bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunohistochemical distribution of the antigenic determinants detected by monoclonal antibodies to carcinoembryonic antigen.
Authors: Yachi A , Imai K , Fujita H , Moriya Y , Tanda M , Endo T , Tsujisaki M , Kawaharada M 
Published: December 2022

Abstract
By using four distinct monoclonal antibodies to CEA, the molecular profile of which was clarified in our accompanying companion paper, immunohistochemical distribution of the antigenic determinants on both cancerous and noncancerous tissues as well as fetal tissues was studied with the use of the immunoperoxidase method. All of the monoclonal antibodies recognize different antigenic determinants on the tissue section. None of the antibodies stained granulocytes in the peripheral blood or in the normal liver tissues tested. Three of our monoclonal antibodies stained columnar epithelial cells in morphologically normal colonic mucosa; however, monoclonal antibody YK024 did not stain them. This antibody was also found to be unreactive with intestinal metaplasia lesions of the stomach, but reacted with a 16-wk-old fetal stomach as well as with cancerous parts of the colon and of the stomach. Moreover, it was found that this monoclonal antibody mainly reacted with moderately or poorly differentiated adenocarcinoma lesions of the colon and the stomach. Periodic acid treatment in this study, together with trypsin treatment on the antigen as described in our accompanying companion paper, may suggest that this antibody recognizes the carbohydrate antigenic determinant in nature.
Streptococcal Fc receptors. II. Comparison of the reactivity of a receptor from a group C streptococcus with staphylococcal protein A.
Authors: Reis K J , Ayoub E M , Boyle M D 
Published: December 2022

Abstract
The reactivity of a soluble Fc receptor from a group C streptococcus ( FcRc ) was compared antigenically and functionally with the staphylococcal Fc receptor, protein A. Protein A and FcRc were found to inhibit each others' binding to the Fc region of human IgG, indicating that they bind to sites that are in close proximity on the Fc region of human IgG. The two bacterial Fc receptors were antigenically unrelated. Differences were observed in the species and subclass reactivity of the two receptors. The patterns of binding of protein A and FcRc under various conditions suggested that these receptors reacted with distinct regions on the Fc region of immunoglobulins. FcRc bound more efficiently to goat, sheep, and cow IgG, protein A bound more efficiently to dog IgG, and neither receptor bound to rat IgG. Differences were also observed in the reactivity towards human IgG subclasses. The FcRc bound to all samples of the four human IgG subclass standards. Protein A bound to IgG1, IgG2, and IgG4, and to one of two IgG3 myeloma proteins tested. The reactivity of our soluble FcRc corresponds to a type III streptococcal Fc receptor classified by the reactivity of intact bacteria.
Treatment of experimental visceral leishmaniasis with lymphokine encapsulated in liposomes.
Authors: Reed S G , Barral-Netto M , Inverso J A 
Published: December 2022

Abstract
Highly susceptible mice were infected with Leishmania donovani chagasi and were treated with supernatants, free or encapsulated in liposomes, from concanavalin A-stimulated or unstimulated mouse spleen cell cultures. Treatment consisted of multiple i.v. injections beginning 2 days before to 2 days after infection. Mice treated with lymphokine-rich supernatants encapsulated in liposomes had significantly fewer liver parasites than the control groups, demonstrating in vivo activity of lymphokine against an infectious organism.
Intracellular destruction of Leishmania donovani and Leishmania tropica amastigotes by activated macrophages: dissociation of these microbicidal effector activities in vitro.
Authors: Hockmeyer W T , Walters D , Gore R W , Williams J S , Fortier A H , Nacy C A 
Published: December 2022

Abstract
Resident peritoneal macrophages were exposed to amastigotes of Leishmania donovani and L. tropica and treated with soluble products of antigen or mitogen-stimulated lymphocytes (lymphokines, LK). Macrophages infected with L. donovani were responsive to lower concentrations of LK for elimination of this parasite than cells infected with L. tropica, and the disappearance of L. donovani amastigotes from activated macrophages preceded that of L. tropica by at least 24 hr. That the differential elimination of amastigotes from LK-treated macrophages may reflect different intracellular killing mechanisms for the two parasites is supported by studies with macrophages activated in vivo; macrophages from BCG-treated C3H/HeJ mice that were incapable of eliminating intracellular L. tropica killed amastigotes of L. donovani. Whether the effector mechanism(s) for intracellular destruction of the two Leishmania are qualitatively or only quantitatively different is as yet unknown.
Fibroblast stimulation in schistosomiasis. V. Egg granuloma macrophages spontaneously secrete a fibroblast-stimulating factor.
Authors: Wyler D J , Stadecker M J , Dinarello C A , O'Dea J F 
Published: December 2022

