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Biomedical subjects

E Clerici

Publications and source records attributed to E Clerici.

At least 19 recordsLinked to original sources
PubMed1991

Reduced natural killer cell activity and IL-2 production in malnourished cancer patients.

Natural killer (NK) cell activity was measured in the peripheral blood mononuclear cells (PBMC) from malnourished (MN) and well-nourished (WN) cancer patients and in healthy controls. A marked depression of NK activity was observed in MN cancer patients with moderate protein-calorie malnutrition (PCM), but not in WN cancer patients nor in the healthy controls. The depression of NK activity did not correlate with the localisation of the tumour, patient's age or body weight reduction. The defective NK activity of PBMC from MN cancer patients was restored to normal by rIL-2, but not by alfa-rIFN. Parenteral nutrition of MN patients with the proper amount of proteins and calories quickly corrected the depressed NK activity, indicating a central role of malnutrition in the genesis of their immune disfunction. PBMC from MN cancer patients produced lower amounts of IL-2, as compared with healthy controls, when stimulated in vitro; the most frequently affected were the responses to recall antigens such as influenza virus vaccine (FLU), while those to allogeneic PBMC (ALLO) and phytohaemagglutinin (PHA) were less affected. However, for each patient the ability to produce IL-2 in vitro did not correlate with NK activity, thus showing how the impairment of NK activity is not subsequent to a decreased production of endogenous IL-2. In summary, it can be concluded that malnutrition, rather than malignancy, plays a major role in the immune dysfunction of cancer patients.

Adult↗
PubMed1991

Influence of sex steroids on the antigen-specific primary antibody response in vitro.

The effect of 17 beta-oestradiol on an Ag-specific primary antibody response in cultures of human peripheral blood mononuclear cells (PBMC), stimulated by sheep red blood cells (SRBC) was studied. Addition of 17 beta-oestradiol (2 x 10(-9) to 100 x 10(-7) M final concentration), to PBMC from adult blood donors significantly augments the Ag-specific immune response. PBMC incubated with the anti-oestrogen agent Tamoxifen (10(-6) to 10(-8) M final concentration) prior to culture were no longer stimulated to produce an increased number of anti-SRBC antibodies as compared to control cultures. The augmentation of the immune response to SRBC in treated cultures is due to an inhibiting effect of 17 beta-oestradiol on CD8+ T suppressor (Ts) cells, since preincubation with Tamoxifen, which acts by competitive binding with CD8+ oestrogen receptors reverses such an effect. The antibody response of PBMC X-irradiated with 10 Gy before culture, (in order to decrease the suppressor activity), and then stimulated with SRBC without addition of oestrogen, was increased about 40% as compared to that of unirradiated PBMC. No further increase by addition of 17 beta-oestradiol to PBMC irradiated cultures was obtained. These findings confirm that oestrogen influences the regulatory radiosensitive CD8+ Ts cells subset. T helper (Th) cells and antigen presenting cells (APC) were not modulated by oestrogens. Our study demonstrates direct immunoregulatory effects of oestrogen on human PBMC and suggests that female sex hormones and anti-oestrogens agents may play a role in the pathogenesis and treatment of some autoimmune diseases and tumors, such as breast cancer.

Antibody Formation↗
PubMed1990

[Malnutrition as a cause of decreased NK activity in cancer patients].

In this work we investigated the effects of malnutrition on the immune response in neoplastic patients. We studied the basal NK activity of 34 neoplastic malnourished patients and 10 neoplastic not malnourished patients and a control group of blood donors, by a standard 51 Cr release assay against K562 cells. We observed that the neoplastic malnourished patients have a defective NK activity in spite of a normal number of NK cells, as ascertained by HNK-1 monoclonal antibodies. The reduced NK activity of the neoplastic malnourished patients is only partially restored by rIFN alpha 2a but is normalized by rIL-2 stimulation. We also found that the endogenous IL-2 production from some of these patients is slightly reduced as compared to controls. On the contrary, there are no significative differences between the neoplastic not malnourished patients and blood donors, as concerns the NK activity. These results suggest that nutritional status plays a very important role in the maintenance of an efficient immune response in neoplastic patients.

Adult↗
PubMed1988

Macrolidic antibiotics: effects on primary in vitro antibody responses.

