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Biomedical subjects

T M Chused

Publications and source records attributed to T M Chused.

At least 91 records · Page 5Linked to original sources
PubMed1979

Expression of xenotropic murine leukemia viruses as cell-surface gp70 in genetic crosses between strains DBA/2 and C57BL/6.

Flow microfluorometry was used to assess levels of xenotropic murine leukemia virus envelope-related cell-surface antigens (XenCSA) expressed on lymphocytes of mice derived from crosses between C57BL/6 (B6) and DBA/2 (D2); 24 recombinant inbred strains (BXD RIs) and 62 backcross mice were studied. The results suggest that XenCSA expression is affected by more than one gene but that the predominant influence is exerted by a single semidominant gene apparently located on chromosome 4 at or in close proximity to the Fv-1 locus. Studies of spontaneous virus production in B6D2F1 X D2 mice suggest that this locus may also affect production by spleen cells of xenotropic MuLV registering in a fluorescent antibody assay of mink lung cells.

Animals↗
PubMed1979

Differences in the clinical manifestations of sicca syndrome in the presence and absence of rheumatoid arthritis.

In this restrospective study we review the clinical features of patients with the sicca syndrome in the presence and absence of rheumatoid arthritis. All patients were followed at the National Institutes of Health for at least five years after the diagnosis of sicca syndrome was established. Twenty-two patients had sicca syndrome alone, and 21 patients had definite rheumatoid arthritis and the sicca syndrome. Rheumatoid arthritis tended to precede the developement of sicca syndrome. The mean age at diagnosis of sicca syndrome is the same in both groups. No significant differences in serum innumoglobulins, the third component of complement (C3), rheumatoid factor titer and salivary histopathology were found. However, the clinical features were quite distinct. Patients with sicca syndrome alone had a significantly greater frequency of recurrent parotitis, Raynaud's phenomenon, purpura, lymphadenopathy, myositis and renal involvement. The clinical characteristics of these two groups coupled with the known serologic and genetic differences suggest that sicca syndrome alone is a distinct pathologic entity.

Arthritis, Rheumatoid↗
PubMed1979

Phenotypic and functional effects of the motheaten gene on murine B and T lymphocytes.

Lymphoid cells from C57BL/6 mice homozygous for the me gene exhibit multiple phenotypic and functional abnormalities from early as one week of age. In the B cell population these include a reduction in the frequency of detectable surface Ig+ cells, alterations in the level of expression of surface IgM and IgD, an increase in the frequency of large cells, plasma cells and TNP-specific plaque forming cePS. Together these findings provide strong evidence for polyclonal activation of B cells. The high level of expression of xenotropic MuLV gp70 by me/me spleen and lymph node cells provides further evidence for lymphoid cell activation. In preliminary studies, me/me T cells appeared to be phenotypically and functionally less affected by the me gene. The distribution of Thy 1.2 on the surface of spleen and lymph node T cells varied from low to normal and the mitogenic responses to Con A and PHA were depressed. It remains to be determined what the basic deficiency in me/me mice is and whether it affects primarily B cells or all lymphoid cells.

Animals↗
PubMed1979

Variations in expression of xenotropic murine leukemia virus genomes in lymphoid tissues of NZB mice.

Lymphocytes from Thy, Sp, LN, and BM and NZB mice were tested for expression of X-MuLV genomes as cell surface gp70 (XenCSA) or infectious virus. The results demonstrate major dissociations for these parameters of X-MuLV expression in different lymphoid compartments and suggest that factors involved in T lymphocyte differentiation modify the levels of expression in these two modes.

Animals↗
PubMed1978

B lymphocyte antigens in sicca syndrome.

All individuals tested in this study with sicca syndrome, a human autoimmune disease, bear two immunologically distinct and genetically unrelated B lymphocyte antigens that appear similar to the immune response associated (Ia) antigens of the mouse. The genes coding for these two antigens are present in only 37 and 24 percent of normal controls. In animal models Ia antigen genes are closely linked to immune response genes. Our findings suggest that two such genes may be required for the development of sicca syndrome.

