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Results for “genetic resistance”

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At least 19 recordsLinked to original sources
PubMed1977

Effects of pre-irradiation on isogeneic and semi-isogeneic CFU growth: a study on genetic resistance.

The genetic resistance to a parental bone marrow transplant as demonstrated, when transplantation was performed early after irradiation, failed to occur if the interval between irradiation and transplantation was increased to 4 days. A similar radiation induced weakening of genetic resistance to a parental bone marrow graft in spleen and bone marrow could be demonstrated in mice, which had been irradiated with a sublethal dose at 7 days prior to the lethal irradiation and transplantation. The pre-irradiation of the recipient with a sublethal dose induced an enhancement of the growth in spleen and bone marrow of isogeneic transplanted CFU. The pre-irradiation of a single tibia also resulted in a significant weakening of the resistance in the spleen. The experiments with partial body pre-irradiation suggested a local effect of the pre-irradiation, but it could be shown that the enhanced CFU growth is not caused by an enhanced seeding of CFU in pre-irradiated bone marrow. The role of microenvironment in the phenomenon of genetic resistance is discussed.

Animals↗
PubMed1976

Genetic resistance to marrow transplantation as a leukemia defense mechanism.

(C57 X AKR) F1 hybrid mice show genetic resistance to C57 parental bone marrow cells, but not to AKR parental bone marrow cells. (C3H X AKR) F1 hybrids show no genetic resistance to bone marrow transplantation from either parental strain. Transplantation of AKR lymphoma cells into lethally irradiated "resistant" (C57 X AKR) F1 and "non-resistant" (C3H X AKR) F1 hybrids produce lymphomatous spleen colonies in "non-resistant" hybrids but not in "resistant" hybrids. Thus "resistant" (C57 X AKR) F1 hybrids can recognize and reject AKR lymphoma cells, but not normal AKR bone marrow cells. A normal biological role of lymphoma surveillance is postulated for genetic resistance.

Animals↗
PubMed1976

Genetic resistance to lethal flavivrus encephalitis. II. Effect of immunosuppression.

Genetic resistance of C3H/RV mice to lethal infection with Banzi virus (flavivirus) was severely compromised by immunosuppression with cyclophosphamide, sublethal X-irradiation, or thymus (T-) cell depletion. The mortality rate among immunosuppressed mice was usually 100%, but average survival times were shorter for mice treated with cyclophosphamide or for X-irradiated mice (10 days) than for T-cell-depleted mice (17 days). Mice treated with cyclophosphamide had high titers of virus in brain, lymphoid tissues, pancreas, and serum. Viral antigen was widespread in brain and pancreas, and mice developed nonsuppurative meningoencephalitis and pancreatitis. Yields of virus, spread of viral antigen, and lesions in T-cell-depleted mice were similar but less severe. Mice treated with cyclophosphamide did not have detectable hemagglutination-inhibiting antibody. T-cell-depleted mice developed hemagglutination-inhibiting antibody but were not protected from lethal infection. These results indicate that genetic resistance of C3H/RV mice to Banzi virus requires immunological factors, and that T-cells play a significant role in resistance to infection with Banzi virus.

Animals↗
PubMed1976

Macrophages genetically resistant to mouse hepatitis virus converted in vitro to susceptible macrophages.

Genetic resistance to mouse hepatitis, which resides largely in the macrophages of resistant C3H mice, may be altered by exposing the cells in vitro to fluid from allogeneic mixed lymphocytes. A 1,000-fold increase in susceptibility was produced in these genetically resistant cells by exposure to this fluid. This presumed lymphokine was effective without producing any change in host adaption of the virus.

Animals↗
PubMed1975

Effect of immunosuppression on the genetic resistance of A2G mice to neurovirulent influenza virus.

