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Biomedical subjects

F Di Padova

Publications and source records attributed to F Di Padova.

60 records · Page 4Linked to original sources

Influence of autologous serum on in vitro reactivity of peripheral lymphocytes of patients with breast cancer.

The influence of autologous serum on DNA synthesis and phytohemagglutinin (PHA) or pokeweed mitogen (PWM) stimulation of peripheral blood lymphocytes from mammary tumor-bearing women has been studied. Blood samples were collected from patients at the 4 stages of the TNM classification who had not undergone any therapeutic treatment. Lymphocyte functions were significantly reduced only in patients with the largest tumors and in the latest stage of disease. Autologous cancer sera inhibited spontaneous DNA synthesis of lymphocytes and did not inhibit lymphocyte stimulation by mitogens. It is possible that unrecognized inhibiting and stimulating factors, possibly acting in synergism with mitogens, are present in mammary cancer sera.

Adult↗

[Susceptibility of leukemias with increased antigenicity to immunological lysis].

Leukaemic sublines obtained following in vivo treatment with antineoplastic drugs present increased antigenic properties and these are transmitted in heredity after suspension of treatment. The pharmaco-altered sublines are rejected by compatible animals with related lymphoma. Susceptibility to humoral and cellular immunological lysis on the part of pharmaco-altered sublines with respect to related lines has been studied. Lymphocytes of C3HC57Bl/10 mise and non-inbred rats immune to histocompatibility antigens of mouse DBA/2 exert the same lysis action towards related cells as towards pharmaco-altered cells. The same susceptibility to lysis on the part of various cell populations was observed with cytotoxic antisera obtained in the same animals. Nor did the immunitary response obtained by inoculating the tumours show any different "fragility" to immunological lysis. Rejection of the pharmaco-altered sublines does not appear to be even partially due to increased fragility with respect to immunitary functions.

Animals↗

p55 and p75 tumor necrosis factor receptors are expressed and mediate common functions in synovial fibroblasts and other fibroblasts.

There is increasing evidence that TNF-alpha is a cytokine of major importance in the pathogenesis of rheumatoid arthritis. Since TNF-alpha mediates its effects via high affinity receptors, we were interested in investigating their expression and function in cells from rheumatoid tissue. Synovial fibroblasts derived from rheumatoid synovial tissue are stimulated by TNF-alpha to proliferate and release cytokines, prostaglandins, proteases and protease inhibitors. We have evaluated through which receptor stimulation of DNA synthesis and the release of the proinflammatory agents, IL-6, IL-8 and PGE2 are induced. It was found that rheumatoid synovial fibroblasts express both the p55 and p75 TNF receptor, in a ratio of 4:1. TNF-alpha-stimulated synovial fibroblast DNA synthesis and the release of IL-6, IL-8 and PGE2 was inhibited by antagonist monoclonal antibodies against either the p55 or the p75 TNF receptor, although the blockade of the p55 TNF receptor had a more potent effect than inhibition of the p75 TNF receptor alone. Similarly, specific monoclonal antibodies, agonistic for either the p55 or p75 TNF receptor stimulated synovial fibroblast DNA synthesis, as well as IL-6, IL-8 and PGE2 release. Both p55 and p75 TNF receptors on dermal and gingival fibroblasts were also involved in TNF-alpha-mediated DNA synthesis and IL-6, IL-8 and PGE2 release, although differences in the levels of DNA synthesis and release of inflammatory cytokines and PGE2 were observed between the three fibroblast types.

Antibodies, Monoclonal↗