bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal anti-Id antibodies react with varying proportions of human B lineage cells.
Authors: Kiyotaki M , Cooper M D , Bertoli L F , Kearney J F , Kubagawa H 
Published: December 2022

Abstract
Monoclonal antibodies to idiotypic determinants are being used with increasing frequency for analysis and treatment of B cell malignancies. In the present study we have compared the idiotypic specificities of a panel of 39 mouse monoclonal anti-idiotype (anti-Id) antibodies developed against 16 monoclonal human immunoglobulins (Ig). The Id cross-reactivities of these antibodies with Ig products of normal and abnormal B cells were examined by immunofluorescence and immunochemical methods. The reactivity patterns of these anti-Id antibodies with a normal population of plasma cells were highly variable in the immunofluorescence assay. Six were reactive with 2 to 10% of normal plasma cells, 30 with 0.1 to 2% of plasma cells, and three with less than 0.1% of plasma cells from blood, bone marrow, spleen, or tonsils. These reactivity patterns were relatively consistent among samples from 23 Caucasian, black, and Oriental adults. Although the reactivities of most anti-Id antibodies in the panel were not restricted to a particular Ig isotype, several were preferentially reactive with a particular heavy or light chain isotype: one IgM-, two IgA-, two kappa-, and three lambda-restricted antibodies. The immunofluorescence data was confirmed by biosynthetic analysis of Id+ molecules produced by a normal plasma cell population. When the reactivity of this panel of anti-Id antibodies with nonhomologous B cell neoplasms was examined, seven of 30 myelomas or leukemia-derived products and one of nine B cell leukemias or lymphomas without paraproteins were found to be cross-reactive with one or two of the anti-Id antibodies. Although clearly significant, the cross-reactivity between the Id of these paraproteins appeared to be of lower affinity than the reactivity of the homologous Id with their respective anti-Id antibodies. The results reveal a remarkable diversity in the specificities of monoclonal antibodies classified by conventional criteria as anti-Id antibodies, and indicate the potential usefulness of a panel of antibodies for analyzing clonal diversity in normal and abnormal B cell development.
Tumor necrosis factor-alpha enhances cytolytic activity of human natural killer cells.
Authors: Ostensen M E , Thiele D L , Lipsky P E 
Published: December 2022

Abstract
The effect of recombinant tumor necrosis factor-alpha (rTNF alpha) on human natural killer (NK) function was examined. Lysis of both the NK-sensitive K562 erythroleukemia line and the relatively insensitive renal carcinoma line Cur by nonadherent peripheral blood lymphocytes was significantly enhanced as a result of an 18-hr preincubation with either rTNF alpha or recombinant interleukin 2 (rIL 2). When cells were preincubated with rTNF alpha and low doses of rIL 2 (1 to 10 U/ml), marked additional augmentation of lysis of both targets was noted which was greater than that caused by either cytokine alone. Similar results were observed when responses of CD16+ large granular lymphocytes selected with the fluorescence-activated cell sorter after staining with the NK-specific monoclonal antibody Leu-11 were examined, indicating that the action of the cytokines was directly on the cytotoxic cells. Augmentation of tumor cell lysis could not be ascribed to a cytolytic activity of rTNF alpha on the targets, because no combination of rIL 2, rTNF alpha, or interferon-gamma caused lysis of K562 or Cur. By flow cytometric analysis, it was found that expression of IL 2 receptors was induced on purified CD16+ large granular lymphocytes by rTNF alpha alone and to an even greater degree by the combination of rTNF alpha and rIL 2. Additional analysis of the expression of surface antigens and blocking studies with monoclonal antibodies showed that enhanced tumor cell lysis was not caused by the augmentation of leukocyte function-associated antigen-1-mediated effector/target interactions. These data indicate that rTNF alpha alone, or in combination with rIL 2, directly augments NK cytotoxic activity.
Autocrine growth of T cells independent of interleukin 2: identification of interleukin 4 (IL 4, BSF-1) as an autocrine growth factor for a cloned antigen-specific helper T cell.
Authors: Kupper T , Horowitz M , Lee F , Robb R , Flood P M 
Published: December 2022

