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At least 37 records · Page 2Linked to original sources
PubMed1992

Evidence for an alpha/beta T cell-independent mechanism of resistance to mycobacteria. Bacillus-Calmette-Guerin causes progressive infection in severe combined immunodeficient mice, but not in nude mice or in mice depleted of CD4+ and CD8+ T cells.

Depleting thymectomized mice of CD4+ T cells, or CD4+ plus CD8+ T cells, rendered them incapable of resolving Bacillus-Calmette-Guerin (BCG) infection in their lives, spleens, kidneys, and lungs. However, it did not render them incapable of stabilizing infection in the latter three organs after an initial period of BCG growth. Athymic nude mice showed a similar capacity to control BCG growth in these organs after a certain stage of infection. In contrast, congenitally severe combined immunodeficient (SCID) mice appeared to offer no resistance to BCG infection, in that the organism grew progressively in all organs of these mice and was lethal for them beginning on day 55 of infection. The results suggest that, although CD4+ T cells are important for resolving BCG infection, an alpha/beta T cell-independent mechanism of resistance can be acquired at 2-3 wk of infection that is capable of inhibiting further BCG growth in all organs except the lungs. Because this mechanism is absent from SCID mice, it is likely that it depends on the functions of gamma/delta T cells, B cells, or both types of cells. In keeping with this possibility is the additional finding that SCID mice engrafted with lymph node cells depleted of CD4+ or CD8+ T cells were capable of expressing an appreciable level of resistance against BCG infection.

Animals↗
PubMed1980

Recovery of Schistosoma mansoni from the skin, lungs and hepatic portal system of naive mice and mice previously exposed to S. mansoni: evidence for two phases of parasite attrition in immune mice.

New or improved techniques for recovering Schistosoma mansoni from the skin, lungs and liver have enabled us to trace the attrition of a challenge infection in naive (i.e. previously uninfected) and chronically infected mice. Within each experiment, numbers of schistosomes recovered from the skin of naive mice on day 2 after challenge or from the skin and lungs on days 3, 4 or 5, did not differ significantly from the numbers recovered from the liver on days 14, 21, 28 or 35. Approximately 65% of cercariae which penetrated the skin failed to be recovered from naive mice by any of the assays and it appeared that these schistosomes had already died in the skin in the first 24 h. No further significant loss of the infection was detected in naive mice. In chronically infected mice a further attrition of the challenge infection was demonstrated in two distinct phases. An 'early phase' occurred within the first 3 days of exposure and accounted for the death of 30% of the remaining parasites. A 'late phase' occurred between days 6 and 14 and accounted for an additional 43% of deaths. Thus, the two phases of attrition accounted for a loss of approximately 73% of the infection that would have survived in a naive mice. The late phase of attrition could be demonstrated before the primary infection had matured, in contrast to the early phase of attrition which was seen only after egg laying had commenced. We believe that the early phase of attrition takes place in the skin and the late phase occurs after the schistosomes have left the lungs, either en route for the liver or as soon as they arrive in that organ. The results suggest that there are two distinct mechanisms of immunity against re-infection with S. mansoni in mice.

Animals↗
PubMed1983

Idiotypic manipulation in mice: BALB/c mice can express the crossreactive idiotype of A/J mice.

The response of A/J mice to arsonate-coupled keyhole limpet hemocyanin is characterized by a crossreactive idiotype (CRIA). CRIA+ antibodies are restricted to the Igh-Ic haplotype and are never expressed in BALB/c mice after immunization with antigen. Studies at the DNA level suggest that the gene encoding the CRIA heavy chain in A/J mice is probably absent in the genome of BALB/c mice. Despite this, using the immunization cascade tool, we have been able to induce the expression of CRIA+ antibodies in BALB/c mice. These studies led to an apparent paradox, whose understanding will provide new insights into the regulatory mechanisms of the immune system. We suggest that clones secreting CRIA-like Igs in BALB/c mice are "somatic variants" that could arise from gene conversion events.

Animals↗
PubMed1980

Tumorigenicity of human malignant lymphoblasts: comparative study with unmanipulated nude mice, antilymphocyte serum-treated nude mice, and X-irradiated nude mice.