A2G mice are genetically resistant to lethal infection with neurotropic and pneumotropic influenza viruses. A possible immunological explanation for this resistance was sought by assessing the effect of cyclophosphamide and X irradiation immunosuppression on the infection of A2G mice with lethal doses of neurovirulent virus. Immunosuppressed A2G mice survived lethal infection enen though rendered unable to produce specific antiviral antibody or to generate cell-mediated delayed-type hypersensitivity responses. Measurement of infectious virus replication and detailed observation of the infection by immunofluorescence microscopy show that immunosuppression does not potentiate or allow spread of the virus in A2G brains. Interferon levels were essentially the same in normal and immunosuppressed A2G brains but were 3 to 5 times lower than in the brains of susceptible mice dying of the infection. The results strongly suggest that the genetic resistance of A2G mice to the acute lethal effects of neurovirulent influenza virus infection does not depend on the induction of primary immune mechanisms as we currently understand them. Other possible explanations for this resistance are considered.

Animals↗
PubMed1976

Mechanisms of genetic resistance to Friend virus leukemia. III. Susceptibility of mitogen-responsive lymphocytes mediated by T cells.

Friend leukemia virus (FV) suppressed the proliferative responses of spleen, lymph node, marrow, and thymus cell populations to various T- and B-cell mitogens. Cells taken from mice, e.g. BALB/c genetically susceptible to leukemogenesis in vivo were much more susceptible to suppression of mitogenesis in vitro than similar cells from genetically resistant mice, e.g., C57BL/6. Nylon wool-purified splenic T cells from BALB/c and C3H mice lost susceptibility to FV-induced suppression of mitogenesis but became suppressible by addition of 10% unfiltered spleen cell. Thus, FV mediates in vitro suppression of lymphocyte proliferation indirectly by "activating" a suppressor cell. The suppressor cell adhered to nylon wool but not to glass wool or rayon wool columns. Pretreatment of spleen cells with carbonyl iron and a magnet did not abrogate the suppressor cell function. Suppressor cells were not eliminated by treatment with rabbit antimouse immunoglobulin (7S) and complement (C). However, high concentrations of anti-Thy-1 plus C destroyed suppressor cells of the spleen; thymic suppressor cells were much more susceptible to anti-Thy-1 serum. Nude athymic mice were devoid of suppressor cells and their B-cell proliferation was relatively resistant to FV-induced suppression in vitro. The suppressor cells in the thymus (but not in the spleen) were eliminated by treatment of mice with cortisol. Thus, FV appears to mediate its suppressive effect on mitogen-responsive lymphocytes by affecting "T-suppressor cells." Spleen cells from C57BL/6 mice treated with 89Sr to destroy marrow-dependent (M) cells were much more suppressible by FV in virto than normal C57BL/6 spleen cells. However, nylon-filtered spleen cells of 89Sr-treated C57BL/6 mice were resistant to FV-induced suppression in vitro, indicating that the susceptibility of spleen cells from 89Sr-treated B6 mice is also mediated by suppressor cells. Normal B6 splenic T cells were rendered susceptible to FV-induced suppression of mitogenesis by addition of 10% spleen cells from 89Sr-treated B6 mice. Thus, M cells appear to regulate the numbers and/or functions of T-suppressor cells which in turn mediate the immunosuppressive effects of FV in vitro. Neither mitogen-responsive lymphocytes nor T-suppressor cells are genetically resistant or susceptible to FV. The genetic resistance to FV is apparently a function of M cells, both in vitro as well as in vivo.

Animals↗
PubMedDate not supplied

Two levels of genetic resistance to lymphoid leukosis.

Two levels of genetic resistance to lymphoid leukosis are recognized: 1) cellular resistance to virus infection; and 2) resistance to tumor development in leukosis-virus-infected birds. Resistance to infection is simply inherited but is very specific for the subgroup of virus. Inheritance of resistance to tumor development is more complex but appears to be less subgroup-specific. A breeder may wish to select for resistance to infection of virus eradication is the goal. If his goal is the reduction of lymphoid tumors, with virus infection not important, he may choose to select for resistance to tumor development.

