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V Colizzi

Publications and source records attributed to V Colizzi.

At least 109 records · Page 6Linked to original sources
PubMed1988

Low doses of recombinant interleukin-2 enhance delayed type hypersensitivity to PPD in mice infected with Mycobacterium bovis-BCG and fed a diet supplemented with vitamin A acetate.

Mice infected intravenously with high doses of M. bovis, strain BCG, showed a marked impairment of delayed-type hypersensitivity to PPD evaluated in vivo as skin test and in vitro as splenocyte blast transformation. Furthermore, this state of unresponsiveness is partially reversed either by the intraperitoneal injection of high doses of IL-2 or by feeding mice a diet supplemented with vitamin A acetate (VAA) at least 6 weeks before the BCG injection. This paper shows that low doses of recombinant IL-2 together with a supplementation of VAA in the diet at the moment of BCG infection is sufficient to induce in mice a positive skin reaction and blast transformation to PPD.

Animals↗
PubMed1988

Induction and regulation of cytotoxic T cells by microbial antigens and recombinant interleukin 2.

The proliferation and development of cytotoxic T cells was investigated in human peripheral blood mononuclear cell (PBMC) cultures stimulated with an antigenic extract from Candida albicans (MPPS), or with the purified protein derivative from Mycobacterium tuberculosis (PPD), or with human recombinant interleukin 2 (rIL-2). Microbial antigen- and rIL-2-induced cytotoxic T cells were able to lyse both natural killer (NK) sensitive and resistant targets. No correlation was observed between the development of T cell cytotoxicity and interferon (IFN) production in vitro. The addition of anti-class II monoclonal antibodies at the beginning of MPPS/PPD-stimulated cultures inhibited the cell proliferation, IFN production and T cell cytotoxicity, while all these cellular activities were not inhibited by anti-class II antibodies in rIL-2-stimulated cultures. Finally, antibodies to class I determinants inhibit T cell cytotoxicity, suggesting a role of such determinants in the development of the non-adaptive immunity to microbial infections.

Adult↗
PubMed1987

Epstein-Barr virus-transformed B cells process and present Mycobacterium tuberculosis particulate antigens to T-cell clones.

We have analyzed the presentation of mycobacterial antigens by Epstein-Barr virus-transformed human B (EBV-B) cells to mycobacteria-specific T-cell clones and lines, and to purified resting T cells. EBV-B cells were able to process and present not only soluble forms of antigen, such as PPD and the expressate preparation of M. tuberculosis strain H37Rv, but also particulate forms of antigen, such as whole mycobacterial H37Rv or M. bovis organisms. Electron microscopy studies demonstrated the capacity of EBV-B cells to phagocytose mycobacterial cells in 18 hr and pulsing experiments confirmed that an 18-hr of incubation is required for an efficient processing and presentation of mycobacterial determinants to T cells. The processing of whole-H37Rv particulate antigen by EBV-B cells was inhibited by the lysosomotrophic compound chloroquine and by high doses of irradiation. Finally, the analysis of the presentation of soluble and particulate mycobacterial antigens by PPD-positive and PPD-negative EBV-B cell clones has shown a preferential presentation of both forms of antigen by PPD-positive EBV-B clones.

Antigen-Presenting Cells↗
PubMed1987

Inhibition of contact sensitivity to oxazolone by the calmodulin inhibitor trifluoroperazine.

Topical application of trifluoroperazine (TFP), a calmodulin inhibitor, on the skin of CBA mice previously immunized with 2-phenyl-4-ethoximethylene-oxazolone (oxazolone) blocks the expression phase of contact sensitivity. More detailed analysis of the TFP-mediated inhibition of contact sensitivity shows that TFP significantly suppresses the passive transfer of contact sensitivity when added in vitro to oxazolone-immune cells at a molar concentration of 10(-4) -10(-5). Furthermore, the DNA synthesis of draining lymph node cells from immune mice challenged with oxazolone was suppressed when cultured in the presence of TFP. The exposure of spleen and lymph node cells from immune animals to recombinant IL-2 fails to modify the TFP-mediated inhibition of passive transfer and cell proliferation. The TFP topical application opens the possibility to use this compound in the treatment of delayed hypersensitivity-caused skin disorders.

Administration, Topical↗
PubMed1986

Nonspecific T suppressor factor (nsTsF) cascade in contact sensitivity: nsTsF-1 causes an Ly-1+2- I-A+ immune T cell to produce a second, genetically restricted, nsTsF-2.

