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At least 19 recordsLinked to original sources
PubMed1977

Immunologic tolerance to HGG in mice. I. Suppression of the HGG response in normal mice with spleen cells or a spleen cell lysate from tolerant mice.

Adoptive transfer of spleen cells or spleen cell lysates from mice tolerant to human-gamma-globulin (HGG) specifically suppressed the response of normal syngeneic recipients to HGG. The suppressive activity could be transferred for over 100 days after tolerance induction. The suppression induced by both spleen cells and spleen cell lysate was found to be specific as evidenced by a normal response to a challenge with turkey-gamma-globulin or goat erythrocytes. The activity of the suppressive lysate could be removed by passing the material through an HGG immunoadsorbent column but not by passing it through an anti-HGG column or a BSA column. These results indicated that the factor had antigen specificity and was probably not antigen-antibody complexes. That this suppression was not due to a shifting of the kinetics of the antibody response has also been demonstrated. The antigen-specific suppressor factor in the tolerant spleen cell lysates was a protein with a m.w. of approximately 45,000 daltons. The kinetics of the appearance of both suppressor cells and suppressor factor were consistent with a mechanism of active suppression functioning in the maintenance of tolerance to HGG.

Animals↗
PubMed1977

Differences in the mechanism of tolerance to dinitrophenylated bovine gamma globulin when induced in normal adult mice or in reconstituted irradiated mice: dependence of the mechanism of tolerance on the structural organization of the lymphoid system.

Tolerance can be induced in adult mice by a single intravenous injection of 0.5 mg dinitrophenylated bovine gamma globulin. The cellular mechanism of the unresponsive state is different depending upon whether the tolerance is induced in normal intact adult mice or in reconstituted, irradiated mice. The tolerant state induced in intact mice is characterized by a high avidity of the residual antibody-forming cells in partially tolerant animals and a prompt reversibility on cell transfer. The overall properties of this unresponsive state are consistent with the hypothesis that it is mediated by the production of small amounts of high affinity antibody in response to the tolerance-inducing injection of antigen. In contrast, the unresponsiveness induced in reconstituted, irradiated mice by the same procedure was characterized by a low avidity of the residual antibody-forming cells in partially tolerant animals and stability on transfer of spleen cells from unresponsive into irradiated recipients. No suppressor cell activity was detected and mixed cell transfer studies were consitent with the view that this unresponsive state represented a B-lymphocyte clonal deletion. The presence or absence of T lymphocytes in the population of cells used for reconstituting the irradiated recipients did not effect the ease of tolernace induction or the cellular mechanism of the tolerant state which was produced. If irradiated mice reconstituted with B and T lymphocytes were rested for 2 wk before tolerance induction then a reversible "high affinity"-type tolerance is obtained such as is typical of normal intact animals. Restorationof a "normal" response to the tolerance-inducing injection of antigen is dependent upon the presence of thymus cells in the population of cells used for reconstitution. It is suggested that the structural integrity of the lymphoid tissue is critical in determining whether B cell will be rendered tolerant after exposure to antigen in vivo.

Age Factors↗
PubMed1978

Histocompatibility difference between C3HfeB/HeN and C3H/HeN mice: tumour induced in C3HfeB/HeN mice expresses C3H/HeN-associated alloantigen.

A transplacentally induced lung tumour of C3HfeB/HeN mouse origin expresses, as a tumour-associated antigen, a normal tissue component of strain A mice. The genetic locus coding for this alloantigen has been shown to be linked to the H-2 major histocompatibility complex. In the present study we demonstrate that this antigen is also expressed on normal tissues of C3H/HeN mice. Skin grafts exchanged between C3HfeB/HeN and C3H/HeN mice are reciprocally rejected at approximately 3 weeks after grafting. C3HfeB/HeN mice were derived from C3H/HeN mice in 1945. These strains have apparently deviated since then in their genetic regulation of the expression of the MHC-linked genetic locus. The finding of the C3H/HeN-associated antigen on a C3HfeB/HeN mouse-derived lung tumour indicates that this deviation is reversible.

Animals↗
PubMed1977

Studies on delayed hypersensitivity in mice. I, Physicochemical and biological properties of preferential antigens for inducing delayed hypersensitivity in mice.

Variously modified protein antigens were tested by footpad assay to clarify the effect of these medications in producing delayed hypersensitivity in mice. The most potent antigen examined was carboxyl-methylated serum albumins. These antigens were highly basic proteins and hydrophobic compared with native serum proteins. They stimulate humoral antibody response in mice poorly, and remain at the subcutaneous injection site much longer than native serum albumins. In vitro tests of susceptibility of thymus and spleen cells and peritoneal macrophages to the antigens revealed that methylated serum albumins possessed the stimulatory activity to the latter and were toxic to the former. As for macrophage, fluorescein-labelled methylated serum albumin showed an affinity to their membrane and were phagocytosed, but FITC-BSA did not show any affinity to the macrophages. These biological activities to tissue or cells may be contributable to render methylated serum albumins to induce and elicit delayed hypersensitivity preferentially in mice.