The ability of unmanipulated, antilymphocyte serum (ALS)-treated, and X-irradiated nude BALB/c female mice (in their 13th backcross generation) to serve as hosts for 10 human lymphoblastoid cell lines as well as for peripheral blood lymphocytes from healthy humans was compared. The 10 lymphoma lines included 7 previously characterized and reported in the literature. Significant differences with respect to both latency period for tumor appearance and success rate for tumor transplantation were detected among the 3 experimental groups. The unmanipulated mice were poor recipients for lymphoma heterotranplants, and tumors were produced in only two instances. In contrast, 6 tumor lines were successfully transplanted in mice inoculated with ALS, and all 10 lines were successfully transplanted in X-irradiated recipients. Although tumors were readily produced in ALS-treated and X-irradiated mice, no gross or histologic evidence of focal or distant metastases was apparent. Human lymphoblastoid cells were recultured, essentially unchanged, from the heterotransplants from 6 of 7 tumors tested. Although the tumor line HT 1460, originally from a human lymphoma, was successfully transplanted in all 3 groups, only mouse cells were recultured. The use of X-irradiation, rather than ALS, to immunosuppress nude mice offers a more standardized method for heterotransplanting human tumor cell lines and permits ready comparisons between laboratories. Furthermore X-radiation permits transplantation and subsequent study of lymphoblastoid tumors that are otherwise difficult to successfully transplant in nude mice.

Animals↗
PubMed2005

Regional variations in the distributions of small intestinal intraepithelial lymphocytes (IELs) in outbred laboratory mice (Mus musculus domesticus) and the inbred strain of mice established from Japanese fancy mice (Mus musculus molossinus).

Previously, we reported regional variations in small intestinal IELs of mice. In this study, we examined the regional variations of IELs in outbred laboratory mice (ddY: Mus musculus domesticus) and the inbred strain of mice established from Japanese fancy mice (JF1: Mus musculus molossinus). IELs were isolated from the proximal, middle and distal parts of the small intestine and analyzed by flow cytometry. The percentages of gammadelta T cells and alphabeta T cell subset of extrathymic origin were higher in the proximal part while the percentages of alphabeta T cell subset(s) of thymic origin were higher in the distal part in both ddY and JF1 mice. Such trends in regional variations of IELs were almost the same as those found in the inbred strains of laboratory mice in our previous reports. This strongly suggests that these regional variations of IELs may be common phenomena in Mus musculus species.

Animals↗
PubMed1988

Increase in basal pulse rate and blood pressure by the diabetic state in KK-CAy mice, alloxan-mice and streptozotocin-mice.

Basal pulse rate (PR) and systolic blood pressure (BP) in the tail artery of diabetic KK-CAy mice were compared with those of alloxan- or streptozotocin (STZ)-induced diabetic ddY mice. Significantly higher PR and BP were obtained by the above three kinds of diabetic states when compared with the pre-diabetic state (KK-CAy) or the non-diabetic state (ddY mice). The PR and BP alteration in diabetic KK-CAy mice were significantly different from the PR one in alloxan-mice and from the BP one in STZ-mice, respectively. Both increases in PR and BP by the diabetic state suggest an anticholinergic state.

Aging↗
PubMed1982

Spleen cells from adult mice given total lymphoid irradiation or from newborn mice have similar regulatory effects in the mixed leukocyte reaction. I. Generation of antigen-specific suppressor cells in the mixed leukocyte reaction after the addition of spleen cells from adult mice given total lymphoid irradiation.

We added spleen cells from adult BALB/c mice treated with total lymphoid irradiation (TLI) to the mixed leukocyte reaction (MLR) using a variety of responder and stimulator cells. The spleen cells nonspecifically suppressed the uptake of [3H]-thymidine and the generation of cytolytic cells regardless of the responder-stimulator combination used. We also examined the effect of the spleen cells on the generation of antigen-nonspecific and antigen-specific suppressor cells in the MLR. The experimental results suggest that the spleen cells from TLI-treated mice inhibit the generation of nonspecific suppressor cells, but do not inhibit the generation of antigen-specific suppressor cells. Thus, alloantigenic stimulation of normal responder cells in vitro in the presence of spleen cells from TLI-treated mice generates large numbers of antigen-specific suppressor cells, but few cytolytic cells or nonspecific suppressor cells. Similar nonspecific inhibition of the MLR was observed with neonatal spleen cells. This in vitro system provides a regulatory model for the induction and maintenance of tolerance in vivo, in which adult mice given TLI or neonatal mice accept allogeneic bone marrow transplants without graft-vs.-host disease.