We studied the mode of action of the nonspecific T suppressor factor (nsTsF-1) made in the picryl (TNP) system when T acceptor cells armed with antigen-specific TsF are triggered by antigen in the context of I-J. This suppressor factor does not inhibit the passive transfer of contact sensitivity directly, as shown by its failure to inhibit passive transfer by immune cells deprived of I-A+ cells. Its immediate target is an immune, antigen-specific, Ly-1+2-, I-A+ T cell. This cell, which may be regarded as a T suppressor effector cell (Ts-eff-2), produces nsTsF-2 when exposed sequentially to nsTsF-1 and antigen. This nsTsF subsequently inhibits the passive transfer of contact sensitivity. The action of nsTsF-2 is MHC genetically restricted. As the nsTsF-2 bears I-A determinant(s), this raises the possibility that it may act by combining with the recognition site for I-A on the T cell that mediates contact sensitivity.

Animals↗
PubMed1986

Mechanism of action of an antigen nonspecific inhibitory factor produced by human T cells stimulated by MPPS and PPD.

Human T lymphocytes cultured in vitro for 5 days with C. albicans purified polysaccharide (MPPS) and with purified protein derivative (PPD) from M. tuberculosis produce an antigen nonspecific inhibitory factor(s) (nsINH). nsINH blocks antigen-driven cell proliferation and the development of natural killer cells (NK) when added at the beginning of peripheral blood mononuclear cell culture. Analysis of the mechanism of action shows that nsINH inhibits the production of interleukin 2 (IL-2), the expression of IL-2 receptor (Tac antigen), and the synthesis of immune interferon (IFN). The biochemical characterization of nsINH shows that the suppressive activity is acid (pH 2.5) and temperature (56 degrees C) resistant. Gel filtration analysis indicates a molecular weight of 30-35K and 60-65K. These results suggest a role for nsINH in the down regulation of the lymphokine cascade.

Candida albicans↗
PubMed1986

Analysis of lysozyme-specific immune responses by synthetic peptides. I. Characterization of antibody and T cell-mediated responses to the N-terminal peptide of hen egg-white lysozyme.

The immunological reactivity against the N-terminal region of hen egg-white lysozyme (HEL) has been investigated by a synthetic peptide (PHEL) comprising residue 1-18 of HEL and by an analogue peptide (PREL) in which phenylalanine at position 3 is substituted by tyrosine. Both peptides are immunogenic in (C57BL/10 X DBA/2)F1 mice genetically responder to HEL. In C57BL/6 mice, genetically nonresponder to HEL, PREL induces anti-peptide antibodies that also bind to PHEL whereas PHEL is not immunogenic. Thus, a single amino acid substitution in a synthetic peptide converts a nonresponder mouse strain into a responder one. Anti-PHEL antibodies demonstrate a higher binding to HEL than anti-PREL antibodies, indicating that phenylalanine at position 3 is important for induction of anti-peptide antibodies able to recognize native HEL. At the T cell level the two peptides show very high bidirectional cross-reactivity between themselves and with HEL for interleukin 2 production, antigen-specific proliferation and delayed-type hypersensitivity response, whereas conservation of phenylalanine at position 3 is required for induction of suppressor cells cross-reactive with HEL. This indicates that the N-terminal region of HEL contains epitope(s) able to induce the same level of helper T cell activity as the native HEL molecule. However, helper T cells do not discriminate between PHEL and PREL whereas phenylalanine at position 3 is critical for HEL-specific suppressor T cell induction.

Animals↗
PubMed1986

Immunoregulation of lysozyme-specific suppression. III. Epitope-specific amplification of immunosuppression induced by monoclonal suppressor-T-cell products.

The hen egg-white lysozyme (HEL)-specific suppression induced by soluble molecules produced by a monoclonal T-cell lymphoma line (LH8-105) obtained from HEL-specific suppressor T lymphocytes has been examined. Injection of I-J+ molecules from LH8-105 cell culture supernatant (TsFa) in HEL-primed mice during the afferent phase of the response induced Lyt-2+ second order suppressor T (Ts) cells which, upon transfer into HEL-CFA-primed syngeneic recipients, inhibit the delayed-type hypersensitivity (DTH) response to HEL. Transfer of spleen cells from TsFa-injected mice primed with HEL or human lysozyme suppresses the DTH response to HEL in recipient mice whereas this response is not affected by cell transfer from ring-necked pheasant egg-white lysozyme (REL)-primed and TsFa-injected mice, indicating that induction of second order Ts by TsFa is specific for a lysozyme epitope including phenylalanine at position 3. Fine antigenic specificity of second order Ts-cell induction is confirmed by similar results obtained upon injection of TsFa in mice primed with HEL N-terminal synthetic peptide or with an analog in which, as in REL, phenylalanine has been substituted by tyrosine at position 3. The same fine antigenic specificity observed in the induction of second order Ts cells is also present in the expression of TsFe suppressive activity. The similar antigenic specificity of Tsa and Tse suggests that Tse cells could result from amplification of the Tsa cell population or these two cell subsets could reflect different maturation stages of the same cell type rather than distinct T-cell populations activated in cascade.