The effect of two macrolidic antibiotics, josamycin and erythromycin, on the primary immune response in cultures of human peripheral blood mononuclear cells (PBMC), were studied using a soft agar hemolytic plaque assay. Both compounds induced an appreciable reduction in the primary antibody response in total PBMC cultures. The removal of plastic-adherent cells, however, profoundly modified the effect of macrolides on the immune response. Both josamycin and, to a lesser extent, erythromycin enhanced, rather than suppressed, the antibody response. Furthermore, the macrolide-induced immunodepression in cultures of total PBMC was completely reversed by the addition of catalase (8000 U/ml). Taken together, these findings suggest that the macrolide-induced depression of the antibody response depends upon the presence of adherent monocytic cells and is mediated by the production of hydrogen peroxide.

Antibody Formation↗
PubMed1988

[Graft versus host reaction and hybrid resistance in experimental models and clinical practice].

The "F1 hybrid transplantation law" states that F1 hybrids of two unrelated inbred strains of mice accept grafts from either parent strain while neither parent accept grafts from the F1 hybrid. However, there are two notable exceptions to this law. Indeed, parent grafts containing immunologically competent cells (spleen cells, bone marrow etc.) react against the F1 normal hosts in which they are placed. In the absence of a host-versus-graft reaction, the graft-versus-host reaction (GvH) may dominate the field and cause untoward reactions which not only negate any benefit derived from the graft, but also cause significant, and often fatal morbidity of the host, that is, a GvH Disease (GvHD). Furthermore, irradiated F1 mice are refractory to the grafting of parental bone marrow, lymphoma cells and normal lymphocytes because of a restriction by non-co-dominant, besides that of codominant MHC-H2 genes. These non-co-dominant genes have been designated Hh genes for Hybrid histocompatibility and the phenomenon itself, hybrid resistance. The cellular, humoral and genetic mechanisms involved in the GvH and hybrid resistance production are explained and discussed in the first, while in the second section of the present review, their equivalent in three human pathological situations are taken into consideration. We focus in detail on two principal immunologic aspects of human bone marrow transplantation: GvH and hematopoietic engraftment; each one of these immunologic aspects has considerable impact on the course and outcome of marrow transplantation in humans. The allograft implantation between HLA-genetically-identical siblings, HLA-aploidentical family members or HLA-phenotypically identical donor-recipient couples are herewith examined, while the autologous bone marrow rescue approach is not taken into consideration. The outcome of bone marrow transplantation depends not only on the degree of genetic disparity between the donor and the recipient, but also on the underlying disease. Bone marrow transplantation is the therapy of choice for patients with aplastic anemia, severe combined immunodeficiency (SCID) and other genetic and acquired immunodeficiency, some leukemias and a few other diseases, mainly if HLA-genetically-identical siblings are available. However, in many cases such siblings are not available. Therefore, the probability of acute or chronic GvHD or graft rejection increases significantly. The clinical and pathologic manifestations, the prognostic factors, and the treatment and prevention of acute and chronic GvHD are illustrated in detail.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1987

[Antibody response in cultures of lymphocytes from patients with Hodgkin's lymphoma: role of monocytes].

In the present study we investigated the role of monocytes and of their soluble products (prostaglandins and hydrogen peroxide) in the modulation of the immune response in 50 untreated patients with Hodgkin's disease (HD) compared with a group of healthy donors. The primary response in vitro has been studied with the method of haemolytic colonies in soft agar. A defective in vitro antibody production has been observed in HD patients. Both Indomethacin addition (10(-6) M, final concentration) and depletion of plastic adherent cells, slightly increased the number of haemolytic areas in cultures from HD patients as compared with healthy donors. Similarly, the addition of catalase (8000 U/ml) which destroys H2O2, that is the main mediator of monocytes suppressor activity in normal subjects, did not restore the response of peripheral blood mononuclear cells (PBMC) from HD patients. These results suggest that monocytic cells play a minor role, if any, in the depression of the immune response in HD patients.

Adolescent↗
PubMed1986

The interference of antibiotics with antigen-specific antibody responses in man.

The effect of a series of antimicrobial drugs on human antigen-specific primary antibody response in vitro was investigated. Of the five agents tested, only streptomycin and gentamicin induced an appreciable reduction in the antibody response; penicillin G, rifampin and amikacin had a poor or irregular effect. The precise mechanisms of action of these substances on mammalian cells remain to be elucidated since an assessment of their capacity to interfere with the immune system is of particular importance in those patients with induced or acquired immunodeficiencies. In this respect, we provide an inexpensive and sensitive method for the preliminary screening of potentially immunosuppressive drugs.

