Dorf M E 
Published: December 2022

Abstract
We have described a trinitrophenyl (TNP)-specific inducer clone, clone Ly-1-T1, which responds to a variety of different stimuli, including a) soluble TNP-protein conjugates plus syngeneic (H-2d) spleen cells, b) TNP directly coupled to syngeneic or allogeneic spleen cells, and c) activated I-A identical B cells in the absence of nominal antigen. In the present study we used a panel of antibodies to investigate the recognition structures involved in the activation of clone Ly-1-T1 by these different stimuli. We show that allogeneic spleen cells must be conjugated by using relatively high concentrations of TNBS to be efficient stimulators of the clone. In contrast, syngeneic spleen cells conjugated by using a much wider range of concentrations will activate the clone. The response of the clone to TNP-coupled allogeneic spleen cells is inhibited by anti-L3T4 and anti-Ia antibodies. In contrast, stimulation of the clone with syngeneic spleen cells coupled by using the same concentrations of TNBS is not inhibited with either anti-Ia or anti-L3T4 antibody. The inhibition pattern observed with anti-Ia and anti-L3T4 antibodies was also determined by the nature of the accessory population used to present soluble TNP-protein conjugates. Anti-I-Ad antibodies blocked the activation of clone Ly-1-T1 by TNP-protein plus splenic adherent cells, indicating the involvement of polymorphic I-A determinants in this response. Anti-L3T4 antibody had little or no effect on this response, suggesting that a significant L3T4-Ia interaction is not required. Finally, the response of the clone to activated B cells in the presence or absence of TNP-protein is exquisitely sensitive to inhibition by anti-L3T4 as well as anti-I-A antibodies. The data suggest that the requirement for an L3T4-I interaction depends on the combination of antigen and accessory cell type used to stimulate the clone.
Human monocyte adherence to cultured vascular endothelium: monoclonal antibody-defined mechanisms.
Authors: Wallis W J , Beatty P G , Ochs H D , Harlan J M 
Published: December 2022

Abstract
We have evaluated the binding of human peripheral blood monocytes to cultured vascular endothelium as an in vitro model of monocyte interaction with the vessel wall. Monocytes were purified (91% +/- 4 SE esterase positive) by elutriation to avoid contact with surfaces before assay. Adherence of 51Cr-labeled monocytes after 45 min (36% +/- 11 SE) was significantly higher than that observed with autologous radiolabeled neutrophils (9% +/- 5 SE) and was greater on monolayers of human umbilical vein endothelium than on bovine aortic endothelium. Peripheral blood mononuclear cells treated with monoclonal antibody (MoAb) 60.3, a reagent that binds leukocyte membrane complex CDw18, implicated in multiple adherence-dependent functions, failed to adhere and flatten on artificial surfaces. Mononuclear cells treated with MoAb 60.3 simulated cells from a patient with recurrent infections whose phagocytes failed to react with MoAb 60.3 and failed to emigrate to extravascular sites in vivo. Incubation of monocytes with MoAb 60.3 inhibited (by 32 to 61%) monocyte adherence to endothelium in a dose-dependent manner for periods up to 24 hr, but had negligible effects on basal (unstimulated) neutrophil adherence. Basal monocyte adherence in the presence of MoAb 60.3 remained significantly greater than basal neutrophil adherence. Augmentation of phagocyte adherence to endothelial monolayers by autologous plasma or phorbol ester (PMA) was abrogated by incubation with MoAb 60.3. Studies with immunofluorescence flow cytometry indicated that PMA stimulation of monocytes resulted in a specific 40% increase in monocyte surface expression of the epitope recognized by MoAb 60.3. These in vitro findings, in conjunction with observations from two patients, support the hypothesis that monocyte adherence to endothelium and emigration to tissues is mediated by mechanisms both dependent upon and independent of the CDw18 complex and the epitope recognized by MoAb 60.3.
The tumor promoter teleocidin induces IL 2 receptor expression and IL 2-independent proliferation of human peripheral blood T cells.
Authors: Isakov N , Bleackley R C , Shaw J , Altman A 
Published: December 2022

Abstract
In testing the recently discovered tumor promoter teleocidin (TCD), we found that like phorbol esters, TCD was mitogenic to human peripheral blood lymphocytes (PBL) and preferentially stimulated sheep erythrocyte-rosetted (ER) T cell-enriched populations. Stimulation of PBL with TCD induced synthesis and expression of receptors for interleukin 2 (IL 2), as shown by dot-blot analysis with the use of a synthetic oligonucleotide probe, cell surface staining with anti-Tac antibody followed by fluorescence-activated cell sorter analysis, and a functional proliferation assay in which TCD-stimulated cells were washed free of TCD and were recultured with human recombinant IL 2 (rIL 2). Increased expression of cell surface markers after TCD stimulation of PBL is not general, because TCD did not affect the expression of Leu-2a antigen, and it also reduced the density of Leu-3a and Leu-4 antigens. Stimulation of cultured, IL 2 receptor-positive PBL with rIL 2, but not TCD, was blocked by anti-rIL 2 antibodies. Furthermore, IL 2-specific mRNA was not detected in TCD-stimulated PBL, demonstrating that IL 2 was not required for TCD-induced T cell proliferation. In addition, TCD replaced IL 2 in inducing short-term proliferation of IL 2-dependent murine cytotoxic T cell lines. The findings that TCD induced IL 2-independent proliferation of T cells, and TCD and IL 2 synergized in inducing T cell proliferation, suggest that they initiate T cell proliferation via different mechanisms. The IL 2-independent activation of T cells, and the induction of IL 2 receptor expression by TCD, may be related to its ability to activate protein kinase C in cell membrane.