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Biomedical subjects

M Ziff

Publications and source records attributed to M Ziff.

At least 127 records · Page 7Linked to original sources
PubMed1974

Serum heat-labile opsonins in systemic lupus erythematosus.

To study possible mechanisms responsible for the increased susceptibility to infection of patients with active systemic lupus erythematosus (SLE), a study of the serum heat-labile opsonic capacity (HLOC) in such patients was undertaken. With leukocytes from normal donors, the sera of 12 of 30 patients with active SLE demonstrated decreased HLOC for E. coli 075. The phagocytic activity was partially restored by normal serum, suggesting that decreased HLOC was responsible for the defective phagocytosis. While 8 of 10 patients with active SLE and concomitant infections showed deficient opsonic capacity to E. coli 075, only 4 of 20 such patients without infections showed the defect (P = 0.01). None of 12 patients with inactive disease had deficient opsonic capacity. Similar results were obtained with S. aureus 502A as the test bacterium. In the patients surviving infection, recovery of normal serum opsonic capacity was rapid and usually coincided with an increase of serum complement to normal levels. In three patients with active SLE and infection, the causative microorganisms were isolated and opsonic capacity for these organisms tested with the individual patients' sera. In each case, sera obtained at the onset of the infectious episode had low opsonic capacity when compared with normal sera. Serum C3 proactivator levels were low in 9 of 11 sera with deficient opsonic capacity. However, similar low values were found in other SLE sera with normal HLOC, suggesting that other factors of the opsonic system were also depleted. Addition of the classical complement components C1, C4, C2, C3, and C5 to sera with deficient HLOC failed to restore activity. Addition of pure C3 proactivator also failed to restore activity. However, addition of C3 proactivator together with 50 degrees C-heated normal serum restored activity, indicating that factors active at the early steps of opsonic activation via the alternative pathway of complement were necessary to restore opsonic activity. These findings indicate that in active SLE, a decrease of components of the alternate pathway of complement activation results in an acquired defect of serum HLOC and perhaps other related complement-mediated functions. This defect may be an important factor in the increased susceptibility to infections of patients with active systemic lupus erythematosus.

Complement C2↗
PubMed1974

Immunoglobulin in clinically uninvolved skin in systemic lupus erythematosus: association with renal disease.

23 of 42, or 55%, of patients with systemic lupus erythematous had immunoglobulin deposits along the epidermal basement membrane of uninvolved skin (positive lupus band test [LBT]). In patients with low serum complement levels, 91% had a positive LBT), as compared with 15% in those with normal complement levels. The LBT was positive in 70% of patients with clinical and laboratory evidence of renal disease, but in only 31% of patients without renal disease. 81% of patients with the more severe histologic forms of lupus nephritis, i.e., proliferative glomerulonephritis and membranous glomerulonephritis, and positive tests, whereas only 23% with mesangial glomerulitis or normal histologic findings were positive. Immunoglobulins of the same class found in the skin were detected in the glomeruli of patients examined by renal biopsy. These results suggest that there is a relationship between the occurrence of immunoglobulin in the epidermal basement membrane and the presence of the more severe forms of lupus nephritis.

Adolescent↗
PubMed1972

The pathogenesis of chronic inflammation in experimental antigen-induced arthritis. II. Preferential localization of antigen-antibody complexes to collagenous tissues.

In an experimental arthritis induced by injection of bovine serum albumin or egg albumin into the joints of previously immunized animals, it has been demonstrated that the major portion of the radioactively labeled antigens injected was localized to avascular collagenous tissues in the joint, i.e., articular cartilage, menisci, and intra-articular ligaments. The antigens were partially eluted from the tissues with 5 M guanidine solution, but not with acid buffers or by 3 M magnesium chloride. The radioactive material eluted with guanidine was at least 80% precipitable by specific antisera. The radioactively labeled-inducing antigen was identified on the surface of articular collagenous tissues from arthritic joints by radioautography and immunofluorescence. Rabbit immunoglobulin and C3 were demonstrated in the same sites by immunofluorescence. The presence of specific antibody in collagenous tissues was demonstrated by the selective in vitro binding of (125)I-labeled-inducing antigen to menisci from arthritic joints of immunized animals. The evidence obtained indicates that in this model of chronic arthritis, the inducing antigen persists for long periods of time in the form of immune complexes in the surface layers of the intra-articular collagenous tissue. The antigen retained in this form may be responsible for the chronicity of the synovitis by serving as a direct stimulus for the maintenance of prolonged antibody synthesis in the synovium and by providing a source of complement-fixing antigen-antibody complexes for the mediation of joint inflammation.

Animals↗
PubMed1972

Lymphotoxin formation by lymphocytes and muscle in polymyositis.

Muscle pieces from 11 patients with dermatomyositis or polymyositis were incubated with autologous peripheral blood lymphocytes and the supernates examined for the production of lymphotoxin, a mediator of delayed hypersensitivity, using human fetal muscle monolayers as the target cell. In the case of all 10 active patients, production of lymphotoxin was demonstrated. This mediator was also demonstrated when muscle alone was incubated from two patients with extensive cellular infiltration. Lymphotoxic activity was not found in supernates obtained by incubation of muscle from nine control subjects with their autologous peripheral blood lymphocytes. Addition of methyl prednisolone to active cultures inhibited the action of lymphotoxin on the muscle monolayers. Lymphotoxin was not demonstrated when breast tumor tissue from a patient with dermatomyositis was incubated with autologous lymphocytes. The lymphotoxic agent in the active supernates had similar chromatographic properties to those of a sample of purified lymphotoxin. These findings suggest that muscle injury in polymyositis is a result of a cellular immune response to an antigen present in involved muscle tissue.

Adolescent↗
PubMed1971

Response of the rheumatoid synovial membrane to exogenous immunization.

The secondary immune response to tetanus toxoid in 14 patients with rheumatoid arthritis (RA) has been studied in suspension cultures of peripheral blood lymphocytes (PBL) and synovial membrane obtained at synovectomy. Sequential cultures of PBL from three normal subjects established the optimal time of antibody response at 5 days. At this time, the antitetanus antibody produced was predominantly IgG, comprising half of this immunoglobulin fraction. Rheumatoid synovium synthesized 5-9 times more IgG than PBL, expressed as per cent of total protein synthesis, but only negligible amounts of tetanus antibody. The same results were observed in synovial cultures following repeated immunization and after the additional intra-articular injection of tetanus antigen. This marked limitation of the synovium to respond to exogenous antigen in spite of its large immunoglobulin production was considered consistent with a prior commitment of the synovial lymphoid infiltrate to other antigen.

Antibody Formation↗