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Biomedical subjects

G Forni

Publications and source records attributed to G Forni.

At least 163 records · Page 9Linked to original sources
PubMed1984

In vitro reeducated T helper cells from sarcoma-bearing mice inhibit sarcoma growth in vivo.

Spleen cells from BALB/c mice bearing a small, but already clinically evident transplantable methylcholanthrene-induced sarcoma (CE-2) are not able to release interferons, proliferate and perform a cytotoxic response against CE-2 cells, nor able to inhibit their growth in vivo in a Winn-type neutralization assay. They can, however, be reeducated to be efficiently active against the tumor. Spleen cells (25 X 10(6) ) and 10(6) mitomycin C-treated CE-2 cells were cultured in 20 ml of medium for 6 days. The surviving spleen cells were then cultured for another 5 days under the same conditions plus 10% interleukin 2-rich supernatant from a clone of EL-4 thymoma cells stimulated with phorbol-12-myristate-13-acetate. Reeducated spleen cells were then able to inhibit the growth of a 100% lethal dose of CE-2 tumor cells in a Winn-type assay, even when the lymphocyte to tumor cell ratio was 5:1. In vitro, they released interferon-gamma when restimulated by CE-2 cells, and displayed a marked cytotoxicity in an 18-hr assay. Their in vivo tumor-neutralizing activity was not affected by the removal of Lyt-2.2+ lymphocytes, nor by the absorption of cytolytic cells on CE-2 monolayers. The absorbed cell population no longer contained cytotoxic cells nor cytotoxic cell precursors, but still contained CE-2-specific helper cells, which assist the in vitro induction of cytotoxic cells by normal thymocytes. Lyt-2.2-, noncytotoxic, reeducated spleen cells from tumor-bearing mice thus play an important role in tumor neutralization in vivo.

Animals↗
PubMed1983

In vivo requirements for the immune recognition of L1210 leukemia cells by allogeneic T-lymphocytes.

The resistance of normal BALB/c mice (H-2d) against the L1210 Ha leukemia of DBA/2 mouse (H-2d) origin is due to the T-lymphocyte-dependent reaction towards DBA/2 multiple minor histocompatibility antigens (Mhas). These Mhas are displayed by the leukemic cells, though in a poorly immunogenic manner. The simultaneous presence of mitomycin C-inactivated DBA/2 leukocytes induces a significantly stronger T-lymphocyte-dependent reaction. This efficient presentation of target Mhas is restricted to Ia+ leukocytes. Their presence significantly increases BALB/c resistance, even when they are injected 3 days after the L1210 Ha challenge.

Animals↗
PubMed1983

H-Y antigen entrance into the immune system: relationship between lymphokine release, proliferation, cytotoxicity and delayed hypersensitivity.

In this paper we tested in parallel lymphokine release, proliferation, cytotoxicity and delayed hypersensitivity (DTH) reactions to H-7 antigen in high responder C57Bl/6 female mice. In vivo priming and in vitro restimulation are required in order to activate all the in vitro T-lymphocyte functions, and the ability to locally transfer DTH reactions. By contrast, a discrepancy is found between in vitro and in vivo tests of T-lymphocyte reactivity. In primed mice DTH reactions are evident, whereas no in vitro reactivity to H-Y is detectable.

Animals↗
PubMed1983

Rous sarcoma virus-induced tumours in mice. II. Contribution of H-2 and non-H-2 alloantigen barriers to tumour immunogenicity in vivo.

The features of the immune recognition of a murine fibrosarcoma induced by Rous sarcoma virus were tested in histocompatible and histoincompatible mice. No evidence of a genetic regulation of spontaneous reactivity to tumour-associated antigens was found in various histocompatible F1 hybrids. Incompatibility in multiple minor histocompatibility antigens triggers a host reaction incapable of causing tumour rejection in some cases. The growth rate of incipient tumours is unaffected, whereas that of already visible tumour masses is significantly delayed. Admixture to the challenge of inactivated leukocytes bearing the same minor histocompatibility antigens as the tumour triggers a significantly stronger reaction. The reaction of hosts incompatible in the H-2K or H-2DL regions is quite efficient. However, the intensity of the immune reaction of H-2DLs antigens displayed by tumour cells is markedly dependent on the alleles of genes located in the central regions of the H-2 complex.

Animals↗
PubMed1982

Suppressor macrophages in tumor-bearing mice. Inconsistency between in vivo and in vitro findings?

