PubMed Health⌕ Search

Biomedical subjects

D Segre

Publications and source records attributed to D Segre.

11 recordsLinked to original sources
PubMed1979

Inhibition of the humoral response by spleen cells from cyclophosphamide-treated mice.

Spleen cells obtained from mice injected with cyclophosphamide (200 mg/kg body weight) suppressed the secondary IgG antibody response of memory cells to a T-dependent antigen, DNP-HGG, in Millipore diffusion chambers. Significant suppression (greater than 50%) was found from 5 to 14 days following cyclophosphamide treatment, with peak suppression (86%) on day 7. The primary IgM antibody response to DNP-Ficoll, a T-independent antigen, was not suppressed by these cells. In contrast, suppression was observed in the primary IgM response to sheep red blood cells, a T-dependent antigen. In addition, treatment of the suppressor cell population with anti-Thy-1 serum and complement did not inhibit suppressor activity. We concluded that the suppressor activity was not attributable to a typical T cell, and that the target of suppression was not a B cell. Preliminary evidence suggests that the suppressor activity is regulated, directly or indirectly, by a T cell.

Animals↗
PubMed1978

A time study of the requirement for carrier-specific helper cells in the response of mice to dinitrophenylated keyhole limpet hemocyanin.

The anti-hapten response of spleen cells from mice primed with hapten-carrier (dinitrophenylated keyhole limpet hemocyanin) was decreased by depletion of T cells during the first four days after secondary antigenic stimulation, but was unaffected when the T cells were depleted on day 5. The response of cultures that were depleted of T cells prior to secondary antigenic stimulation was restored by addition of carrier-primed cells during the first two days of culture, partially restored on day 3, but not at later times. Thus, T cells were required only at about day 4 of a secondary response to a T-dependent antigen that peaked on day 8. Autoradiography experiments showed that the frequency of antigen-binding cells increased with time regardless of the presence of T cells in the cultures. We conclude that helper T cells are not required for B cell proliferation, but are required for the differentiation of B cells to antibody-secreting cells.

Animals↗
PubMed1977

[Gastric leiomyoma. Presentation of a case].

The only case of gastric leiomyoma observed at the S. Croce Hospital of Cuneo, in over 15 years of surgical activity, is described. On the basis of the literature on the subject, the clinical aspects of the disease are then discussed.

Adult↗
PubMed1976

[Our experience with reparative and derivative operations for non-cancerous lesions in the extrahepatic bile ducts].

17 reparative operations on the bile ducts, 7 of which were immediate (5 for peroperative lesions and 2 for "spontaneous" lesions) and 10 reoperations to deal with sclero-cicatricial lesions, were studied. 7 reconstructive operations (plastic or end-to-end anastomosis) and 10 derivative operations with a preference for hepato- or choledocho-jejunostomy on defunctionalized loop were carried out. The former were reserved for lesions without or with minimum loss of substance, the latter for extensive lesions. Operative mortality is high and higher still in immediate interventions. Long term results were good in all cases but one.

Adult↗
PubMed1976

Humoral immunity in aged mice. I. Age-related decline in the secondary response to DNP of spleen cells propagated in diffusion chambers.

The secondary response of young-adult and old BC3F1 mice to DNP was assessed by boosting spleen cells from primed mice with DNP-KLH, propagating them in diffusion chambers implanted into irradiated recipient mice, and by counting the DNP-specific PFC. There was no difference between young-adult and old cells in the antigen dose response and in the kinetics of the immune response. There were marked differences in the magnitude of the peak response. The response of 2-year-old mice was significantly smaller than the response of young-adult mice. Two and one half-year-old mice had the smallest response. In the old mice, there was an inverse correlation between the number of nucleated cells in the spleen and the log of the number of PFC.

Aging↗
PubMed1976

Humoral immunity in aged mice. II. Increased suppressor T cell activity in immunologically deficient old mice.

Mixed cultures of DNP-primed spleen cells from old and young BC3F1 mice in diffusion chambers yielded significantly fewer secondary PFC than expected from the numbers of PFC found when young and old spleen cells were cultured alone. There was a negative correlation between the log of the number of PFC found in cultures of old spleen cells alone and the degree of immunosuppression exerted by the cells. The immunosuppressive effect was abolished by pretreatment of the old spleen cells with anti-theta serum and complement. Thus, the effect was attributed to the presence of large numbers of suppressor T cells in the spleen of primed old mice. No suppression was found in mixed cultures of spleen cells from old unimmunized mice and young primed mice.

Aging↗
PubMedDate not supplied

Age-related changes in B and T lymphocytes and decline of humoral immune responsiveness in aged mice.

The activity of the immune system declines in an age-related fashion, after reaching a peak in young-adult animals. Although this pattern has been well documented, the mechanisms responsible for the decline of immune potential in senescence have not been fully elucidated. At the same time, it has become apparent that the immune response depends on complex interactions among different cell types. We review the results of the analyses of B- and T-lymphocyte function and activity in the humoral responsiveness of aged mice that have been performed in a number of laboratories, with a variety of experimental techniques. We conclude that an increase in T-cell suppressor function is the first immunologic lesion of aging in mice. This is followed by a decrease in T-cell helper function and finally by a loss of B-cell function.

Aging↗