Abstract
Isolated intact egg granulomas from the liver of Schistosoma mansoni-infected mice have been previously shown to elaborate factors in vitro that can stimulate fibroblasts for biological functions that are of potential importance in the pathogenesis of hepatic fibrosis in schistosomiasis. We report here that cell cultures obtained from monodispersed granuloma cell suspensions, and specifically enriched for macrophages (95% to 100%) spontaneously elaborated fibroblast proliferation-stimulating activity in vitro. These cells possessed functional and phenotyptic characteristics of activated macrophages. In contrast, control peritoneal macrophages from uninfected mice lacked such phenotypic characteristics, and did not spontaneously elaborate fibrogenic activity in vitro. The granuloma macrophage activity was present, pre-formed within the isolated cells, and was continuously elaborated during 72 hr of incubation. By gel infiltration chromatography (Sephacryl S-200 sf), fibroblast-stimulating activity was identified in two pooled fractions, one with estimated molecular radius (Mr) of 46 kd to 57 kd and the other with Mr of 10 kd to 16 kd. Preparative isoelectric focusing in granular gel of crude macrophage culture supernatants identified peak activity in fractions with pI approximately 5. Two different serine esterase inhibitors had no effect on the ability of crude granuloma macrophage supernatants to stimulate fibroblast proliferation. Whereas crude and chromatographed fractions of granuloma macrophage supernatant were active for fibroblasts, they had minimal or no interleukin 1 (IL 1) activity when tested in a thymocyte proliferation assay. In contrast, resident peritoneal macrophages from the same infected mice spontaneously secreted substantial IL 1 and fibroblast-stimulating activity in vitro. We conclude that egg granuloma macrophages are activated in vivo to secrete fibrogenic molecules functionally distinct from IL 1, which might contribute to the pathogenesis of hepatic fibrosis in schistosomiasis.
Antiviral activity of a thymic factor in experimental viral infections. I. Thymic hormonal effect on survival, interferon production and NK cell activity in Mengo virus-infected mice.
Authors: Klein A S , Fixler R , Shoham J 
Published: December 2022

Abstract
A partially purified thymic factor, thymostimulin (TS), significantly increased the survival rate of adult, immune-intact mice infected with the neurotropic Mengo virus. TS treatment was begun after virus inoculation by daily i.p. injections. In untreated C57BL/6 mice, LD50 was reached with 1 X 10(4) PFU, but 10-fold more virus (i.e., 1 X 10(5) PFU) was needed to reach LD50 in TS-treated animals. TS effect on survival, though, could be observed with several virus doses (1 X 10(3) to 1 X 10(6) PFU) (p less than 0.001). A significant effect on survival was also observed with outbred ICR mice (p less than 0.005). Serum interferon (IFN) levels in the Mengo virus-infected mice were relatively low (average peak 300 U/ml), but were significantly increased (two- to ninefold) in the TS-treated mice. Peak serum levels were reached earlier in TS than in control animals (24 hr and 72 hr, respectively). Both acid-labile and acid-stable type I IFN production were augmented by TS in the Mengo virus-infected mice. Natural killer activity was also enhanced by TS, in particular on the second day after virus inoculation. In addition, MP-virus was used as a second, unrelated virus challenge. This virus caused a nonlethal infection, with relatively high levels of serum IFN (average peak 10,000 U/ml). TS increased IFN levels (two- to eight-fold) also in this challenge system. In conclusion, TS causes a nonspecific enhancement of endogenous production of IFN and has a significant effect on the survival of lethally infected mice. The data indicate a potential application of thymic factors for the treatment of viral infections.
Requirement for protein synthesis for induction of macrophage tumoricidal activity by IFN-alpha and IFN-beta but not by IFN-gamma.
Authors: Blasi E , Herberman R B , Varesio L 
Published: December 2022