Adolescent↗
PubMed1978

Immune complex glomerulonephritis in sicca syndrome.

In three patients with the sicca syndrome (Sjögren's syndrome), who were followed for one to seven years, glomerulonephritis developed. None of these patients fulfilled the diagnostic criteria for systemic lupus erythematosus. All of these patients had circulating immune complexes as detected by the Clq binding assay. Glomerular histology by light and electron microscopy revealed changes compatible with membranoproliferative glomerulonephritis in two of the patients and membranous glomerulonephritis in the third. All patients showed rapid improvement in renal function following moderate doses of corticosteroids. In addition, the treatment decreased the level of circulating immune complexes in two patients who were followed for a sufficient period of time.

Adult↗
PubMed1978

Increased risk of lymphoma in sicca syndrome.

The risk of cancer was ascertained in 136 women with sicca syndrome followed at the National Institutes of Health (NIH). Seven patients developed non-Hodgkin's lymphoma from 6 months to 13 years after their first admission to NIH. This was 43.8 times (P less than 0.01) the incidence expected from the rates of cancer prevailing among women of the same age range in the general population during this time. In addition, three cases of Waldenström's macroglobulinemia occurred in this study group. Eight patients developed cancers other than lymphoma, similar to the number expected based on the rates prevailing in the general population. Patients with a history of parotid enlargement, splenomegaly, and lymphadenopahy had an increased risk of lymphoma. These clinical conditions did not appear to be early manifestations of undiagnosed lymphoma but rather seemed to identify a subgroup of patients with sicca syndrome with marked lymphoid reactivity, who had a particularly high risk of subsequently developing lymphoma.

Adult↗
PubMed1977

Sjögren's syndrome associated with HLA-Dw3.

Sjögren's syndrome is associated with a serologically defined histocompatibility antigen of the HLA-B locus, HLA-B8. Another closely linked locus, HLA-D, determines lymphocyte-defined cell-surface antigens. In laboratory animals such antigens are closely linked to immune response genes. To determine whether Sjögren's syndrome is primarily associated with an HLA-D antigent or with HLA-A and HLA-B antigens as well as HLA-Dw3, which is known to be in linkage disequilibrium with HLA-B8. We found the primary association of association of Sjögren's syndrome to be with HLA-Dw3, which we observed in 84 percent of patients with Sjögren's syndrome in the absence of rheumatoid arthritis as compared to 24 percent in controls (P less than 0.00001). The frequency of HLA-B8 and HLA-Dw3 in patients with both Sjögren's syndrome and rheumatoid arthritis did not differ from that in controls. Patients with Sjögren's syndrome and rheumatoid arthritis comprise genetically distinct groups.

Adult↗
PubMed1977

Sjögren-type syndrome after allogeneic bone-marrow transplantation.

Four patients, treated for hematologic disorders with bone-marrow transplants from HLA-identical siblings, spontaneously complained of dry eyes 8 to 12 months after transplantation. Four allograft recipients and two recipients of autologous bone-marrow transplants were evaluated for xerophthalmia and xerostomia. Three allogeneic marrow recipients had evidence of keratoconjunctivitis sicca, and two had decreased parotid gland function. All four allograft recipients had minor salivary gland histopathology identical to that of Sjögren's syndrome. The severity of symptoms and histologic lesions corresponded with the severity of chronic graft-versus-host disease. In addition, one patient developed sclerodermatous skin changes, another had discoid lupus erythematosus, and two patients had laboratory evidence of cholestasis. None of the patients had autoantibodies but all had hypergammaglobulinemia. In contrast, none of the recipients of autologous bone marrow had clinical, laboratory, or histologic findings resembling Sjögren's syndrome.

Adolescent↗
PubMed1977

Demonstration of activation of B lymphocytes in New Zealand black mice at birth by an immunoradiometric assay for murine IgM.