Animals↗
PubMed1986

Nonspecific inhibitor of DNA synthesis elaborated by T-acceptor cells. II. Requirements for its production and action.

The production of a nonspecific inhibitor of DNA synthesis (nsINH) appears to be one of the final events in the T-suppressor cell circuit in mice exposed to contact sensitizers. We report here that: The nsINH suppresses the proliferative response to a polyclonal T-cell mitogen, concanavalin A (Con A), regardless of the dose of Con A used. It also suppresses DNA synthesis in lymphoid cells stimulated with alloantigens. This suppression can be completely eliminated by adding exogenous interleukin 2 (IL-2). DNA synthesis in lymphoid cells exposed to nsINH before the proliferative stimulus is uninfluenced so that activation of the lymphoid cells at the same time as exposure to nsINH seems to be a requirement for its action. Since the activity of nsINH can be absorbed by activated Lyt-1+ or Lyt-2+ lymphocytes, the early activated T cell appears to be a target of the action of nsINH. The production of nsINH is abolished or severely reduced by adult thymectomy. Natural killer (NK) cells are resistant to nsINH action and no interferon (IFN)-like activity can be demonstrated in nsINH preparation using a conventional assay for IFN.

Animals↗
PubMed1986

Effects of dexamethasone on human natural killer cell cytotoxicity, interferon production, and interleukin-2 receptor expression induced by microbial antigens.

Dexamethasone inhibits the expression of the interleukin-2 receptor, the synthesis of immune interferon, and the development of natural killer cells when added to peripheral blood mononuclear cells cultured with soluble microbial antigens (purified protein derivative and a polysaccharide extract from Candida albicans [MPPS]) or human recombinant interleukin-2.

Antigens, Bacterial↗
PubMed1986

An overview of T-suppressor cell circuits.

This review gives an overview of two main suppressor circuits. In its complete form, the first circuit form has an early acting Ts-inducer that behaves like a T-helper cell for the production of idiotype-directed Ts-transducer or antigen-directed Ts-effector cells. In this circuit, the T-suppressor effector cell (Ts-eff) produces antigen-specific T-suppressor factor (TsF). This has a mode of action through the T-acceptor cell (T-acc), a cell that requires immunization, but not specific immunization, for its production. This cell, when armed with TsF-eff and then triggered with antigen and I-J, releases nonspecific TsF that blocks the passive transfer of contact sensitivity. It also blocks the production of IL-2. The biological significance of the complexities of this circuit is discussed in relation to the control of unresponsiveness and the handling infection and antigenic variation of microorganisms. The second set of suppressor cells, T suppressor afferent cells, inhibits only when given early in the immune response but differs from the Ts-inducer by lacking an obligatory mode of action through the Ts-eff/T-acc circuit. In general, the antigen-specific T-helper and T-suppressor factors have a two-chain disulfide-bonded structure. One chain carries the antigen-binding site and the other chain MHC-related determinants. Both chains are required for biological activity, and the genetic restriction in this complementation implies that the antigen-binding chain has a recognition site for MHC determinant(s). The generalization can be made that the MHC-related determinants carried by the factors and the genetic restriction in their induction, in their action, and in the interchain complementation between their separated chains all map to the same region of the genome. This is intelligible on the assumption that the T-cell receptor on the cell that produces the factor has a recognition site for antigen and MHC determinants and that the antigen-binding chain of secreted factor has the same properties.

Animals↗
PubMed1986

Regulation of immune interferon production during the response to soluble microbial antigens.

Human peripheral blood mononuclear cells (PBMC) stimulated in vitro with purified protein derivative (PPD) or with a Candida albicans polysaccharide extract (MPPS) released immune interferon (IFN) and interleukin 2 (IL-2). Kinetic studies showed a biphasic production of IFN with maximum levels at days 3-4 and days 5-6 of culture. In contrast, the IL-2 production is only observed at days 2-3 of culture. The relationship between IFN and IL-2, analysed both in responder and nonresponder PBMC cultures, showed that the early peak of IFN production appears to be IL-2 independent whereas the second peak seems strictly related to the presence of IL-2 culture. Furthermore, monoclonal antibodies against class I and class II products of the major histocompatibility complex (MHC) inhibited IFN production when added at the beginning of culture, whereas only anti-class I antibodies interfered with the release of IFN when added to antigen-primed lymphocytes.

Adult↗
PubMed1986

Inhibition of lymphocyte mitogenesis in mice infected with Newcastle disease virus: viral interference with the interleukin system.