Abstract
Peritoneal mouse macrophages elicited by proteose-peptone (pM phi) were treated in vitro with IFN-alpha, IFN-beta, or IFN-gamma in the presence or absence of cycloheximide (Cy), a reversible inhibitor of protein synthesis, and were assayed for cytolytic activity against tumor cells. Inhibition of protein synthesis during treatment of pM phi with IFN-alpha or IFN-beta prevented the development of cytotoxic activity. In contrast, IFN-gamma was fully capable of inducing cytotoxic pM phi in the presence of Cy. Moreover, pM phi treated with mixtures of IFN in the presence of Cy were activated for cytotoxicity only by IFN-gamma together with IFN-alpha or IFN-beta, but not by IFN-alpha plus IFN-beta. These results indicate that the activation of pM phi by IFN-gamma is independent of new protein synthesis, whereas the activation of pM phi by IFN-alpha and/or IFN-beta requires active protein synthesis, suggesting that the mechanism of induction of cytotoxic pM phi by IFN-gamma differs from that by the other types of IFN.
Estrogen immunosuppression is regulated through estrogenic responses in the thymus.
Authors: Luster M I , Hayes H T , Korach K , Tucker A N , Dean J H , Greenlee W F , Boorman G A 
Published: December 2022

Abstract
Previous studies have clearly established that physiologic and pharmacologic levels of estrogens modulate immunologic responses that result in simultaneous activation of the reticuloendothelial system and depression of cell-mediated immunity. The mechanisms of estrogen immunoregulation were examined in adult female mice administered pharmacologic levels of exogenous estrogens. Evaluation of steroidal and nonsteroidal compounds with varying degrees of estrogenicity (i.e., uterotrophic activity) provided evidence that their immunotoxicity, for the most part, correlates with estrogenicity. The mechanisms responsible for these effects appear to be complex, mediated through a direct chemical interaction with lymphoid target cells, as well as with nonlymphoid tissue, resulting in the release of soluble immunoregulatory factors. The latter phenomenon was examined in detail and it appears to constitute a regulatory factor(s) produced by thymic epithelium in response to an estrogen stimulus. This response is not only estrogen specific but may involve specific binding to estrogen receptors or receptor-like structures present in cytosol preparations from thymic epithelial cells.
Molecular mechanisms of lymphocyte extravasation. II. Studies of in vitro lymphocyte adherence to high endothelial venules.
Authors: Braaten B A , Spangrude G J , Daynes R A 
Published: December 2022

Abstract
Lymphocyte migration from the blood into the lymph nodes in most species occurs across post-capillary high endothelial venules (HEV). In a previous study, we proposed that lymphocyte extravasation involves receptor-mediated binding followed by adenylate cyclase-dependent activation of lymphocyte motility. This hypothesis was, in part, based on observations of in vitro lymphocyte adherence to HEV by employing pertussigen, which is a known inhibitor of lymphocyte recirculation. In vitro lymphocyte-HEV binding requires a cold (6 degrees C) incubation step and binding is poor to nil if the assay is attempted at room (23 degrees C) or physiologic temperature. We decided to investigate why this assay is temperature restricted, because of the possibility that pertussigen or fucoidin -treated lymphocytes might interact with HEV differently at higher temperatures. We now report that O.C.T. compound (OCT), the embedding matrix generally used to cut frozen lymph node sections, is toxic to lymphocytes at temperatures above 6 degrees C. Exclusion of OCT from the assay system will allow lymphocyte-HEV binding to occur at 23 degrees C and to a lesser extent at 37 degrees C. With this modified protocol, lymphocytes treated with either pertussigen, fucoidin , or neuraminidase were tested for adherence to HEV at 23 degrees C. No essential difference in binding properties was observed from what had been reported at 6 degrees C. In contrast, trypsin-treated lymphocytes that did not bind to HEV with the standard technique at 6 degrees C did adhere to a minimal extent to HEV at 23 degrees C using the modified procedure. We also report some preliminary work, using the modified assay, on in vitro lymphocyte-HEV binding of rat, rabbit, and guinea pig lymphocytes to sections of lymph nodes from the respective species.
A human monoclonal IgG1 with anti-idiotypic activity against anti-human thyroglobulin autoantibody.
Authors: Zouali M , Fine J M , Eyquem A 
Published: December 2022