We have developed a highly specific and sensitive "two-site" immunoradiometric assay for murine IgM in which antigen bound to immobilized antibody reacts with affinity-purified radiolabeled antibody. We utilized the sensitivity of this assay to study the rate of IgM secretion in short-term cultures by spleen cells from the autoimmune strains, New Zealand Black (NZB) and New Zealand Black by New Zealand White F1 hybrid (BW), and from normal (C57BL/6, DBA/2, NZW) mice. The temperature dependence of IgM secretion in short-term cultures, its pentameric structure, and the similar viability of NZB and normal strain spleen cells indicate that active IgM synthesis is being measured. We observed that the splenic B lymphocytes of NZB and BW mice, in contrast to normal strains, produce IgM in vitro at birth. By 6 to 8 weeks of age NZB and BW spleen cells produce 40 times more IgM than spleen cells from normal strains of mice. The IgM produced in vitro by splenic lymphocytes from NZB and BW mice is not absorbed by synegeneic or allogeneic thymocytes or erythrocytes.

Animals↗
PubMed1976

Macrophage requirement for the in vitro response to TNP Ficoll: a thymic independent antigen.

The in vitro antibody-forming cell response of mouse spleen cells to the thymic independent synthetic polymer, TNP-Ficoll, was found to require the presence of either macrophages or 2-mercaptoethanol. The TNP-Ficoll response and that to the thymic dependent antigen, sheep erythrocytes, demonstrated the same degree of macrophage dependence. However, macrophage-depleted spleen cells which did not produce plaque-forming cells responded normally to T and B cell mitogens. Comparison of the antibody-forming cell response of macrophage-depleted spleen cells in the presence and absence of 2-mercaptoethanol indicated that either macrophages function 10 to 100 times more efficiently in its presence or that 2-mercaptoethanol partially replaces the function of macrophages.

Animals↗
PubMed1975

Increased frequency of HL-A8 in Sjogren's syndrome.

The histocompatibility antigen, HL-A8, was found to be elevated in patients with Sjogren's syndrome. Among 24 patients, the frequency of HL-A8 was 58% compared to 21% among controls (P less than 0.001 after correction). With the addition of this disorder to the list of other autoimmune diseases associated with HL-A8, it now seems possible to postulate a single basis autoimmune defect gene in high linkage disequilibrium with HL-A8.

Adult↗
PubMed1975

Inhibition of proliferation of lymphoma cells and T lymphocytes by suppressor cells from spleens of tumor-bearing mice.

We have recently demonstrated suppressor cells in spleens of mice bearing tumors induced by Moloney murine sarcoma virus (MSV) which were non-T cells and inhibited phytohemagglutinin Molney (PHA)-induced DNA synthesis of syngeneic normal spleen cells. From the present study, the suppressor cells appeared to be macrophages since they were radioresistant, inactivated by carrageenan, and removed by adherence columns and an iron/magnet technique. We have also found that suppressor cells were still fully active when added 16 hr after the mitogen, thus indicating that early mitogen-induced changes were not the target of suppressive action. It appeared that suppressor cells inhibited metabolic events related to the initiation of DNA synthesis and that they had a selective effect on proliferation-dependent lymphocyte effector functions. PHA-induced cytotoxic reactivity which in our system is largely independent of DNA synthesis was not depressed but actually enhanced in MSV spleens. Cytotoxicity of MSV spleen cells against syngeneic lymphoma cells was unaffected by suppressor cells whereas lymphocytes stimulation by mitomycin C-treated syngeneic lymphoma cellls was inhibited. MSV spleen cells also inhibited DNA synthesis of cultured murine lymphoma cells. This function was only slightly diminished after treatment with anti-omicron serum plus guinea pig complement. Furthermore, spleen cells from MSV tumor-bearing nude mice were as effective as spleen cells from their heterozygous littermates, thus suggesting that T lymphocytes are not the main effector cells of inhibition of lymphoma cell DNA synthesis. The inhibitor cells were radioresistnant, inactivated by carrageenan, and removed by adherence columns and the iron/magnet technique. These data strongly suggest that the inihibitor cells of lymphoma cell DNA synthesis are macrophages and that they belong to the same group of cells as the suppressor cells of PHA-induced lymphocyte proliferation.

Animals↗