The growth of a spontaneous adenocarcinoma (ADK-1t) of BALB/c mice (H-2d, MIsb) induces progressive hyporesponsiveness of spleen cells stimulated with PHA or irradiated leukocytes from DBA/2 strain (H-2d, MIsa) in mixed leukocyte culture. This hyporesponsiveness is due to the suppressor activity of macrophage-like cells, since it is abrogated by passage over nylon-wool columns, pretreatment with carrageenans, or carbonyl iron and magnet. BALB/c mice bearing greater than 20 mm mean diameter ADK-1t tumors, and displaying a drastic impairment of T lymphocyte reactivity in vitro, were challenged with the P815 mastocytoma of the DBA/2 strain. These mice rejected increasing numbers of P815 cells to the same extent as normal BALB/c mice. The reactivity towards P815 is abrogated by 450 rad, and can be reconstituted by the adoptive transfer of 2 X 10(7) normal T lymphocytes in either normal or ADK-1t bearing BALB/c mice. These data show that a discrepancy exists between the capacity of T lymphocytes from ADK-1t bearing mice to react against DBA/2 cells tested in vitro or in vivo, and indicates that great caution should be exercised in predicting the responsiveness of the immune system on the basis of in vitro data on the suppressor activity of macrophages.

Adenocarcinoma↗
PubMed1982

Immune recognition of tumor cells in vivo. I. Role of H-2 gene products in T lymphocyte activation against minor histocompatibility antigens displayed by adenocarcinoma cells.

Challenges from ADK-1t adenocarcinoma cells of BALB/c (H-2d, Mlsb) mouse origin are rejected by DBA/2 (H-2d, Mlsa) mice on the basis of differences in a limited number of minor histocompatibility antigens. This T lymphocyte-dependent reaction is highly specific, and efficiently triggered only by Ia+ leukocytes infiltrating the tumor mass. ADK-1t challenges depleted of Ia+ infiltrating BALB/c leukocytes grow and kill DBA/2 mice, whereas the simultaneous injection of Ia+-inactivated BALB/c leukocytes induces tumor rejection. The expression of Mlsb-incompatible determinants on the Ia+ BALB/c leukocyte membrane is irrelevant in the induction of this efficient T lymphocyte reaction against BALB/c minor histocompatibility antigens. By contrast, a critical requirement is H-2 matching between the Ia+ leukocytes and the recipient mice at the inductive phase of the reaction.

Adenocarcinoma↗
PubMed1982

Rous sarcoma virus-induced tumors in mice--I. Macrophage-mediated natural cytotoxicity.

Lymphoid cells from normal untreated A.SW mice showed a cell-mediated cytotoxicity (CMC) towards Rous sarcoma virus-induced tumor lines in a 48-hr microcytotoxicity assay in vitro, using 3[H]-thymidine prelabeled tumor cells. The tissue distribution of this natural CMC shows high levels of activity in the peritoneal cavity, intermediate levels in bone marrow and spleen, and low levels in lymph node, peripheral blood and thymus. Natural CMC of unstimulated resident peritoneal cells against tumor cells was also found in several strains of mice. This was not dependent on the donor's age, since similar levels appeared in mice aged 1-40 weeks. Passage through nylon wool columns or adherence to the plastic surface of resident peritoneal cells removed cytotoxic activity. By contrast, adherent cell displayed significant CMC levels. Treatment with carbonyl iron powder and magnet decreased peritoneal cell cytotoxicity when performed once and abolished it when repeated. All these results suggest that in mice, natural cytotoxicity against Rous sarcoma virus-induced tumors is primarily mediated by macrophages or macrophage-like cells.

Age Factors↗
PubMed1982

Distinct alloantigens trigger proliferative or nonproliferative T lymphocyte activation in CBA/N, CBA/J, and C3H mice.