Spleen cells from mice infected with Newcastle disease virus (NDV) fail to proliferate when cultured with allogeneic cells or with concanavalin A (Con A). This failure is not due to impairment of interleukin-1 (IL-1) production or to a lack of accessory cell function as stimulator cells from NDV-infected mice induce DNA synthesis in the mixed lymphocyte reaction. However, spleen cells from NDV-infected mice fail to produce detectable amounts of interleukin-2 (IL-2) when stimulated with mitogenic doses of Con A and do not respond to exogenous IL-2-containing preparations. Furthermore, absorption experiments suggest that cells from NDV-infected mice fail to bind appreciable amounts of exogenous IL-2. All these events seem to be infection-dependent, as cells from mice injected with ultraviolet-inactivated NDV (UV-NDV) behave normally.

Animals↗
PubMed1985

I-A region genetic restriction in the production and action of an antigen-specific T-helper factor which bears I-A region determinant(s).

Antigen-specific T-helper factor (ThF) augments the contact sensitivity reaction induced by the injection of small numbers of picrylated cells into mice. ThF was produced by injected picrylated spleen cells into the footpads and taking the 24-hr culture supernatant of the regional lymph node cells. Analysis showed that there was a genetic restriction in the induction of ThF, between these picrylated cells and the mouse making the ThF, which maps to the I-A region. This finding suggests that the receptor on the T cell which makes ThF, and by implication ThF itself, bears recognition site(s) for both antigen and I-A. ThF was then prepared from mice painted on the skin with picryl chloride, and the genetic restriction in its action was investigated. There was a requirement for genetic matching between the mouse producing the ThF and the final recipient which mapped to the I-A region. The genotype of the picrylated cell used as a source of antigen was unimportant. This I-A genetic restriction, together with the finding that ThF bears at least some I-A determinants, suggests that ThF may act by binding to the picrylated cells used as a source of antigen through its antigen-binding site and hence provide the I-A determinants needed for the recognition of antigen in the context of self-MHC. The present findings add to the list of antigen-specific factors which have a two-chain structure and show genetic restriction in their induction, action, and in the interaction between their chains which maps to the same region as the MHC-related determinant(s) which they bear.

Animals↗
PubMed1985

Immunosuppression by cell-free translation products from monoclonal antigen-specific suppressor T cell mRNA.

Polypeptides synthesized in a rabbit reticulocyte lysate system directed by mRNA from the T cell line LH8-105, obtained by radiation leukemia virus-induced transformation of hen egg-white lysozyme (HEL)-specific suppressor T lymphocytes, are able, when injected into mice, to specifically suppress the antibody response and delayed-type hypersensitivity to HEL. The suppressive activity exerted by in vitro translated proteins appears to be independent from post-translational modifications. These in vitro translated polypeptides display fine antigenic specificity in immunosuppression and bind to HEL but not to the closely related ring-necked pheasant egg-white lysozyme immunosorbents. Suppressive molecules obtained by cell-free translation of LH8-105 mRNA or by culture supernatant of LH8-105 cells display, by gel filtration, a similar molecular mass of about 82-90 kDa.

Animals↗
PubMed1985

Infection of mice with Newcastle disease virus inhibits the T suppressor afferent cell circuit which regulates contact sensitivity to picryl chloride.

The interaction between Newcastle disease virus (NDV) and the suppressor cell circuit which regulates the induction phase of contact sensitivity reaction to picryl chloride (Pcl) was investigated. NDV infection impairs the activity of the T suppressor afferent cells (Ts-aff) which inhibit DNA synthesis in the draining lymph nodes of mice specifically sensitized with Pcl and the development of contact sensitivity. The inhibitory effect of NDV was evident when the virus was administered up to 2 days before or at the same time as the injection of picrylsulfonic acid; this effect required infectious virus, as NDV inactivated by ultraviolet irradiation failed to inhibit Ts-aff activity. Taken together with the previous finding that the T suppressor efferent cell is unaffected by NDV, the present results support the view that contact sensitivity reaction to picryl chloride is regulated by two distinct T-suppressor-cell circuits.

Animals↗
PubMed1985

The role of dendritic cells in the initiation of immune responses to contact sensitizers. I. In vivo exposure to antigen.

Twenty-four hours after skin painting mice with picryl chloride (PIC) there was a four- to fivefold increase in the numbers of dendritic cells (DC) isolated from the lymph nodes. These DC initiated primary proliferative and cytotoxic responses when added to cultures of normal syngeneic lymph node cells. The proliferative response was enhanced when the donors of the responding lymph node cells were sensitized with the same antigen. Contact sensitivity developed in syngeneic mice injected into the footpads with 30,000-50,000 DC from lymph nodes of mice painted with picryl chloride 1 day previously. Thus, 1 day after skin painting mice, there were dendritic cells in the draining lymph nodes which were able both to initiate primary stimulation of lymphocytes in vitro and to sensitize recipient mice to give specific delayed hypersensitivity reactions.

Animals↗