Abstract
Interleukin 4 (IL 4), formerly known as B cell stimulatory factor 1 (BSF-1), has recently been described as a growth factor for T cells. The role of IL 4 in the putatively IL 2-independent growth of certain cloned T helper cells is unclear. D10.G4.1 (D10) is a conalbumin-specific helper T cell that has been employed extensively in the analysis of T cell activation and as an assay for the detection of IL 1. Previously, it was thought that IL 1 induced the expression of IL 2 receptors on D10 cells, thereby permitting D10 to proliferate in response to endogenously produced IL 2. However, we cannot detect IL 2 mRNA or protein in D10 cells or their supernatants as determined by the following criteria: monoclonal antibodies that neutralize the in vitro activity of murine IL 2 do not block the IL 1-dependent proliferation of D10 cells; no competitive binding for high-affinity IL 2 receptors with 125I-labeled IL 2 can be detected with medium conditioned by activated D10 cells; and Northern blot analysis and S1 nuclease protection assays, performed with cDNA probes for IL 2, do not detect mRNA for IL 2 under a variety of different activation conditions that foster autocrine growth of D10 cells. In contrast, activated D10 cells produce both IL 4 mRNA and protein as judged by similar criteria. Purified IL 4 has significant TCGF activity as measured by proliferation of HT-2 cells. This activity can be blocked completely by a monoclonal antibody to IL 4 (11B11). The proliferation of D10 cells in the presence of 3D3 (a clonotype-specific monoclonal anti-T cell receptor antibody) and IL 1 can be blocked completely by 11B11 antibody. Highly purified IL 4 alone cannot induce the proliferation of resting D10 cells; however, equivalent amounts of IL 4 in the presence of recombinant IL 1 induce significant D10 proliferation. Therefore, IL 1 appears to render D10 cells responsive to their autocrine growth signal. These data indicate that IL 4 serves as the autocrine T cell growth factor for D10 cells, and that exogenous IL 1 is required for the transduction of this growth signal. This may represent a more broadly applicable mechanism for the growth of certain subsets of T helper cells.
Granulocyte-macrophage colony stimulating factor produced by cloned L3T4a+, class II-restricted T cells induces HT-2 cells to proliferate.
Authors: Woods A , West J , Rasmussen R , Bottomly K 
Published: December 2022

Abstract
Cloned L3T4a+ antigen-specific, class II-restricted T cells can be subdivided by function and by cytokine production. All cloned T cell lines produce T cell growth factors that can be distinguished by the ability of monoclonal antibodies to inhibit the proliferation of cytokine-dependent T cell lines induced by these T cell growth factors. From these types of analyses, it has been shown that all cloned T cells that help hapten-specific B cells secrete immunoglobulin, produce interleukin 4 (IL 4). Those cloned T cells that fail to help for anti-hapten responses produce neither IL 4 nor interleukin 2 (IL 2), yet release an activity that induces the proliferation of the cytokine-dependent T cell line, HT-2. Additional analysis of the HT-2 stimulating activity has shown that it is indistinguishable from granulocyte macrophage-colony stimulating factor (GM-CSF)--this activity being produced by all cloned T cells tested. Thus GM-CSF is a product of all cloned L3T4a+ T cell lines tested thus far, and can serve as a T cell growth factor for HT-2, as well as a co-factor for in vivo derived T cells.
Deficiency of the tryptase-positive, chymase-negative mast cell type in gastrointestinal mucosa of patients with defective T lymphocyte function.
Authors: Irani A M , Craig S S , DeBlois G , Elson C O , Schechter N M , Schwartz L B 
Published: December 2022

Abstract
The distribution and concentration of human T (tryptase-positive, chymase-negative) and TC (tryptase-positive, chymase-positive) mast cells were examined in Carnoy's-fixed specimens of the gastrointestinal tract of normal individuals, patients with inflammatory bowel diseases, and patients with immunodeficiency disorders. In normal specimens, T mast cells predominated in the mucosa (89%), with a mean concentration of 17,850 +/- 4,998 per mm3 (+/- SD, n = 16), whereas TC mast cells predominated in the submucosa (90%) with a mean concentration of 7,516 +/- 1,227 per mm3 (+/- SD, n = 16). The concentrations of T and TC mast cells in specimens of ileum from five patients with active Crohn's disease and of colon from three patients with active ulcerative colitis were not significantly different (p greater than 0.4) from normal values. Three patients with combined immunodeficiency disorders demonstrated a marked decrease in the concentration of the T mast cells in the intestinal mucosa, to 540 +/- 630, and a corresponding decrease in the percentage of T mast cells to 9%. Concentrations of TC mast cells were unchanged, both in the mucosa and in the submucosa. In three patients with acquired immunodeficiency syndrome, a similar deficiency of the T mast cell type was observed in the ileal mucosa, with a mean concentration of 788 +/- 534 T mast cells per mm3, but not in the appendiceal and colonic mucosa of one of the three patients. These findings indicate a role for functional T lymphocytes in the development of the T mast cell type in humans, and suggest divergent pathways for development of T and TC mast cells.
An IgG monoclonal antibody to group B meningococci cross-reacts with developmentally regulated polysialic acid units of glycoproteins in neural and extraneural tissues.
Authors: Finne J , Bitter-Suermann D , Goridis C , Finne U 
Published: December 2022