Alleles↗
PubMed1978

Role of B cells in the expression of genetic resistance to growth of Rous sarcoma in the chicken.

Resistance to the development of progressively growing tumors induced by Rous sarcoma virus is a dominant trait controlled by a gene linked to the major histocompatibility complex (MHC). The effect of bursectomy (Bx) on the expression of this trait was studied in two inbred lines of chickens homozygous for different MHC alleles, and which differ with respect to the gene controlling resistance to Rous tumors. The results show that Bx alters the expression of the trait, since genetically resistant birds were rendered highly susceptible to progressive tumor growth. The bursa of Fabricius thus makes an important contribution to resistance. The results do not indicate whether genetic resistance is mediated exclusively by B cells or by another bursa-dependent population.

Animals↗
PubMed1978

Immunological nature of genetic resistance of mice to herpes simplex virus type 1 infection.

Treatment of mice genetically resistant to HSV-1 with agents which impair T-cell or macrophage function markedly diminished resistance. Bone marrow transplantation of genetically susceptible mice with marrow from resistant F1 mice produced chimeras resistant to HSV-1. Resistance thus appears to be immunological in nature. Striking similarities were found between resistance to HSV-1 and allogeneic resistance.

Animals↗
PubMed1977

Role of the major histocompatibility complex in resistance to Marek's disease: restriction of the growth of JMV-MD tumor cells in genetically resistant birds.

B21 is associated with resistance to Marek's disease (MD). Forty populations of chickens from all over the world were examined for the presence of the B21 allele. B21 was found in twelve of these populations and it's presence was confirmed by GVH testing in all ten populations which were tested. The populations in which B21 was detected represent the extreme production types of the species and include the progenitor of the species, the Red Jungle Fowl. Our studies suggest that B21 may have strong survival value for the species. An allogeneic transplantable lymphoma of MD, the JMV tumor cell line, grows more slowly in MD resistant (B21/B21) chicks than in MD susceptible (B2/B2) chicks. This is the first direct evidence that genetic resistance to MD may involve an active (immunological?) restriction of tumor cell growth. JMV cells were further characterized as a transplant of B1 carrying lymphoblastoid cells, an allele which may be associated with susceptibility to MD.

Animals↗
PubMed1975

Weakening of genetic resistance. I. The effect of injection of endotoxin, Freund's complete adjuvant and alloantiserum.

A parent to F1 transplantation combination was used to study the weakening effect of endotoxin, Freund's complete adjuvant and alloantiserum on genetic resistance. The relationship between time of treatment with endotoxin, Salmonella typhosa, and Freund's complete adjuvant, and their weakening effect was assessed by use of the spleen colony technique. CFU growth studies revealed that both endotoxin and alloantiserum were capable of weakening genetic resistance in the spleen but were unable to induce weakening of the resistance in the femoral marrow cavity. These results led us to the conclusion that the agents might not have a direct effect on the effector cells of the resistance. The weakening induced by endotoxin and alloantiserum seemed to be related to a certain immunological phenomenon in the spleen. In this phenomenon macrophages are likely to play a role since a number of agents capable of weakening resistance were known for their capacity to influence the mononuclear phagocytic system.

Animals↗
PubMed1976

Genetic resistance to lethal flavivirus encephalitis. I. Infection of congenic mice with Banzi virus.