Animals↗
PubMed1985

Regulation of pre-B cell proliferation in bone marrow: immunofluorescence stathmokinetic studies of cytoplasmic mu chain-bearing cells in anti-IgM-treated mice, hematologically deficient mutant mice and mice given sheep red blood cells.

To identify factors influencing the in vivo proliferate activity of bone marrow pre-B cells, the metaphase-blocking drug, vincristine sulfate, was injected into (a) mice depleted of B lymphocytes by treatment with anti-mouse IgM antibodies from birth; (b) hematologically deficient W/Wv and Sl/Sld mutants, and (c) mice injected with a foreign agent, sheep red blood cells (SRBC). Subsequently, a quantitative measure of pre-B cell proliferation was provided by examining marrow cells by immunofluorescence labeling for the absolute number of pre-B cells, identified by the presence of cytoplasmic mu chains (c mu) without surface mu (s mu), which had been arrested in metaphase. In anti-IgM-treated mice, some changes were observed in the size of the large pre-B cell population and in the incidence of mitotic cells after vincristine administration, but the overall production rate of pre-B cells did not differ from that in controls given normal rabbit serum. Pre-B cell kinetics in W/Wv and Sl/Sld mice also generally resembled those in homozygous controls. In contrast, after SRBC injection, there was an increase in the rate at which large pre-B cells entered mitosis. Thus, the proliferation of c mu + s mu- bone marrow pre-B cells shows no evidence of feedback control from the mature B lymphocyte pool, as indicated by lack of stimulation of pre-B cell production in anti-IgM-treated mice, and is independent of the hemopoietic defects of W/Wv or Sl/Sld mutants. On the other hand, the increased bone marrow pre-B cell proliferation after SRBC injection demonstrates that the magnitude of B cell genesis in the bone marrow can be influenced by extrinsic agents and thus may be influenced by environmental stimuli.

Animals↗
PubMed2003

Chemical kindling induced by pentylenetetrazol in histamine H(1) receptor gene knockout mice (H(1)KO), histidine decarboxylase-deficient mice (HDC(-/-)) and mast cell-deficient W/W(v) mice.

The role of brain histamine on seizure development of pentylenetetrazol (PTZ)-induced kindling was examined in H(1)-receptor gene knockout (H(1)KO), histidine decarboxylase-deficient (HDC(-/-)) and mast cell-deficient (W/W(v)) mice. All H(1)KO, HDC(-/-) and W/W(v) mice had accelerated seizure development of PTZ-induced kindling when compared to their respective wild-type mice. The daily PTZ-kindling increased histamine content in the cortex and diencephalon of H(1)KO mice, whereas the histamine content in the diencephalon of W/W(v) mice was decreased. The present study indicates that histamine plays a suppressive role in seizure development through H(1)-receptors.

Analysis of Variance↗
PubMed2002

Sleep deprivation in prion protein deficient mice sleep deprivation in prion protein deficient mice and control mice: genotype dependent regional rebound.

We have previously reported a larger and more prolonged increase of slow wave activity (SWA) in NREM sleep after sleep deprivation (SD) in prion protein deficient mice (PrP) compared to wild-type mice. Regional differences in the SWA increase were investigated by comparing the effect of 6 h SD on a frontal and occipital derivation in PrP deficient mice and wild-type mice. The larger increase of SWA after SD in PrP deficient mice was restricted to the occipital derivation. The difference appeared after the waking-NREM sleep transitions, making it unlikely that PrP is involved in the mechanisms enabling the transition to sleep. Our findings may reflect differences between the genotypes in the need for recovery in this particular brain region.

Animals↗
PubMed1985

T cell development in B cell-deficient mice. II. Serological characterization of suppressor T cell factors (TsF1) produced in normal mice and in mice treated chronically with rabbit anti-mouse IgM antibodies.