Animals↗
PubMed1985

Monocyte mediated modulation of the antibody response in vitro.

Human peripheral blood monocytes (PBMC) were isolated by Ficoll-Hypaque density gradient and then fractionated by differential adhesion to plastic surface. Adherent cell-depleted PBMC, non-readherent fraction and firmly adherent fraction so obtained from PBMC, PBMC themselves and a mixture of the above cells, were then sensitized in vitro with sheep erythrocytes (SRBC) so as to produce a primary antigen-dependent, antigen-specific antibody response. It appears that adherent cell-depleted PBMC produce about twice as many haemolytic areas as compared to total PBMC (from 43 to 85). If depleted PBMC are co-cultured with firmly adherent or non-readherent cells, the number of haemolytic areas goes down to 19 or up to 102, respectively. Functional, histochemical, immunochemical and morphological data suggest that the inhibiting firmly adherent fraction is composed of typical phagocytizing cells, while the enhancing cells of the non-readherent fraction are similar to the dendritic cells described in human blood and some lymphoid organs, which do not exhibit active pinocytic activity, but are the principal accessory cells needed to stimulate lymphocyte responses.

Antibody Formation↗
PubMed1979

An assay for estradiol preceptors using a staphylococcal protein-A--estradiol antibody adsorbent.

Antiestradiol antisera were raised in rabbits by immunization with a steroid-protein conjugate Whole antisera and purified antiestradiol antibodies were reacted with heat-killed and formalin-fixed bacteria from the protein-A-bearing strain of Staphilococcus aureus (Cowan I, NCTC 8530). The bacterial immunoadsorbent was used to estimate the estrogen-receptor proteins contained in several specimens from human breast carcinoma. Since the affinity constant for estradiol of antiestradiol antibodies is about 10(8) M-1 while those for breast estrogen-receptor complexes are about 10(9) to 10(10) M-1, it is possible to remove the free steroid from a reaction mixture containing tissue cytosol, radio-labelled estradiol, and the antiestradiol bacterial adsorbent by pelleting the bacteria at low-speed centrifugation. The radiolabelled estradiol molecules bound to their receptors remain in the supernatant and can be easily counted by liquid scintillation counting. The results obtained by this technique on specimens of human breast carcinomas compared more than satisfactorily with those obtained, on separated aliquots from the same specmens, by the dextran-coated charcoal method, according to the EORTC group (1973). The versatility, specificity and stability of the antiestradiol bacterial immunoadsorbent recommend its use, rather than that of charcoal-coated dextran and other non-specific steroid adsorbents, in the mass screening of patients with breast carcinoma which could be amenable to hormonal therapy.

Animals↗
PubMed1978

Immunoadherence and complement in cancer-bearing mice.

Shortly after grafting of Ehrlich ascites carcinoma cells, the serum of tumour-bearing mice loses the capacity to mediate immunoadherence phenomena, because of a sharp decrease in the concentration of C3b and C3d, while the cellular receptors for such factors are unaffected by tumour growth. It is suggested that complement is consumed through the alternative pathway which is activated during the inflammatory responses accompanying tumour growth.

Animals↗
PubMed1976

T-cell precursors in mice bearing the Ehrlich ascites tumors.

Mice bearing Ehrlich ascites tumors and challenged with sheep erythrocytes produced fewer plaque-forming cells than did normal mice. At the same time the immunosuppression developed, the number of T lymphocytes in the thymus and spleen were reduced significantly. In the spleen, the number of B lymphocytes remained constant during carcinogenesis, whereas that of the macrophages increased significantly, as compared to the controls. In this paper, we demonstrated that the mechanism responsible for thymus and spleen depletion of theta antigen-bearing cells had to be ascribed to fewer T-lymphocyte precursors in the bone marrow of mice with cancer. The reduction of T-lymphocyte precursors was probably caused by the same "soluble factor(s)" produced by Ehrlich ascites tumor cells, which also interfered with the proliferation of myelopoietic stem cells in the bone marrow of mice with this neoplasm, as we previously reported. By performing several reconstitution experiments of lethally X-irradiated hosts, we determined that the immunodepression by Ehrlich ascites tumor cells was readily reversible, and the alteration of the T:B lymphocyte ratio in the spleen had a minor function, if any, in the pathogenesis of the immunosuppression.

Animals↗