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Biomedical subjects

M Bennett

Publications and source records attributed to M Bennett.

At least 415 records · Page 23Linked to original sources
PubMed1979

Hybrid resistance to EL-4 lymphoma cells. I. Characterization of natural killer cells that lyse EL-4 cells and their distinction from marrow-dependent natural killer cells.

Natural killer (NK) cells from nonimmunized mice capable of lysing EL-4 (C57BL/6 strain H-2b) tissue culture-adapted lymphoma cells have been analyzed and compared with NK cells which lyse YAC-1 (A-strain, H-2a) lymphoma cells. A correlation was seen in the ability of inbred and B6D2F1 mice to reject C57BL/6 (B6) bone-marrow grafts and the ability of their spleen cells to lyse EL-4 cells in vitro. This suggests that hybrid or hemopoietic histocompatibility antigens, (Hh-1b), relevant in the rejection of B6 stem cells may also be the relevant target structures for the anti-EL-4 NK cells. Certain features of these NK cells are similar to the NK cells reactive against YAC-1 cells. Both types of NK cells are present in athymic nude mice, are not affected by treatment with anti-immunoglobulin plus complement, and are not depleted by techniques that remove macrophages. NK activity against both targets is stimulated 3 d after injection of Corynebacterium parvum, and 24 h after challenge with polyinosinic:polycytidylic acid. Hydrocortisone acetate and cyclophosphamide lead to reduction of NK activity within 2-3 d after administration. However, the anti-YAC and anti-EL-4 NK reactivities differed in several important respects. Treatment of mice with 89Sr, the bone-seeking isotope, to deplete marrow-dependent cells, depleted the anti-YAC-1 but not anti-EL-4 cell functions. Anti-EL-4 NK cells were unaffected by silica particles in vivo or in vitro; the NK cells reactive to EL-4 cells matured functionally much earlier in life (5 d of age) and the function did not decline with age. Irradiated mice reconstituted with syngeneic marrow or spleen cells developed functional NK cells against EL-4 targets before they developed anti-YAC-1 NK cells in their spleen. Thus anti-EL-4 NK cells that express hybrid resistance in vitro appear to differ from anti-YAC-1 NK cells and do not require an intact marrow microenvironment for functional differentiation. Despite differences in the NK-cell types involved in the lysis of YAC-1 and EL-4 cells, these two tumor cells share certain common determinants. This was ascertained both by cold competition and by utilization of YAC-1 and EL-4 cell monolayers as immunoadsorbents. We conclude that Hh-1b is the common antigen present in EL-4 and YAC-1 cells, because B6D2F1 anti-B6 (anti-Hh-1b) cytotoxic T lymphocytes lysed both the tumor cells. Our data suggest that Hh-1b antigen is recognized by both types of NK cells, but that additional determinants must be present on YAC-1 cells. Two models of NK cell lysis compatible with the data are presented.

Animals↗
PubMed1979

Immunosuppression by Friend leukemia virus is H-2 restricted by alloreactive T lymphocytes.

Friend leukemia virus suppresses mitogen-responsive cells in vitro by activating thymus-dependent suppressor cells. The interaction between T suppressor and mitogen-responsive cells is H-2D restricted by a third cell type, called an interfering cell. The interfering cells could be characterized as alloreactive T cells that functionally mature in the spleen at 2 weeks of age and that can be functionally inhibited by mitomycin C, irradiation, and cortisol. Interfering cells are stimulated by H-2D (and not H-2L) alloantigens of the mitogen-responsive cells. H-2D differences between interfering and T suppressor cells are unimportant. Induction of "tolerance" to H-2 alloantigens in semi-allogeneic radiation marrow chimeras resulted in the specific loss of interfering cell function. It is possible that interfering or similar cells participate in other forms of H-2 restriction.

Animals↗
PubMed1979

Effect of age on immune function in terms of chemically induced cancers.