Animals↗
PubMedDate not supplied

[Ontogeny of the immune response in mice. I. Presence of IgG and alpha fetoprotein in the body fluids of mice of various ages].

Alpha protein and IgG were determined by radial immunodiffusion in Swiss mice, in the amniotic fluid, milk and serum of the mice at different ages (fetus, neonates, at the age of 5, 10, 15, 20, 25, 30, 35 and 40 days and adults). The highest alpha-protein concentrations were found in the fetal serum (0.20 mg/ml) ; after birth serum levels rapidly fell and at 20 days could no longer be detected ; it was present in the amniotic fluid and milk collected within the first 24 hours after birth. In contrast, IgG was found in small concentrations in the fetal serum (0.60 mg/ml) but increased with age after birth. This immunoglobulin was present in the amniotic fluid and mothers' milk for 15 days. The significance of the results is discussed.

Age Factors↗
PubMed1979

Immunological unresponsiveness in mice. II. Cellular basis of immunological unresponsiveness induced in foetal and neonatal mice by transfer of human gamma-globulin by the maternal route.

The cellular basis of the mechanism of immunological tolerance to human gamma-globulin (H gamma G) induced in foetal and neonatal mice by materno-foetal or materno-neonatal transfer after a single injection of tolerogen (deaggregated H gamma G) into the mothers was investigated using a cell transfer system and assays of passive haemagglutinating antibodies and plaque-forming cells to H gamma G. The results demonstrated that B cells are mainly involved in the tolerance induced on the fourteenth day of gestation, whereas inactivation of T cells may account for the tolerance induced on the eighteenth day of gestation and in the neonatal stage. Treatment of the mothers with tolerogen and then anti-H gamma G serum reduced the tolerance induced on the fourteenth day of gestation, but did not affect that induced on the eighteenth day of gestation and in the neonatal stage. Cell transfer experiments showed that B-cell tolerance induced on the fourteenth day of gestation was prevented by passive antibody, while T-cell tolerance induced on the eighteenth day of gestation and in the neonatal stage was not affected by passive antibody. Assay of the anti-DNP antibody response after immunization with DNP10-H gamma G showed that treatment of mice with the tolerogen on the eighteenth day of gestation, but not the fourteenth day of gestation, inactivated H gamma G-reactive helper cells. The significance of these results is discussed in relation to the results of the cell transfer experiments described as above.

Animals↗
PubMed1975

Cell-mediated immunity to moloney sarcoma virus in mice. I. Analysis of antigens responsible for lymphocyte stimulation in regressor mice.

Purified viruses, viral antigens, and cell extracts have been tested for their ability to stimulate protein synthesis by MSV-M-1 regressor spleen cells from BALB/c mice. Immune, but not normal cells, responded to MSV-M, but not to MSV-G virus-1, and to the type-specific viral envelope glycoprotein from MSV-M virus. Extracts of mouse embryo fibroblasts transformed by either MSV-M or MSV-G, however, specifically stimulated MSV-M regressor spleen cells. Cells stimulated by different antigens, and by phytohaemagglutinin, had the same sedimentation profile and were identified as T-lymphocytes.

Animals↗
PubMed2024

Bulk serum extracellular vesicles from stressed mice show a distinct proteome and induce behavioral and molecular changes in naive mice.

Chronic stress can trigger several pathologies including mood disorders for which no clear diagnostic molecular markers have been established yet. Attractive biomarker sources are extracellular vesicles (EVs). Evs are released by cells in health and disease and contain genetic material, proteins and lipids characteristic of the cell state. Here we show that Evs recovered from the blood of animals exposed to a repeated interrupted stress protocol (RIS) have a different protein profile compared to those obtained from control animals. Proteomic analysis indicated that proteins differentially present in bulk serum Evs from stressed animals were implicated in metabolic and inflammatory pathways and several of them were previously related to psychiatric disorders. Interestingly, these serum Evs carry brain-enriched proteins including the stress-responsive neuronal protein M6a. Then, we used an in-utero electroporation strategy to selectively overexpress M6a-GFP in brain neurons and found that M6a-GFP could also be detected in bulk serum Evs suggesting a neuronal origin. Finally, to determine if these Evs could have functional consequences, we administered Evs from control and RIS animals intranasally to naïve mice. Animals receiving stress EVs showed changes in behavior and brain M6a levels similar to those observed in physically stressed animals. Such changes could therefore be attributed, or at least in part, to EV protein transfer. Altogether these findings show that EVs may participate in stress signaling and propose proteins carried by EVs as a valuable source of biomarkers for stress-induced diseases.

