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Biomedical subjects

T Maier

Publications and source records attributed to T Maier.

78 records · Page 5Linked to original sources
PubMed1979

Further characterization of thymic suppressor cells and a factor that suppress the generation of cells cytotoxic for a syngeneic tumor in DBA/2 mice.

Antigen-specific suppressor cells and suppressive extracts obtained from the thymuses of DBA/2 mice bearing small syngeneic P815 mastocytomas were compared for their immunogenetic properties and requirements. The assay for specific suppression involved the ability of either cells or extracts to inhibit the primary in vitro cytotoxic response of normal DBA/2 splenocytes to mitomycin-treated P815 cells. It was shown that pretreatment of suooressor cell populations with anti-Iad antiserum plus rabbit complement removed the suppressive activity. Similarly, absorption of the suppressor factor with anti-Iad antiserum removed the suppressive properties of the material. It was found that the suppressor cells, generated in DBA/2 tumor bearers, were capable of specifically suppressing the anti-P815 response of B6D2 F1 radiation chimeras possessing lymphoid cells of the H-2b or H-2t2 haplotype equally as well as they could suppress the response of H-2d-bearing effector cells. This indicates that the suppressor cells are not H-2 restricted with respect to K or D markers on the responder cells in this system.

Animals↗
PubMed1972

Role of the macrophage in natural resistance to salmonellosis in mice.

In vitro, macrophages from normal strain BRVR mice killed Salmonella more quickly than did macrophages from normal strain BSVS mice. Salmonella injected intraperitoneally multiplied more quickly in BSVS mice than in BRVR mice. BRVR macrophages injected intraperitoneally into BSVS mice protected against Salmonella multiplication better than did BSVS macrophages. The populations of peritoneal cells that could be washed from the peritoneal cavity of normal BRVR and BSVS mice were morphologically and numerically identical. In vitro, BSVS macrophages were as efficient as BRVR macrophages in phagocytizing virulent Salmonella. These findings all support the concept that the greater natural resistance of BRVR mice to Salmonella infection may be explained by the greater ability of normal BRVR macrophages to kill ingested Salmonella.

Animals↗
PubMedDate not supplied

Co-occurrence of spondyloarthropathy and connective tissue disease: development of Sjögren's syndrome and mixed connective tissue disease (MCTD) in a patient with ankylosing spondylitis.

Spondylarthropathies (SpA) and connective tissue diseases (CTD) are clinically distinct entities which, at first glance, seem to have little in common. However, a link between SpA and CTD has recently been suggested by a study in which a higher prevalence of Sjögren's syndrome (SS) and sicca symptoms was reported in patients with ankylosing spondylitis (AS) and undifferentiated SpA (1). Another link between SpA and CTD is a possible side effect of a DMARD widely used to treat SpA: sulfasalazine (SAS). SAS was reported to induce antinuclear antibodies (ANA) and systemic lupus erythematosus (SLE)-like syndromes such as drug-induced lupus. This report describes a 54-year-old white male, HLA B27-positive AS patient with some syndesmophytes who, after 15 years of disease, developed SS with salivary gland involvement, Raynaud's syndrome and anti-Ro antibodies. Then, 20 years after the onset of AS, he became acutely ill, suffering severe myositis and myocarditis along with swollen hands and highly elevated autoantibody titers recognizing UIRNP; his condition was interpreted as mixed connective tissue disease (MCTD). The patient had been treated with SAS and azathioprine (AZA) alone several times during the last years because he had not tolerated other DMARDs. A combination of both drugs had been prescribed 3 weeks before a severe flair because of progredient high disease activity with painful peripheral arthritis of the MCP and PIP joints which, however, had not shown radiographic erosions. We describe the rare development of MCTD in an AS patient and report, for the first time, the onset of MCTD potentially triggered by sulfasalazine.

Humans↗