Abstract
Sixty-one human myeloma proteins (HMP) from patients with multiple myeloma and Waldenström macroglobulinemia were tested for anti-idiotypic (Id) activity against autoantibodies to double-stranded DNA, small nuclear ribonucleoproteins, and human thyroglobulin (HTg), by competitive radioimmunoassays and enzyme immunoassays. An IgG1, lambda HMP from patient BEN with anti-Id activity against antibodies to HTg is reported. IgG1 BEN was not directed toward human Fc fragments and its activity was not related to allotypic determinants. IgG1 BEN molecules recognized Id determinants (idiotopes) on F(ab')2 anti-HTg fragments, but not idiotopes of F(ab')2 fragments of antibodies of other specificities. This observation supports the general significance of Id network interactions in regulation and diversification of immune responses in man.
Nuclear DNA degradation in lymphocytes of patients with systemic lupus erythematosus.
Authors: Compton L J , Steinberg A D , Sano H 
Published: December 2022

Abstract
The degradation of nuclear DNA in lymphocytes of patients with systemic lupus erythematosus (SLE) was analyzed. A low m.w. DNA fragment was identified in phytohemagglutinin (PHA)-stimulated lymphocytes from both healthy controls and SLE patients. The rate of appearance of low m.w. DNA was at least fourfold higher in lymphocytes from SLE patients, suggesting that DNA from SLE cells are more easily degraded than that from normal cells. PHA-stimulated lymphocytes from SLE patients were also shown to be more sensitive to UV irradiation than those of controls. These results suggest that DNA metabolism is abnormal in T cells of SLE patients.
Characterization of sequential immune complexes in infective endocarditis by Western blot analysis.
Authors: Inman R D , Rosenberg R A , Redecha P B , Christian C L 
Published: December 2022

Abstract
A patient with cutaneous vasculitis during infective endocarditis due to Lactobacillus casei was studied. Immune complexes (IC) were isolated from serum at the time of diagnosis and after 4 wk of therapy. Purification of IC used differential polyethylene glycol precipitation and competitive binding to staphylococcal protein A. In situ radioiodination of IC was performed, followed by SDS-polyacrylamide gel electrophoresis (PAGE). Anti-IC antisera were raised in rabbits by immunization with purified IC. IC were characterized by SDS-PAGE followed by electrophoretic transfer to nitrocellulose, incubation with antiserum and then with 125I protein A, and autoradiography. Although early and late IC differed quantitatively, there were no differentiating immunochemical features. Both IC contained a 60,000 dalton component that did not react with preimmune serum nor with anti-normal human serum. This component reacted with antiserum rendered specific for L. casei by affinity chromatography. The restricted antigen-antibody representation in IC contrasted with a wider panel of antibody activity in patient serum. The Western blot analysis proves to be an ideal method for the characterization of IC because of its sensitivity, dissociative capability, and preservation of immunoreactivity. IC isolated at a time removed from the original antigenic challenge may provide insight into the nature of the inciting antigen.
Induction of various autoantibodies by mutant gene lpr in several strains of mice.
Authors: Izui S , Kelley V E , Masuda K , Yoshida H , Roths J B , Murphy E D 
Published: December 2022

Abstract
The effect of the autosomal mutant gene lpr (lymphoproliferation) on the development of various autoantibodies and immune complex (IC) glomerulonephritis was investigated in four genetically distinct strains of mice: MRL/ MpJ , C3H/HeJ, C57BL/6J, and AKR/J. The presence of the lpr gene not only enhanced the production of autoantibodies in the autoimmune MRL/ MpJ strain, but also induced the formation of various kinds of autoantibodies in the three other strains of mice without any apparent predisposition to autoimmune disease. Autoantibodies induced by the lpr gene included anti-double-stranded DNA, anti-single-stranded DNA, anti-IgG, anti-thymocyte, and anti-serum glycoprotein gp70. This indicates that the action of the lpr gene on the development of autoantibody response does not require the particular abnormalities of the MRL genome. The differences in amounts and types of autoantibodies among the lpr strains reflect the difference in the background genome of each strain, suggesting the participation of other genes or factors determining the quantity and/or specificity of autoantibodies. In addition to the development of autoantibodies, the three nonautoimmune strains of mice produced high levels of unidentified IC in the presence of the lpr gene, detectable by the C1q and the conglutinin binding tests. Their glomerular lesions, however, were relatively limited when compared with MRL/ MpJ -lpr/lpr mice, which developed severe glomerulonephritis early in their life. These results suggest that the lpr gene is able to induce the formation of various autoantibodies and IC at significant concentrations in nonautoimmune mice, but for the full manifestation of systemic lupus erythematosus there may be a requirement for supplemental genetic abnormalities or factors.
Differential effect of cyclosporin A on the expression of T and B lymphocyte activation antigens.
Authors: Lillehoj H S , Malek T R , Shevach E M 
Published: December 2022

