PubMed Health⌕ Search

Biomedical subjects

M Giovarelli

Publications and source records attributed to M Giovarelli.

At least 91 records · Page 5Linked to original sources
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

Interaction of H-2 and non-H-2 genes in spontaneous resistance to adenocarcinoma ADK-1t in F1 mice.

The genetic control of spontaneous resistance in vivo to increasing doses of a poorly immunogenic spontaneous adenocarcinoma (ADK-1t) of BALB/c origin was studied in F1 hybrid mice. The spontaneous resistance of homozygous parental BALB/c mice was not increased in F1 hybrids of BALB/c and BALB.B or BALB.K mice, even with small tumor challenges (10(3) cells). By contrast, it was significantly enhanced in F1 hybrids of BALB/c and several strains on A or B10 background. Resistance due to the acquisition of a new set of background genes was, however, markedly enhanced or suppressed by the presence of particular alleles located within or closely linked to the H-2 complex, as demonstrated by increasing the tumor challenge to 10(4) or 10 (5) cells. Spontaneous resistance, effective even with high tumor inocula, thus depended on a complex interplay between background and H-2 genes.

Adenocarcinoma↗
PubMed1980

Strain- and sex-linked effects of dietary polyunsaturated fatty acids on tumor growth and immune functions in mice.

In the present paper, we studied the influence of different levels of dietary polyunsaturated fatty acids (PUFA) on the immune system and tumor growth in young mice. Female BALB/c mice fed a PUFA-rich diet display an enhanced body growth, proliferative response to mitogens in vitro, and rate of growth of a spontaneous transplantable adenocarcinoma as compared to PUFA-poor diet-fed females. Such effects are, however, limited by sex and strain background genes located outside the H-2 complex. In effect, the influence of dietary PUFA content is evident in female but not in male BALB/c mice. Moreover, in female DBA/2 mice with the same haplotype (H-2d) of the major histocompatibility complex as that of BALB/c mice, low dietary PUFA determines a reduced tumor growth only, but it does not affect body growth and proliferative response to mitogens in vitro.

Adenocarcinoma↗
PubMed1979

Lymphokine production in primary mixed lymphocyte culture (MLC). III. Alloantigen signals cell-cell interactions involved in migration inhibition factor and immune interferon release.

The alloantigen differences stimulation migration inhibition factor (MIF) and immune interferon (i-IF) release in primary one-way murine mixed lymphocyte cultures are reported. Differences at H-2 and Mls coded alloantigens induce both MIF and i-IF release, while the differences at multiple minor histocompatibility antigens induce MIF release only. Both MIF and i-IF release are T-lymphocytes dependent events. However, while T-lymphocytes are sufficient for MIF release, the presence of macrophages is required for i-IF release.

Animals↗