Abstract
The structurally similar polysialic acid capsules of group B meningococci and Escherichia coli K1 are poor immunogens, and attempts are currently being made to improve their immunogenicity by chemical modifications. An IgG monoclonal antibody to these polysialic acid capsules was used for the study of the presence of structurally similar components in tissue glycoproteins to investigate the reasons for the poor immunogenicity and to evaluate potential dangers in active or passive immunization. By immunoblotting polysialic acid was detected outside the brain in newborn rat kidney, heart, and muscle. It appeared in immunoblots as one component and with similar mobility to the neural cell adhesion molecule N-CAM. Specificity studies of the antibody and endosialidase treatment showed that the polysialic acid glycans detected were composed of chains as long as eight sialic acid residues or more. The polysialic acid was not detected in the corresponding tissues of the adult animal. These results indicate that polysialic acid units are developmentally regulated components of both neural and extraneural tissues, and are bound to components with properties similar to a known cell-adhesion molecule. This together with the presence of low amounts of polysialic acid even in the adult brain, suggests potential hazards in vaccination trials and suggested immunotherapy of meningitis caused by group B meningococci or E. coli K1, which should be carefully assessed.
Salmonella-typhimurium-specific difference in rate of intracellular killing by resident peritoneal macrophages from salmonella-resistant CBA and salmonella-susceptible C57BL/10 mice.
Authors: van Dissel J T , Stikkelbroeck J J , Michel B C , Leijh P C , van Furth R 
Published: December 2022

Abstract
The aim of the present study was to determine whether the difference between the rate of intracellular killing of Salmonella typhimurium by macrophages of salmonella-resistant CBA and salmonella-susceptible C57BL/10 mice also holds for other salmonellae and other bacteria species. After in vivo phagocytosis, the initial rate of in vitro intracellular killing of S. typhimurium phagetype 505, S. typhimurium phagetype 510, and S. typhimurium M206 by macrophages of CBA mice amounted always to approximately 1.7 times the value found for macrophages of C57BL/10 mice (p less than 0.001), indicating that the difference in killing efficiency between CBA and C57BL/10 macrophages holds for various strains of S. typhimurium. However, some other salmonella species, i.e., S. dublin and S. heidelberg, as well as E. coli 054 and 02K1+, Listeria monocytogenes EGD and L347, and Staphylococcus aureus were killed equally efficiently by macrophages of both mouse strains. These findings indicate that the difference between the rates of intracellular killing by macrophages of salmonella-resistant CBA and salmonella-susceptible C57BL/10 does not hold for several other bacteria species and thus might be specific for S. typhimurium. Subsequent experiments showed that the in vivo proliferation of S. typhimurium 510 in the first 2 days after i.v. injection was 2.0-fold to 3.0-fold higher in the spleens and livers of C57BL/10 mice than in those of CBA mice, whereas the in vivo proliferation of S. dublin and S. heidelberg was between 1.0-fold to 1.4-fold higher in the C57BL/10 mice. These findings suggest that the differences between the rate of in vitro intracellular killing of salmonella by CBA and C57BL/10 macrophages are reflected in differences in the rate of in vivo proliferation of these microorganisms in CBA and C57BL/10 mice. To gain insight into the involvement of the oxidative metabolism of CBA and C57BL/10 macrophages in the difference in the rate of intracellular killing of S. typhimurium, the O2 consumption and H2O2 release by resident peritoneal macrophages was determined. The amplitudes of the respiratory burst and the release of H2O2 was identical in macrophages of the two mouse strains after triggering by either preopsonized heat-killed S. typhimurium or phorbol myristic acetate. These findings indicate that the mouse species-associated difference in the intracellular killing of S. typhimurium is not caused by a difference in the oxidative metabolism of CBA and C57BL/10 macrophages.
Different VL and VH germ-line genes are used to produce similar combining sites with specificity for alpha(1----6)dextrans.
Authors: Akolkar P N , Sikder S K , Bhattacharya S B , Liao J , Gruezo F , Morrison S L , Kabat E A 
Published: December 2022

