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Biomedical subjects

M Andreis

Publications and source records attributed to M Andreis.

At least 37 records · Page 2Linked to original sources
PubMed1977

Macrophage migration inhibitory factor in rheumatoid pericarditis.

The pericardial effusion in a case of rheumatoid pericarditis was studied to determine whether immune complexes and mediators of cellular immunity, represented by migration inhibitory factor (MIF), were present. MIF-like activity was detected in the pericardial fluid, but only traces of immune complexes were revealed by ultracentrifugation. The MIF-like activity was partially characterized by column fractionation and sugar inhibition tests. The role of lymphokines in the pathogenesis of this case of rheumatoid pericarditis is strongly suggested.

Aged↗
PubMed1977

Phagocytosis of immune complexes by polymorphonuclear leucocytes in patients with Felty's syndrome.

The possible role of phagocytosis of circulating immune complexes by neutrophils in the production of the neutropenia of Felty's syndrome has been investigated. Normal neutrophils phagocytosed massive inclusions from the sera from twelve of fifteen patients with Felty's syndrome when incubated with these sera. Such inclusions were phagocytosed from only three of fifteen patients with seropositive RA who did not have Felty's syndrome. Normal neutrophils were more effective than patient neutrophils with regard to phagocytosis of inclusions from the patients' serum suggesting a defect in phagocytic function of Felty's neutrophils. The titre of granulocyte-reactive antinuclear antibodies did not appear to be related to the degree of neutropenia. The data suggest that phagocytosis of circulating immune complexes by neutrophils may interfere with the function of these cells in combating infection and also render them susceptible to removal from the circulation thus leading to the development of neutropenia.

Antibodies, Antinuclear↗
PubMed1975

Lymphokines in rheumatoid synovitis.

In antigen-induced experimental arthritis of rabbits, a macrophage migration inhibitory factor was released from the inflamed synovial tissues. A migration inhibitory factor, blastogenic factor, and B-cell-stimulating factor were also found in human rheumatoid synovial fluids and culture supernatants of rheumatoid tissue explants. Joint fluids from patients with inflammatory conditions other than RA sometimes also displayed these activities. OA fluids were usually inactive. At present, little is known of the origin or role in vivo of the lymphokine-like activities observed in the joints of rheumatoid patients. In related experiments, injection of lymphokine-rich antigen-free lymphocyte supernatants into normal rabbit knee joints produced a synovitis characterized by lining layer hyperplasia and infiltration of the sublining layer by macrophages. The lymphocytic and plasmacytic components seen in active antigen-induced synovitis were absent. It seems likely that some of the changes observed in active chronic synovitis are mediated by soluble factors of the lymphokine variety.

Animals↗
PubMed1975

Experimental arthritis produced by injection of mediators of delayed hypersensitivity.

Synovitis was produced in the rabbit knee by repeated intraarticular injection of a preparation of mediators of cellular immunity. The mediators were prepared by incubation of KLH with lymph node cells of animals previously immunized with KLH in Freund's adjuvant. Following three intraarticular injections, a chronic synovitis resulted in which hyperplasia of the lining layer and infiltration of the sublining layer occurred. The cell types in the sublining layer were predominantly histiocytes and fibroblasts. These experiments demonstrate that mediators of cellular immunity may produce a chronic inflammatory reaction when injected repeatedly into normal joints. They indicate that the cellular immune response may play a role in the development of the synovitis of immunologically induced arthritides.

Animals↗