Neonatal, fetal, and very old animals are particularly sensitive to chemical carcinogenesis. Reasons for this increased sensitivity could be due to increased susceptibility of "target" organs or cells, peculiar hormonal levels at these age groups, relatively deficient immune functions, or combinations of these and/or other factors. During the late fetal and first three weeks of neonatal life, the immune system is rapidly maturing, is relatively incompetent, and its diverse components are developing at different rates. For example, thymus-dependent (T) alloreactive cells capable of proliferating in mixed lymphocyte reactions (T helper cells) develop by 7 days of age, but precursors of T killer cells are not competent until approximately 14 days of age. Bursa equivalent-dependent (B) cells capable of generating antibody responses are present in fetal liver but are extremely sensitive to tolerance induction until 10-14 days of age when IgD cell surface receptors are detectable. Marrow-dependent (M) cells responsible for regulation of suppressor cells and for natural cytotoxicity to transformed tumor cells do not mature until 3 weeks of age. In very old animals, the thymus is atrophic and cell-mediated immunity is moderately suppressed. Natural cytotoxicity against tumor cells is less than normal but antibody formation (B cell function) is adequate. Gonadotrophic hormones of the pituitary or placenta are high during pregnancy, the early neonatal period, after the menopause, and in a large fraction of men over 60 years of age. These and other hormones are immunosuppressive and could theoretically facilitate carcinogenesis. The particular immune cell type, if any, responsible for resistance to chemically induced tumors has not been determined. One can only state that susceptibility to chemical carcinogenesis is associated with a relative dysfunction of the immune system and that age is an important factor.

Aging↗
PubMed1979

New motility medium for nonfermenting bacilli.

Researchers compared use of a semisolid agar plate to wet mount examinations of broth cultures (16 to 18 hours) for the detection of motility of 96 reference and clinical strains of gram-negative rods. In this double blind study, 83 nonfermentative and 13 oxidase-producing, fermentative bacilli were tested by the two methods. Overall accuracy of the semisolid agar motility test was 96.8 percent compared to 89.6 percent for the broth method. Reproducibility of agar plate tests using selected reference strains was 100 percent in contrast to 90 percent for broth examinations. These findings indicate that the semisolid agar plate offers a convenient and more accurate method than wet mount examination for determining motility of unusual gram-negative bacilli.

Bacillus↗
PubMed1978

Successful cardiac allografts in syngeneic radiation chimeras.

Successful cardiac allografts were accomplished across the major histocompatibility complex of rats. LEW and F344 (Ag-B2) rats were lethally irradiated and grafted with WF (Ag-B1) hearts on day 0. Either on day 0 or day 2, the hosts were repopulated with syngeneic hemopoietic cells. The best results were obtained (86%) when a mixture of 3.0 x10(7) non-adherent syngeneic bone marrow and thymus cells were used to repopulate the recipients. In contrast, all of the WF to LEW heart grafts were rejected within 30 days if syngeneic thoracic duct and bone marrow cells were used to repopulate the host. Tolerant rats bearing a functioning WF heart graft were able to mount a normal antibody response to SRBC and a proliferative response to Con A. They accepted a second WF heart or a WF kidney graft but rejected WF skin and bone marrow grafts as well as "third-party" ACl or BN hearts. The lymphocytes of tolerant rats had a reduced response to WF antigens as assayed by local or systemic graft-versus-host reactions in (LEW x WF)F1 recipients. Tolerance to the WF hearts was resistant to a large innoculum of normal spleen and lymph node cells. The unresponsive state could be transferred to unirradiated LEW rats with a mixture of spleen, thymus, lymph node and bone marrow cells.

Animals↗
PubMed1978

Prevention of acute porphyric attacks by intravenous haematin.

A thirty-three-year-old female with acute intermittent porphyria (A.I.P.) was having regular attacks of the disease with her menstrual periods. During several of these attacks she received intravenous haematin, which was followed by chemical and clinical remissions. Hormones failed to prevent the regular attacks, which were completely prevented by 200 mg of haematin, given approximately once a week for six months. There were no changes in menstruation. The monthly attacks recurred on withdrawal of haematin.

Acute Disease↗
PubMed1978

Mechanisms of genetic resistance to Friend virus leukemia in mice. IV. Identification of a gene (Fv-3) regulating immunosuppression in vitro, and its distinction from Fv-2 and genes regulating marrow allograft reactivity.

Friend leukemia viru (FV) suppresses the proliferative response of normal lymphocytes to mitogens. The in vitro suppressive effect of FV on lymphocyte mitogenesis is mediated by T-suppressor cells and is under host genetic control. Lymphocytes from strains of mice of the C57BL background (e.g., C57BL/6) are resistant while cells from other strains (e.g., 129 and DBA/2) are susceptible. Genetic analyses utilizing resistant and susceptible parental strains, their F1, intercross and backcross progeny indicated that susceptibility to in vitro suppression is regulated by a single autosomal gene, dominant for susceptibility to suppression. This gene, which is not linked to the H-2 complex, segregated independently of the Fv-2 gene which controls resistance to spleen focus formation in vivo. The gene is also unlinked to the Ir-like genes which regulate the ability of H-2d mice to reject H-2b bone marrow grafts. The gene is therefore designated as Fv-3. Fv-3 may mediate its effect by regulating the numbers and/or functions of T-suppressor cells.