Abstract
Monoclonal antibodies to alpha(1----6)dextrans produced in mice immunized with the T-independent antigens alpha(1----6)dextran or the stearylisomaltosyl oligosaccharides have been characterized immunochemically. To correlate the immunochemical properties of these monoclonal antibodies with their primary structure, we have sequenced the variable (V) regions of the light (L) and heavy (H) chains. Three V kappa germ-line genes belonging to two major gene families were used; differential J usages also contribute to diversity. Five different VH germ-line genes belonging to three major VH families were used. The VH genes were further modified by junctional diversity and differential J usage and possibly by somatic mutations. The effects of these modifications on the fine specificities of anti-alpha(1----6)dextrans are discussed. Thus far, six different combinations of VLJL-VH(D)JH chains that form groove-type combining sites specific for alpha(1----6)dextran have been found. We conclude that entirely different VL and VH can form combining sites specific for the internal linear sequence of alpha(1----6)dextran.
Differential expression of the human Thy-1 gene in rodent-human somatic cell hybrids [corrected].
Authors: Rettig W J , Nishimura H , Yenamandra A K , Seki T , Obata F , Beresford H R , Old L J , Silver J 
Published: December 2022

Abstract
Thy-1 is a cell surface differentiation marker which shows distinct patterns of tissue-specific expression in different species. In man, the Thy-1 antigen is encoded by chromosome 11. We have examined the regulatory signals determining human Thy-1 expression through serologic analysis of rodent-human somatic cell hybrids retaining human chromosome 11 in which the fusion partners belong to distinct differentiation lineages. Cell surface expression of human Thy-1 was determined by mixed hemadsorption assays with two monoclonal antibodies (mAb), K117 and L127, shown to detect authentic human Thy-1 through analysis of COS-7 monkey kidney cells transfected with a cloned human Thy-1 gene. Three different patterns of human Thy-1 expression were observed when hybrid cells, constructed with different human and rodent cell types, were tested with mAb K117 and L127. Hybrids formed between Thy-1+ human neuroblastoma cells and Thy-1- mouse neuroblastoma cells, or hybrids between Thy-1+ human fibroblasts and the Thy-1- mouse kidney carcinoma, RAG, retain human Thy-1 expression. In contrast, hybrids formed between either Thy-1+ human neuroblastoma cells or Thy-1+ human fibroblasts and Thy-1- mouse L cells lose expression of human Thy-1 even though chromosome 11 is retained. Finally, hybrids formed between Thy-1- human peripheral lymphocytes or a Thy-1- lymphoblastoid B cell line and Thy-1- Chinese hamster fibroblasts begin to express human Thy-1. These studies suggest that both positive and negative trans-acting signals may play a role in the tissue-specific regulation of the human Thy-1 gene.
Monoclonal antibodies against murine IFN-gamma abrogate in vivo tumor immunity against RSV-induced murine sarcomas.
Authors: Prat M , Bretti S , Amedeo M , Landolfo S , Comoglio P M 
Published: December 2022

Abstract
Previous work has shown that immunization of syngeneic mice with v-src-induced sarcomas gives rise to specific protection against a lethal dose of v-src-transformed fibroblasts. This immune response is mediated by Lyt-1+, Lyt-2,3+ T lymphocytes, with no apparent involvement of cytotoxic T cells, as shown in Winn-type assays. Immune cells mediating tumor rejection in this system have now been further characterized, and it was found that L3T4+ T lymphocytes alone provided full protection against v-src-induced sarcomas. Moreover, the role of interferon-gamma (IFN-gamma) in the tumor rejection was analyzed. A monoclonal antibody directed against this lymphokine was able to reverse the protective effect displayed by immune T lymphocytes, by eliciting highly effective T suppressor cells. It was thus concluded that T cells with L3T4 surface marker are the main thing responsible for the adoptive immunity in this tumor system, and the activity of these cells is positively modulated by lymphokines such as IFN-gamma.
Suppression of anti-mouse immunoglobulin antibodies in subhuman primates receiving murine monoclonal antibodies against T cell antigens.
Authors: Lowder J N , Miller R A , Hoppe R , Levy R 
Published: December 2022