Animals↗
PubMedDate not supplied

Models for assessing the effect of toxicants on immunocompetence in mice. II. Effect of cyclophosphamide on the antibody responses to type III pneumococcal polysaccharide and tetanus toxoid in BALB/c female mice.

A mixture of antigens was used to detect alterations in immunocompetence. Type III pneumococcal polysaccharide (S3) and tetanus toxoid (TT) stimulate different cellular components, and can therefore be used to assess different compartments of the immune mechanism. Cyclophosphamide (CP), a known immunosuppressant, had a potent effect upon the antibody responses to both S3 and tetanus toxoid. All doses of CP administered within 2 days of priming with S3 resulted in a dose-related immunosuppressive action which persisted even after reinjection of S3. 300 mg/kg of CP given up to 14 days prior to or following primary immunization resulted in a marked suppression of antibodies to S3. Doses of S3 which were partially tolerogenic were made even more so by injections of CP. The effect persisted over a 96 day experimental period. CP also suppressed the formation a memory cells necessary for induction of a secondary-type IgG response to TT. The time of injection for maximum suppression was days 10 to 14 after priming. Therefore, the suppression must involve cellular mechanisms different from those responsible for S3 antibody suppression. In addition, there was a difference in the degree and persistence of the suppressive effect, since the suppressed animals were able to mount an immune response to subsequent injections of TT. Double injections of a high dose (300 mg/kg) of CP 4 weeks after priming completely suppressed the acquired immunity to both S3 and TT. Low and moderate doses of CP appeared to induce a mild augmentation of S3 antibody response when given 4 weeks after priming. However, an immunosuppressive effect occurred if the primed animals were reinjected with S3 or challenged with TT within a period of 2 days prior to or after receiving the CP treatment. Doses of CP, injected prior to challenge and resulting in suppressed tetanus antitoxin production, elevated the titers of specific IgE antibody. This class of antibody is associated with adverse hypersensitivity reactions. These data provided background for the development of models to assess immunocompetence in mice, based on a study of immune profiles following exposure to selected T-dependent and T-independent antigens. Such models may be used to detect potentially hazardous chemicals found in the environment of incorporated into foods, drugs, or cosmetics.

Animals↗
PubMed1975

Normal tissue alloantigens and genetic control of susceptibility to tumors: microcytotoxicity studies on resistant C3Hf and susceptible (A X C3Hf) F1 mice inoculated with transplacentally induced C3Hf lung tumor.

The immune response of mice to a transplacentally induced lung tumor was investigated with the microcytotoxicity (MC) assay. The tumor, originally induced in C3Hf mice, does not grow readily when transplanted to normal syngeneic C3Hf recipients. It grows readily, however, in (A C3Hf)F1 hybrids and in strain C3H mice, which express in their normal lung tissue a component which constitutes a strong lung tumor-associated transplantation antigen (TATA) in C3Hf mice. Both lung tumor-immunized C3Hf and tumor-bearing (A X C3Hf)F1 and C3H mice possessed lymphoid cells reactive against cultured lung tumor cells in the MC assay. Reactivity was also observed against cells cultured from normal lungs of (A X C3Hf)F1 and C3H mice, but not against cells similarly cultured from C3Hf of C57BL/6 mice. Anti-tumor MC was inhibited by serum-blocking factors present in some but not all tumor-bearing and tumor-immunized mice. The MC assay and detection by it of serum-blocking factors does not distinguish the effective anti-C3Hf lung tumor immune response of immunized C3Hf mice from the ineffective immune response of tumor-bearing (A X C3Hf)F1 and C3H mice. Furthermore, in lung tumor-bearing mice cells reactive in the MC assay may be directed against a normal tissue antigen rather than a tumor-associated antigen.

Adenocarcinoma, Bronchiolo-Alveolar↗
PubMed2020

Tissue specificity of senescent cell accumulation during physiologic and accelerated aging of mice.

Senescent cells accumulate with age in vertebrates and promote aging largely through their senescence-associated secretory phenotype (SASP). Many types of stress induce senescence, including genotoxic stress. ERCC1-XPF is a DNA repair endonuclease required for multiple DNA repair mechanisms that protect the nuclear genome. Humans or mice with reduced expression of this enzyme age rapidly due to increased levels of spontaneous, genotoxic stress. Here, we asked whether this corresponds to an increased level of senescent cells. p16Ink4a and p21Cip1 mRNA were increased ~15-fold in peripheral lymphocytes from 4- to 5-month-old Ercc1-/∆ and 2.5-year-old wild-type (WT) mice, suggesting that these animals exhibit a similar biological age. p16Ink4a and p21Cip1 mRNA were elevated in 10 of 13 tissues analyzed from 4- to 5-month-old Ercc1-/∆ mice, indicating where endogenous DNA damage drives senescence in vivo. Aged WT mice had similar increases of p16Ink4a and p21Cip1 mRNA in the same 10 tissues as the mutant mice. Senescence-associated β-galactosidase activity and p21Cip1 protein also were increased in tissues of the progeroid and aged mice, while Lamin B1 mRNA and protein levels were diminished. In Ercc1-/Δ mice with a p16Ink4a luciferase reporter, bioluminescence rose steadily with age, particularly in lung, thymus, and pancreas. These data illustrate where senescence occurs with natural and accelerated aging in mice and the relative extent of senescence among tissues. Interestingly, senescence was greater in male mice until the end of life. The similarities between Ercc1-/∆ and aged WT mice support the conclusion that the DNA repair-deficient mice accurately model the age-related accumulation of senescent cells, albeit six-times faster.