Lymphokine release and proliferation take place during one-way murine mixed leukocyte cultures (MLCs) when responder and stimulator cells differ in H-2 alloantigens, whereas a dissociation of these two functions can be observed where there are incompatibilities in non H-2 alloantigens, It is possible that this dissociation depends on different thresholds of activation of the two responses, or that some non H-2 alloantigens selectively activate lymphokine release or proliferation. To investigate this question we used H-2-matched CBA/N, CBA/J. C3H/HN, (CBA/N x CBA/J)F1, and (CBA/N x C3H/HN)F1 leukocytes, both as responder and stimulator cells. CBA/N mice and the male F1 hybrids obtained from CBA/N mothers carry an X-linked immune defect that results in an arrest of B lymphocyte maturation. In the majority of MLC combinations tested, migration inhibition factor (MIF) release and proliferation took place in parallel. However, CBA/N, but not F1 leukocytes, stimulated MIF release and not proliferation by CBA/J responders, whereas C3H/HN leukocytes stimulated proliferative responses but not MIF release by CBA/J responders. Since proliferation and MIF release have a similar threshold of activation, their dissociation indicates that different non-H-2 alloantigens can specifically activate distinct T cell functions. Moreover, previously unsuspected alloantigen differences between CBA/N and CBA/J are revealed by MIF release.

Animals↗
PubMed1982

Interferon production in mixed cultures of murine leukocytes and syngeneic L1210 leukemia cells.

Spleen cells from DBA/2 mice did not proliferate, but released interferon (IFN) when cultured in the presence of mitomycin C-treated syngeneic L1210 leukemia cells apparently free from mycoplasma and common non-oncogenic viral infections. IFN titers reached a plateau after 18 h of culture. The biological activity of this IFN was stable at pH 2 and could be inactivated by antibody raised against alpha and beta-IFN. Removal of phagocytes from the spleen cell suspensions caused a decrease in IFN production. By contrast, suspensions depleted in Thy 1.2-positive cells had an enhanced capacity to produce IFN in response to the L1210 cells.

Animals↗
PubMed1981

Immune depression in Trypanosoma brucei brucei infected mice. Sequential histological and immunological findings.

Pathological findings in various organs and tissues, T and B lymphocyte inability to proliferate towards several mitogens, and the appearance of serum interferon at progressive stages after intraperitoneal infection of BALB/c mice with Trypanosoma brucei brucei are reported. Heavy parasitaemia is evident throughout infection and complete hyporesponsiveness is already present on day 3. A sharp interferon production peak appears after 48 hours. The anatomopathological picture makes it clear that infection is substantially restricted to the blood. Secondary involvement of liver, lung and kidney takes the form of perivascular cuffs. These appear at relatively early stages. By contrast, spleen and lymph nodes appear to be greatly altered.

Animals↗
PubMed1980

Polygenic control of interferon production induced by poly I:C in vivo. Brief report.

Poly I:C-induced interferon production shows quantitative differences in various mouse strains depending on multiple interactions among genes located both inside and outside the major histocompatibility complex. Moreover, circulating interferon levels do not appear to be under direct genetic control but, rather, to depend on the gene-coded intensity of specific recognition of the inducer.

Animals↗
PubMed1980

Bacterial phagocytosis by macrophages from lipopolysaccharide responder and nonresponder mouse strains.

The phagocytic capacity of macrophages from C3H/H3J mice was assessed against lipopolysaccharide-producing (Escherichia coli) and -nonproducing (Staphylococcus aureus) bacteria. Despite their gene-coded unresponsiveness to lipopolysaccharide endotoxin and lymphokines and their defective tumoricidal activity, proteose peptone-induced C3H/HeJ macrophages did not display a defective phagocytic capacity, but rather displayed an enhanced phagocytosis of both bacterial strains compared with macrophages from closely related C3H/HeN mice. Unstimulated peritoneal resident C3H/HeJ macrophages, on the other hand, displayed a normal phagocytic activity toward E. coli and enhanced phagocytosis toward S. aureus.

Animals↗
PubMed1980

Lymphokine production in primary mixed lymphocyte reactions. I. Characteristics of responding and stimulating cells.

The characteristics of the responder and stimulating cells involved in migration inhibition factor (MIF) production in primary 'one-way' mouse mixed lymphocyte reactions (MLR) were analyzed by using an indirect agarose droplet assay. T-lymphocytes are mainly responsible for MIF release, as shown by pretreatment with anti-Thy 1.2 serum plus complement or purification over a nylon wool column. On the other hand, macrophages and B-lymphocytes appear to be optimal stimulating cells. T-lymphocytes as stimulating cells induce MIF release, but to a much lesser degree than macrophages and B-lymphocytes. The kinetics of MIF production in MLR is related to the kind of stimulating cells employed. Lastly, the ability to release MIF is already present in the spleen of 1- to 2-week-old mice, lasts until 20 weeks of age and declines to undetectable levels at 50 weeks of age.

Aging↗