Adult C3H/RV mice were highly resistant and adult C3H/He mice were highly susceptible to lethal encephalitis after intraperitoneal inoculation of Banzi virus (flavivirus), but the infectivity of the virus was the same for both strains of mice. Yields of virus were similar from lymphoid tissues of C3H/He and C3H/RV adult mice, but titers of virus in the brain were significantly lower in C3H/RV mice. Lesions of encephalitis developed in both strains but remained mild and self-limiting in C3H/RV mice, whereas widespread necrosis occurred in the brains of C3H/He mice. Resistance to lethal infection after intraperitoneal inoculation developed postnatally in C3H/RV mice and did not reach significant levels until mice were at least four weeks old. Mortality rates among C3H/RV and C3H/He mice were comparable after intracerebral inoculation of virus. Yields of virus, brain lesions, and immunofluorescent staining patterns for viral antigen were similar in intracerebrally inoculated C3H/He and C3H/RV mice. Results indicate that tissues of resistant and susceptible mice in vivo can support replication of Banzi virus about equally well. Thus, genetic resistance to lethal infection with Banzi virus in these strains of mice does not seem to be solely dependent on resistance of tissues to viral replication.

Animals↗
PubMed1979

Apparent identity of mechanisms of genetic resistance to marrow transplantation and natural killer cell activity.

Because the phenomenon of in vitro lysis of lymphoma cells by spleen natural killer (NK) cells bears genetic and effector cell resemblances to genetic resistance to bone marrow transplantation, they were compared for additional known unique characteristics of the latter phenomenon. Like GR to BMT, NK cell activity first appeared abruptly at about 3 weeks of post-natal age; was radioresistant to 1 100 R whole body irradiation, but was quantitatively diminished by higher exposures or delay of test post-irradiation; was suppressed by pretreatment with either cyclophosphamide, carrageenan, silica particles, anti-bone marrow serum or anti-thymus serum. The many unique identical characteristics of these two effector mechanisms indicates that they represent two manifestations of the same basic phenomenon of natural immunity. This is in accord with other data indicating that GR to BMT is directed at Hh antigens which, like TL antigens, may in some mouse strains appear on both leukemic cells and normal hemopoietic cells.

Animals↗
PubMed1975

Fowl immunoglobulins: quantitation and antibody activity during Marek's disease in genetically resistant and susceptible birds.

Five-week-old birds of resistant (N) and susceptible (P) genetic lines were inoculated with the JM strain of Marek's disease (MD) virus. MD occurred only in P-line birds; one-third had died by the end of the experiment (63 days after inoculation). Sera were examined for antibodies (precipitating, virus neutralizing,and fluorescing), and immunoglobulins were measured. Antibodies were associated with immunoglobulin classes by density gradient centrifugation and utilization of specific antisera to gowl immunoglobulins in indirect immunofluorescence. Precipitating antibodies were found in both lines; they first appeared 7 days after inoculation in P-line birds and 14 days after inoculation in N-line birds, but thereafter there was no difference between the two genetic lines. A peak of neutralizing antibody occurred in both lines between 6 and 12 days. Thereafter neutralizing antibodies increased gradually throughout the experiment. Neutralizing antibody levels were at this stage often higher in N-line than in P-line birds. The fluorescent antibody test showed transient immunoglobulin (Ig) M antibody from 7 to 9 days in N-line birds and 5 to 12 days in P-line birds; this corresponded with the initial peak of neutralizing antibody. Antibodies were seen from 7 to 8 days after inoculation and increased gradually durin gthe experiment, generally paralleling the secondary increase in neutralizing antibodies. Ultracentrifugation confirmed the presence of IgM and IgG antibodies as described. Antibodies of the IgA class were not found. The alterations in serum immunoglobulin levels occurred in three phrases: (i) 1 to 9 days postinfection, there was an increase in IgM and IgA compared with uninfected control birds; (ii) 10 to 20 days postinfection, Ig M and IgA levels were lower than in control birds; and (iii) 21 days postinfection, until the end of experiment, IgA returned to normal levels, IgG increased to about eight times higher than in control birds, and IgM in P-line birds returned to normal levels and in N-line birds reached and maintained levels about double those of control birds. Another experiment was designed to examine the separate effects of moving and inoculation of uninfected kidney cells and virus-infected kidney cells. The changes in immunoglobulins observed in the first experiment occurred only after infection with MD virus and were not related to movement or handling stress. It was concluded that no significant primary difference exists in the humoral immune system between fowls resistant and susceptible to MD; all differences could be related to the immunosuppressive effects of MD, which are greater in susceptible birds apparently due to the greater lymphoid tissue damage in these strains.

