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Biomedical subjects

D Venza-Teti

Publications and source records attributed to D Venza-Teti.

14 recordsLinked to original sources
PubMed1988

Depression by Fc gamma receptor ligands of SRBC-induced IgM-PFC generation in human blood mononuclear cell cultures.

A tissue-culture system to stimulate human peripheral blood mononuclear cells (PBMC) has been employed in which IgM plaque-forming cell (IgM PFC) generation in response to sheep erythrocytes (SRBC) is dependent on macrophages and T suppressor and helper lymphocytes. In this system PBMC from normal subjects give IgM PFC responses ranging from 26 to 938 PFC/culture. Heat-aggregated human IgG or immune complexes present for the duration of culture induce a significant depression of PFC. Unaggregated IgG has no effect on the response or only a moderate stimulatory effect at the highest dose. The results of these experiments are compatible with previous results in a murine system, which indicated that Fc gamma receptor-positive (Fc gamma R+) cells in the suppressor subset are the target for aggregated IgG and induce depression of the PFC response. A similar mechanism may be operating in the human system described here, although the target cell has not been identified. These results may reflect a mechanism of immunomodulation dependent on interaction of Fc receptor (FcR) ligands with FcR, which may play a role in the pathogenesis of immune complex disorders.

Antibody-Producing Cells↗
PubMed1988

Mononuclear cells from rheumatoid arthritis patients exhibit a depressed IgM response to sheep erythrocyte stimulation in vitro.

Human peripheral blood mononuclear cells when cultured for the short term (11 days) produce an optimal IgM plaque-forming cell (PFC) response to sheep erythrocytes, which is dependent on macrophages and T suppressor and helper lymphocytes. With this system we have investigated the PFC response of individuals with rheumatoid arthritis and compared this to the response of normal sex- and age-matched controls and of patients with osteoarthritis. The response of rheumatoid arthritis patients was significantly lower than that of subjects in the other two categories.

Animals↗
PubMed1984

Depression of direct plaque-forming cell response in mouse spleen cell cultures by aggregated IgG2b-induced factors.

Mouse spleen cells were treated with concanavalin A (Con A) or aggregated mouse IgG2b for 48 h in culture. When cells thus treated were added to fresh mouse spleen cell cultures immunized with SRBC they depressed the response of B lymphocytes as measured by enumerating plaque forming cells (PFC) on the fourth day of culture. When supernatant from cells cultured with IgG2b was added to immunized cultures this resulted in depression of PFC generation similar to that observed by addition of treated cells. The depression observed was essentially in the same range as that observed by addition of Con A treated cells or their supernatant. These observations extend previous work suggesting that IgG2b-induced PFC depression may result from activation of suppressor T cells with elaboration of soluble suppressor factors. This mechanism of immunomodulation may be important in the pathogenesis of immune complex disorders.

Animals↗
PubMed1983

Redistribution of mouse spleen cell Fc receptors following treatment with mouse or human aggregated immunoglobulin G.

Mouse spleen cells treated with the Fc receptor ligands mouse IgG2b and human IgG, followed or not by a second antibody, exhibit different patterns of redistribution. In the work reported here we have examined the redistribution of Fc receptors (FcR) after binding of aggregated mouse IgG2b (Alg) or of Alg followed by anti-lg. We were particularly interested in learning whether binding of isologous Alg to FcR is followed by significant redistribution and shedding of Alg-FcR complexes. Mouse IgG2b alone will not induce capping even after 60 min at 37 degrees C. Human IgG induces some capping with minor shedding of complexes. Human IgG followed by anti-IgG readily induces capping by 15 min on 70% of the cells. This treatment also induces capping by 60 min at 20 degrees C on about 80% of the cells with a moderate degree of shedding of complexes. This is in agreement with the concept that the crosslinking required for FcR capping can be best induced with a second antibody. It is of interest, however, that heterologous IgG, unlike isologous, can induce a modest degree of capping and slight shedding even without the second antibody, suggesting that some crosslinking occurs with heterologous IgG.

Animals↗
PubMed1981

Cytochalasin A inhibits B-lymphocyte capping and activation by antigens.

Cytochalasin B (CB) has been shown to be a potent depressant of the antigen-induced clone expansion and terminal differentiation of mouse B-lymphocytes to antibody-forming cells. This effect could be the result of the microfilament-disrupting effect of CB with subsequent inhibition of antigen-sIg complex redistribution, a series of events which seems to be necessary for B-lymphocyte activation. CB is not very active in depressing capping and will inhibit glucose transport. To further investigate the mechanism of action of cytochalasins, the effect of cytochalasin A (CA) on cap formation and plaque-forming cell generation was studied, since CA is less inhibitory of glucose transport and more inhibitory of cap formation. The results presented here indicate that complexes of anti-Ig-sIg will be prevented from capping by as little as 1 microgram of CA, a quantity sufficient to depress markedly the generation of plaque-forming cells to SRBC in culture. These results further confirm our conclusion that the depression of B-lymphocyte activation may be related to the depression of cap formation. It also strongly suggested that inhibition of glucose transport can be regraded as a negligible factor in this depression.

Animals↗
PubMed1980

Effect of prostaglandins on mouse erythrocyte rosette-forming human lymphocytes.

Prostaglandins (PGs) E2 and F2 alpha, preincubated with human lymphocytes for short periods of time inhibit mouse erythrocyte rosette formation. The presence of calcium ions does not influence this effect, which is dose-dependent and relatively temperature-independent. These observations indicate the PG treatment of lymphocytes may be useful to distinguish a subclass of IgM-bearing mouse erythrocyte rosette-forming B lymphocytes, which is sensible to the modulating effect of Pgs.

Animals↗
PubMed1980

Interaction between prostaglandins and human T lymphocytes: effect of PGE2 on E-receptor expression.

E-rosette formation is not modified by preincubation of lymphocytes with prostaglandins (PGs) E1, F1 alpha, and F2 alpha. On the contrary, short preincubation with PGE2 affects active rosette-forming cells (Ea-RFC) and, only slightly, total RFC. This effect appears to be dose-dependent and relatively temperature-independent; it does not require calcium ions. Incubation with a fraction enriched in late RFC showed that PGE2 does not affect late rosette formation. It is postulated that PGE2 may redistribute surface receptors for sheep erythrocytes on T lymphocyte membranes. Thus, sensitivity to PGE2 may be considered another difference between early and late RFC.

Animals↗
PubMedDate not supplied

Lack of effect of exogenous prostaglandins on Fc receptor expression of mouse splenocytes.

Previous work has shown that Prostaglandin E1 (PGE1) and other cyclic AMP elevating agents increase the expression of Fc receptors for IgG (FcR) on the murine pre-B cell lymphoma ABE-8 (Burchiel and Warner, 1980). We have investigated here the effect of Prostaglandins E1, E2, F1alpha, F2alpha on FcR expression of normal mouse lymphocytes. FcR were detected by an indirect fluorescent technique on B lymphocytes. The results show that Prostaglandins in culture did not induced any significant change of FcR + lymphocytes. The results are discussed in terms of the role of FcR in the ontogeny and functions of B lymphocytes.

Animals↗