Abstract
We have used a monoclonal antibody (Mab) to the interleukin 2 (IL 2) receptor as well as a Mab to the transferrin receptor to analyze the effects of cyclosporin A (CsA) on the induction and expression of these activation antigens on mitogen-stimulated murine T and B lymphocytes. The same concentration (0.25 microgram/ml) of CsA that produced optimal inhibition of the T cell proliferative response to concanavalin A (Con A) was also very effective at inhibiting IL 2 production and the induction of IL 2 responsiveness, as well as the expression of the IL 2 and transferrin receptors when measured 72 hr after mitogen activation. Surprisingly, CsA only minimally inhibited expression of these receptors 24 hr after the addition of mitogen; however, T cell blasts recovered from these cultures failed to respond to IL 2 even though IL 2 receptor expression was only modestly decreased. These results suggest that inhibition of the maturation of receptor expression is secondary to an early effect of CsA in blocking the induction of IL 2 responsiveness or to an arrest in the sequence of events required for maturation of T cells that bear high densities of these receptors. In contrast to the results observed with T lymphocytes, CsA had no effect on the B cell proliferative response to lipopolysaccharide (LPS) or on the induction of the IL 2 and transferrin receptors on activated B lymphocytes.
Dexamethasone-mediated inhibition of human T cell growth factor and gamma-interferon messenger RNA.
Authors: Arya S K , Wong-Staal F , Gallo R C 
Published: December 2022

Abstract
Glucocorticoids suppress the proliferation of human T lymphocytes. Activated T lymphocytes require T cell growth factor (TCGF) for proliferation. TCGF is produced by a subset of T lymphocytes, and this production is regulated at the TCGF mRNA level. Dexamethasone, a synthetic glucocorticoid, strongly inhibits the synthesis of TCGF mRNA in human normal peripheral blood lymphocytes stimulated in culture with phytohemagglutinin. It also inhibits the accumulation of gamma-interferon mRNA in these cells. This dual effect may in part explain some of the immunosuppressive and anti-inflammatory effects of glucocorticoids.
Biochemical comparison of murine colony-stimulating factors secreted by a T cell lymphoma and a myelomonocytic leukemia.
Authors: Prestidge R L , Watson J D , Urdal D L , Mochizuki D , Conlon P , Gillis S 
Published: December 2022

Abstract
Factors that stimulate the proliferation and differentiation of murine bone marrow cells have been purified from a cloned T cell lymphoma, LBRM-33, and a cloned myelomonocytic leukemia cell line, WEHI-3. These colony-stimulating factors (CSF) have been purified by sequential fractionation by using salt precipitation, gel filtration, anion and cation exchange chromatography, and high pressure liquid chromatography. Both LBRM-33 and WEHI-3 cells secrete a CSF species with similar chemical and biologic properties. This CSF species appears to exist in two forms, termed CSF-2 alpha and CSF-2 beta, both of which stimulate the growth of bone marrow cells in the granulocyte, macrophage, megakaryocyte, mast cell, and erythrocyte lineages, as well as the growth of a CSF-dependent cell line, FDC-P2. These properties of CSF-2 alpha and -2 beta are similar to those reported for interleukin 3, hematopoietic cell growth factor, mast cell growth factor, and persisting cell growth factor. However, LBRM-33 cells secrete another CSF species, not produced by WEHI-3 cells. This CSF species, unique to LBRM cells, is termed here CSF-2 gamma and it stimulates the proliferation of granulocytes and macrophages from bone marrow but does not support the growth of FDC-P2 cells.