Animals↗
PubMed1978

Genetic resistance to helminths. The influence of breed and haemoglobin type on the response of sheep to re-infection with Haemonchus contortus.

The influence of genetic factors on acquired resistance to Haemonchus contortus infections in sheep was investigated. Animals whose primary infections were terminated with an anthelmintic failed to develop any immunity against subsequent challenge as judged by worm numbers. Nevertheless, all were better able to retard the development and reduce the fecundity and haematophagic activities of their parasite populations than animals undergoing primary infections. High levels of resistance, as judged by all these parameters, were observed in most animals when the challenge larvae were superimposed on existing worm populations. The patterns of worm establishment and disease indicated that genetic factors operated in determining resistance, since fewer worms became established and less severe clinical and pathophysiological changes were observed in Scottish Blackface than in Finn Dorset sheep with the same haemoglobin type. Similar advantages were displayed by animals with haemoglobin AA and to a lesser extent those with haemoglobin AB over haemoglobin BB types. The importance of breed was further indicated by the occurrence of 'self-cure' in the majority of the Scottish Blackfaces but in only one Finn Dorset. There was no evidence that this reaction was associated with haemoglobin type.

Animals↗
PubMed1976

Genetic resistance to Marek's disease.

A programme to control MD by genetic selection was tested by selecting breeding sires and dams whose progeny were found to have above average resistance to MD following inoculation at day old with infectious material. Under conditions of natural exposure, Australorp pullets from parents selected for resistance had a lower incidence of MD lesions than an unselected Australorp group. In experimentally challenged Australorp chickens the incidence of MD was significantly lower in progeny derived from mating resistant Australorp sires with unselected dams than in progeny from an unselected Australorp line. Under conditions of experimental and natural exposure to MD, crossbred chickens derived from resistant White Leghorn sires and Australorp dams had a lower incidence of MD lesions than the chickens derived from susceptible White Leghorn series and unselected Australorp dams.

Animals↗
PubMed1976

Mechanisms of genetic resistance to Friend virus leukemia in mice. II. Resistance of mitogen-responsive lymphocytes mediated by marrow-dependent cells.

Friend leukemia virus suppresses the proliferative responses of normal thymus-dependent (T) and bursa equivalent-dependent (B) lymphocytes from spleen, thymus, lymph node, and bone marrow to mitogens. The suppressive effect of Friend virus complex (FV) requires fully infectious virions. Friend erythroleukemic cells, washed to removed extracellular virus, fail to suppress concanavalin A (Con-A)-induced mitogenesis of normal spleen cells. This indicates that FV does not mediate its immunosuppressive effect via transformed erythropoietic cells. The in vitro suppressive effect of FV on lymphocyte mitogenesis is under host genetic control. Spleen, bone marrow, and thymus cells from strains of mice susceptible to FV-induced leukemogenesis in vivo were quite susceptible to the suppressive effects of FV in vitro. On the other hand, similar cells from strains of mice such as C57BL/6 resistant to Friend erythroleukemia, were quite resistant to in virto immunosuppression by FV. Mitogenesis of splenic T cells from resistant B6 mice, previously treated with 89Sr, became susceptible to suppression by FV. This indicated that the in vitro resistance of lymphocytes to FV-induced suppression is not an intrinsic property of T cells, but is controlled by marrow-dependent (M) cells which are selectively eliminated by treatment with 89Sr. M-cell function does not develop in mice less than 3-wk old. The Con A response by thymus cells from 2-wk-old B6 mice was susceptible to suppression by FV, further supporting the concept that M cells may regulate the genetic resistance to FV.

Age Factors↗