Serological analysis of idiotypic specificities present in azobenzenearsonate (ABA)-specific first-order suppressor T cell factors (TsF1) from C.AL-20 and BALB/c mice revealed a significant difference between TsF from these two strains of mice. The idiotypic composition of TsF1 from BALB/c mice appears to be more heterogeneous, and at least two different fractions can be readily identified. One bears the characteristic BALB/c-associated CRI(C) (crossreactive idiotype) determinants, and the other is non-CRI(C)-bearing. Analysis of ABA-specific TsF1 from animals lacking B cells uncovered a fundamental change in the expression of their idiotypic specificities. TsF from rabbit anti-mouse IgM (anti-mu)-treated C.AL-20 mice failed to express the characteristic CRI(A) determinants. Instead, they express CRI(C) specificities. Similarly, TsF1 from anti-mu-treated BALB/c mice did not express their characteristic CRI(C) specificities, but rather express CRI(A) determinants. These experiments provide strong evidence that the Igh restriction specificity of TsF is dictated by the particular idiotypic specificities expressed. They also clearly demonstrate that B cells and their products play an important role in establishing the idiotypic composition and repertoire of suppressor T cells.

Animals↗
PubMed1989

[Studies on the possible causes of decreasing NK cell activity in tumor-bearing mice. I. The number of NK cells in the spleens of tumor-bearing mice is higher than that in normal mice].

In studies of viral immunotherapy of cancer, we found that NK cell activity in tumor-bearing mice was usually below the normal level, a universal phenomenon in tumor-bearing animals and patients. Our data show that the depressed NK cell activity in tumor-bearing mice was not due to a decrease of NK cell number. The percentage of NK cells in the spleens of tumor-bearing mice was much higher than that in normal mice. Using morphological and 3H-TdR uptake methods, we found that there were many NK blast cells in the spleens of tumor-bearing mice, and blastogenesis was sustained up to the day of death.

Animals↗
PubMed1982

Spleen cells from adult mice given total lymphoid irradiation (TLI) or from newborn mice have similar regulatory effects in the mixed leukocyte reaction (MLR). II. Generation of antigen-specific suppressor cells in the MLR after the addition of spleen cells from newborn mice.

Spleen cells from newborn BALB/c mice were added to the mixed leukocyte reaction (MLR) between a variety of responder and stimulator cells. The newborn cells nonspecifically suppressed the uptake of (3H)-thymidine and the generation of cytolytic cells regardless of the responder-stimulator combination used. Suppressor cell activity fell rapidly during the first 4 days after birth, and could not be detected by day 20. Newborn spleen cells inhibited the generation of nonspecific suppressor cells during the MLR but did not inhibit the generation of antigen-specific suppressor cells. Thus, newborn spleen cells exhibit a pattern of regulation of the MLR similar to that reported previously for spleen cells from adult mice given total lymphoid irradiation (TLI). These regulatory interactions provide a model that explains the ease of induction of transplantation tolerance in vivo in newborn mice and in TLI-treated adult mice.

Animals↗
PubMed2003

Malformation of the radial glial scaffold in the dentate gyrus of reeler mice, scrambler mice, and ApoER2/VLDLR-deficient mice.

We studied the postnatal development of the radial glial scaffold in the dentate gyrus of reeler mice, lacking the extracellular matrix protein Reelin, in scrambler mice, deficient in the intracellular adaptor protein disabled1 (Dab1), which is required for the transmission of the Reelin signal into the cell, and in mutant mice lacking the Reelin receptors apolipoprotein receptor 2 (ApoER2) and/or the very low density lipoprotein receptor (VLDLR), known to transmit the Reelin signal via Dab1. By immunolabeling for the glial fibrillary acidic protein (GFAP), we show that a regular dentate radial glial scaffold fails to form in mutants deficient of Reelin, Dab1, and VLDLR and ApoER2. Mutant mice lacking only one of the Reelin receptors, VLDLR or ApoER2, display a gradual expression of the radial glial defects seen in mutants that lack both receptors. Our results suggest that Reelin signaling via ApoER2, VLDLR, and Dab1 is required for the formation of a regular radial glial scaffold in the dentate gyrus.