Animals↗
PubMed1978

Cerebral haemorrhage in haemophilia.

A young male haemophiliac child is here described in whom intracerebral haemorrhage required craniotomy and the subsequent insertion of a ventriculo-peritoneal shunt. These procedures can now be attempted in severe haemophilia A because of the ease in clotting factor replacement therapy.

Cerebral Hemorrhage↗
PubMed1978

Mechanism of genetic resistance to Friend virus leukemia in mice. V. Relevance of Fv-3 gene in the regulation of in vivo immunosuppression.

Infection with the Friend murine leukemia virus complex (F-MuLV) suppressed humoral antibody synthesis in vivo and lymphocyte mitogenesis in vitro. Both these effects of F-MuLV were under host genetic control. In vitro suppression of lymphocyte mitogenesis was regulated by a single autosomal gene called Fv-3 that is dominant for susceptibility. Genetic analyses, with the use of the susceptible DBA/2 and resistant B10.D2/n parents, their F1, intercross, and backcross progeny, indicated that a single autosomal gene dominant for susceptibility regulated the in vivo susceptibility to immunosuppression by F-MuLV. Individual [(DBA/2xB10.D2)F1xB10.D2] mice were typed both for susceptibility to F-MuLV-induced suppression of lymphocyte mitogenesis in vitro (an Fv-3 function) and susceptibility to immunosuppression by F-MuLV in vivo. Such an analysis indicated that the same mice that were susceptible or resistant to immunosuppression in vivo were susceptible or resistant to suppression of lymphocyte mitogenesis in vitro. Spearman's rank analysis of the data also indicated that the in vivo and in vitro immunosuppressive effects of F-MuLV were correlated with and not independent of each other. Thus Fv-3, which regulates the effect of F-MuLV on lymphocytes in vitro, also appears to regulate the effect of F-MuLV on antibody-forming cells in vivo.

Animals↗
PubMed1978

Casein-induced experimental amyloidosis. IX. Alterations in marrow dependent function.

CBA/J mice receiving multiple injections of sodium caseinate (CAS) or bovine serum albumin (BSA) were assayed for marrow dependent functions by measuring their ability (i) to reject bone marrow allografts and (ii) to resist Friend virus (FV)-induced suppression of lymphocyte mitogenesis. Mice that developed amyloidosis following 25-30 injections completely lost the ability to reject allogeneic marrow cells, whereas nonamyloid BSA-treated mice had enhanced rejection of marrow allografts. There was increased resistance to the suppressive effects of FV in spleen cells from 'preamyloid' mice receiving CAS injections and nonamyloid mice receiving 10-40 BSA injections. Amyloid mice appeared to be as susceptible to the effects of FV-induced suppression as control (untreated) animals. These data indicate that alterations in marrow dependent function may be related to the pathogenesis of amyloid disease.

Amyloidosis↗
PubMed1978

In vitro activation of suppressor cells from spleens of mice treated with radioactive strontium.

Mice were treated with two 100-muCi injections of 89Sr to deplete marrow-dependent (M) cells. Mice so treated responded normally to immunization with sheep red blood cells (SRBC) in vivo; moreover, spleen cells from 89Sr-treated mice were able to respond to SRBC after infusion into irradiated recipient mice. However, spleen cells from mice treated with 89Sr did not respond to SRBC in vitro and mixtures of normal spleen cells with the latter were also not able to respond in vitro. The discrepancy between in vivo and in vitro responses was abolished by culturing spleen cells for 24 hr before testing their ability to respond to SRBC in the adoptive transfer in vivo. Pretreatment of spleen cells from 89Sr-treated mice with 1000 R of gamma-radiation lessened their suppressive activity. The suppressor cells were detected in spleens of athymic nude mice treated with 89Sr. The suppressive activity, after the 24-hr culture period, was not abolished by irradiation and was active in vivo as well as in vitro. Thus, depletion of M cells by 89Sr results in the appearance within the spleen of thymus-independent suppressor cells, which require a short period of in vitro cultivation before becoming functionally active.

Animals↗