Aging↗
PubMed1976

Histamine hypersensitivity in mice induced by Bordetella pertussis or pharmacologic beta adrenergic blockade. Effects of adrenergic, cholinergic, and other drugs.

The effects of prostaglandin E1, E2, F2alpha (PGE2 PGF2alpha), isoproterenol, epinephrine, norepinephrine, salbutamol, practolol, atropine, aminophylline, and corticosterone on the hypersensitivity to anaphylaxis, histamine, and serotonin in Bordetella pertussis-treated mice and propranolol-treated mice were investigated. Female HLA-SW (ICR) mice, 27-29 gm, were injected with pertussis vaccine intravenously 4 days before challenge with antigen, histamine, or serotonin. Alternatively, instead of pertussis vaccine, propranolol was injected intraperitoneally 45 min before histamine challenge. Test drugs were administered intraperitoneally 15 min before challenge. PGE1 and PGE2 at a narrow range of between 10 and 100 mug and epinephrine at 100 mug protected both pertussis- and propranolol-treated mice. Isoproterenol (25 mug) and aminophilline (800 mug) protected beta-blocked mice, but did not protect pertussis-treated mice even with very high doses (1,000 and 3,2000 mug, respectively), although salbutamol (500 mug) did. PGF2alpha, norepinephrine, and atropine were not protective at all. Practolol, a beta 1-blocker, given intraperitoneally 30 min before histamine neither sensitized normal mice nor changed the effect of isoproterenol or salbutamol in pertussis-treated mice. Corticosterone 10 mg/kg reduced the number of deaths from histamine in beta-blocked mice, but not in pertussis-treated mice. The protective effect is discussed in connection with probable effects of the drugs on intracellular cyclic adenosine monophosphate (cAMP) levels.

Adrenergic beta-Antagonists↗
PubMed1976

Effect of sera from immunologically altered mice on phytohemagglutinin-induced mouse lymphocyte transformation.

The DNA-synthetic response of mouse spleen cells to phytohemagglutinin in vitro is depressed by the addition of normal mouse serum. The effects of sera from mice that had been modified immunologically were examined. Increased depressive activity was found in sera from nude mice and from mice recently treated with anti-thymocyte globulin, but no change was found in sera from thymectomized, irradiated, bone marrow-reconstituted mice, nor from lethally or sublethally irradiated or cyclophosphamide-treated mice. Base line DNA synthesis was, however, less inhibited by sera from irradiated or cyclophosphamide-treated mice. Increased depressive activity was found in sera from mice with graft-versus-host reaction and from mice injected with Salmonella enteritidis 11RX, in which macrophage stimulation occurred. Increased depressive activity was also found in the sera of mice injected with sheep erythrocytes. T cells do not appear to be a source of depressive activity but B cells, macrophages and nonlymphoid cells may be sources.

Animals↗
PubMed1977

Theta-bearing cells in the bone marrow of thymus-deprived mice. Numbers and nature.

Theta-bearing cells in lymphomyeloid tissues of thymus-deprived and normal mice have been studied by the use of anti-theta antiserum and cytotoxicity tests in addition to functional tests. In contrast to the findings in peripheral lymphoid tissues, increased percentages and numbers of theta-bearing cells were found in the bone marrow of neonatally and nude mice as compared with normal and sham-thymectomized mice. In adult thymectomized mice, percentages comparable to those in sham-operated littermates were found. The findings were not due to irrelevant antibodies in the anti-theta antiserum, and neonatally thymectomized mice grafted with a thymic lobe showed percentages of theta-positive cells in the bone marrow comparable to those of sham-operated animals. Adrenalectomy did not lead to diminished percentages of theta-positive cells in the bone marrow of neonatally thymectomized mice, and the serum levels of hydrocortisone and corticosterone were within normal ranges in thymus-deprived mice. The mitogen responses and graft-versus-host activity of bone marrow cells from neonatally thymectomized mice suggest that most theta-positive cells in the bone marrow of these mice are functionally immature cells.

Adrenalectomy↗