Animals↗
PubMed1998

2-Mercapto-propylamine: radiopharmacology in mice, pharmacokinetic studies in mice and in rats, mutagenicity and differential distribution between tissues and EMT6 tumour in mice.

Radiopharmacological studies conducted with 2-mercapto-propylamine (2MPA), a methylated derivative of cysteamine, indicated a good efficiency in whole body irradiated mice as observed over a period of 9 months. Its efficacy was also checked for supralethal irradiations of restricted body parts: in the brain and the rectum. The diffusion of 14C-labelled 2MPA was assessed by an autoradiographic study and measurement of its distribution in the main organs in mice. 2MPA penetrated the blood brain barrier but concentrated preferentially in the liver, kidney and skin. Fixation on plasmatic proteins was much lower in rats than in mice but urinary and faecal eliminations were of the same order for the two species. An important biliary excretion of 2MPA or its metabolites in rats combined with their lack in the faeces underlies an entero-hepatic cycle. A differential diffusion of 2MPA between normal tissues in mice and EMT6 tumours was clearly revealed by autoradiographic observations. The ability of 2MPA to trap 2,2'-diphenyl 1-picryl hydrazyl, an organic free radical, was checked by in vitro studies. Its performance indicated that 2MPA acted at least as a free radical scavenger. Ames test demonstrated that 2MPA whatever the dose employed was not a mutagenic agent. Pharmacological and pharmacokinetical observations provided a better understanding of the activity of this drug.

Animals↗
PubMed1986

Induction of early-phase endotoxin tolerance in athymic (nude) mice, B-cell-deficient (xid) mice, and splenectomized mice.

Early-phase endotoxin tolerance was inducible in mice which were T cell deficient (nude), B cell deficient (xid), or asplenic, which suggests that these lymphoid cell subsets and the spleen do not contribute significantly to the induction of acquired lipopolysaccharide hyporesponsiveness. C3H/HeJ mice did not exhibit the hematopoietic changes observed in mice made endotoxin tolerant, which suggests that multiple mechanisms may underlie lipopolysaccharide hyporesponsiveness.

Animals↗
PubMed1983

Regulation of bone marrow lymphocyte production. IV. Cells mediating the stimulation of marrow lymphocyte production by sheep red blood cells: studies in anti-IgM-suppressed mice, athymic mice, and silica-treated mice.

Some cellular requirements have been examined for the stimulation of lymphocyte production in mouse bone marrow by injected sheep red blood cells (SRBC). The increased genesis of marrow lymphocytes after a single dose of SRBC assayed radioautographically after [3H]thymidine labeling was unimpaired in the marrow of mice treated with anti-IgM antibodies from birth to eliminate B lymphocytes, and in congenitally athymic mice lacking T lymphocytes. However, pretreatment of mice with silica to depress macrophage function completely abolished the SRBC effect both on the total lymphocyte production and on the number of B and null small lymphocytes in the marrow. Comparative studies were performed on the thymus and spleen. The results demonstrate that the stimulation of marrow lymphocytes production by SRBC is mediated by a silica-sensitive mechanism, does not require B or T lymphocytes, and is independent of the humoral immune response. Thus, extrinsic agents may amplify the production of primary B cells and other lymphocytes in the bone marrow by an antigen-nonspecific mechanism, putatively mediated by macrophages.

Animals↗
PubMed1966

Autoimmune disease in NZB/BL mice. 3. Induction of membranous glomerulonephritis in young mice by the transplantation of spleen cells from old mice.

The transplantation of spleen cells from old NZB/Bl mice with renal disease induced both the structural and the functional changes of membranous glomerulonephritis in young NZB/Bl mice within a few weeks and well in advance of its usual spontaneous occurrence. The development of hypergammaglobulinemia and lymphoid cell hyperplasia in the young mice indicated that immunologically competent cells, derived from either the transplant or the recipient, proliferated during this process. These experiments, together with other findings, provide further support for the view that membranous glomerulonephritis in NZB/Bl mice is produced by immunological, and probably autoimmune, mechanisms and that the renal disease is apparently almost wholly unrelated to the hemolytic process.

Animals↗