Abstract
Murine monoclonal antibodies stimulate the production of human anti-mouse immunoglobulin antibodies (AMIA) when administered to patients. This limits their long-term usefulness as therapeutic and diagnostic agents. We report the use of three maneuvers to suppress AMIA against T cell-specific monoclonal antibodies in cynomolgus monkeys. Twelve monkeys received daily i.v. infusions of 1 mg each of anti-Leu-2a, -3a, and -5 on days 1 through 10. One group (control) received no suppressive regimen. The second group received cyclosporine, 12.5 mg/kg daily on days -7 to +14. The third group (PI) were passively immunized with 0.4 ml of hyperimmune monkey AMIA serum on days -7, -1, 2, 4, 6, and 8. The fourth group (TLI) received 1700 rad fractionated total lymphoid irradiation ending on day -1. The animals treated with TLI were markedly delayed in the onset of AMIA, which was suppressed to less than 1% of the control group. The AMIA specific for the constant region of animals receiving PI was also suppressed to one-third of control. The majority of the AMIA in all the animals was anti-idiotypic and wholly anti-idiotypic in the TLI animals.
Gender differences in eicosanoid production from macrophages of arthritis-susceptible mice.
Authors: Leslie C A , Gonnerman W A , Cathcart E S 
Published: December 2022

Abstract
Collagen-induced arthritis (CIA) in rodents is an experimental animal model that shares many clinical and pathologic findings with rheumatoid arthritis in man. Our previous findings suggested that the amelioration of CIA in mice by a fish oil diet was associated with macrophage accumulation and metabolism of eicosapentaenoic acid and a subsequently altered prostaglandin (PG) profile. In these experiments, we examined the role of gender and found that macrophages from female arthritis-susceptible B10.RIII or B10.G mice synthesized more PG and thromboxane than macrophages isolated from the males. Compared with males, female mice had higher circulating anti-type II collagen antibodies but were less likely to develop CIA. Females, especially those on a fish oil diet, developed a much less severe disease than the males. This supports our hypothesis that the type and/or amount of eicosanoid produced from the macrophage may alter the course of experimentally induced arthritis.
Expression of leukocyte adherence-related glycoproteins during differentiation of HL-60 promyelocytic leukemia cells.
Authors: Hickstein D D , Smith A , Fisher W , Beatty P G , Schwartz B R , Harlan J M , Root R K , Locksley R M 
Published: December 2022

Abstract
We used the HL-60 human promyelocytic leukemia cell line to analyze the surface expression of a family of adherence-related leukocyte surface antigens during myeloid differentiation. These antigens are composed of discrete alpha subunits, designated alpha L, alpha M, and alpha X, that are each noncovalently associated with a common beta subunit. Monoclonal antibodies directed against the individual subunits served as markers in both indirect immunofluorescence studies and immunoprecipitations from HL-60 cells differentiated preferentially towards mature granulocytes (DMSO, retinoic acid) or monocyte/macrophages (PMA, vitamin D3). In undifferentiated HL-60 cells, the alpha L and alpha X subunits were constitutively expressed, whereas the alpha M subunit was not. Differentiation of HL-60 cells along the granulocytic pathway with DMSO resulted in a marked increase in alpha M and minimal increases in alpha L and alpha X. The phenotypic expression of these antigens on DMSO-treated HL-60 cells closely resembled that on normal circulating PMN. Differentiation along the monocyte/macrophage pathway when using PMA or vitamin D3 resulted in major increases in alpha L and alpha X expression, as well as alpha M. These changes resulted in a surface phenotype characteristic of that present on human monocyte-derived macrophages. Triggering of undifferentiated HL-60 cells with PMA caused no increase in subunit expression, whereas stimulation of DMSO-differentiated HL-60 cells with PMA produced more than a 1.5-fold enhancement of both the alpha M and alpha X subunits, and stimulation of human PMN with PMA increased the surface expression of alpha M more than fourfold and alpha X subunit twofold. Stimulation with PMA produced no change in expression of the alpha L subunit in any of the three cell populations. These results indicate that the alpha subunits of this glycoprotein family can be selectively regulated during in vitro differentiation of a human promyelocytic leukemia cell line. Second, DMSO-differentiated HL-60 cells and human PMN possessed an intracellular pool of alpha M and alpha X, but not alpha L, that could be translocated to the surface. Thus, despite structural and functional relationships among the alpha subunits in this glycoprotein family, they undergo disparate surface expression and intracellular regulation during differentiation.