PubMed Health⌕ Search

Biomedical subjects

V Colizzi

Publications and source records attributed to V Colizzi.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1985

Dissociation between interleukin-1 and interleukin-2 production in proliferative response to microbial antigens: restorative effect of exogenous interleukin-2.

The relationship between the production of interleukin-1 (IL-1) and interleukin-2 (IL-2) after stimulation of human mononuclear cells within an antigenic extract from Candida albicans was analyzed in both responder and nonresponder donors. Culture supernatants from responders contained both IL-1 and IL-2 activity, whereas the supernatants from nonresponders contained only IL-1 and no appreciable IL-2. However, the addition of exogenous IL-2 to nonresponder cultures restored the normal proliferative response. Similar observations were made when cells from mice infected intravenously with high doses of Mycobacterium bovis BCG were cultured; these cells showed a marked impairment of the proliferative response to purified protein derivative. Spleen cells from BCG-induced unresponsive mice failed to produce IL-2 despite the fact that normal IL-1 activity was present in the culture. Again, the addition of exogenous IL-2 fully reversed the proliferative unresponsiveness. Thus, the presence of IL-1 does not necessarily induce production of IL-2, and the proliferative unresponsiveness is therefore due to a primary lack of IL-2.

Animals↗
PubMed1985

Two-chain disulphide-bonded structure of antigen-specific T-helper factor: both chains are necessary for activity and their interaction is I-A restricted.

The molecular structure of the antigen-specific T-helper factor (ThF) which augments contact sensitivity in mice was studied. ThF was split into two types of polypeptide chain by mild reduction and alkylation; one antigen binding (which determined the specificity), the other non-antigen binding. The two chains were, by themselves, inactive but complemented each other and reconstituted biological activity. In addition, a genetic restriction was observed in the complementation of the two chains which mapped to the I-A subregion of the H-2 complex.

Animals↗
PubMed1985

Synthetic peptides in the analysis of the induction and regulation of delayed-type hypersensitivity to lysozyme.

T cells mediating hen egg lysozyme (HEL)-specific delayed hypersensitivity can be activated by synthetic peptides of the 1-18 amino acid residues of hen egg lysozyme. The N-terminal 1-18 peptides of hen egg (PHEL) and ring-necked pheasant lysozyme (PREL) are highly cross-reactive in the induction of T cells mediating delayed hypersensitivity. The N-terminal 1-18 peptides of hen egg and ring-necked pheasant lysozyme (PHEL and PREL) are not cross-reactive in the induction of suppressor T cells, demonstrating that phenylalanine at amino acid residue 3 is critical for the formation of an epitope recognized by T suppressor cells.

Amino Acid Sequence↗
PubMed1985

The control of the contact sensitivity skin reaction: T-suppressor afferent cell blocks the production of antigen-specific T-helper factor.

Lymph node cells from mice painted with the contact sensitizers picryl chloride or oxazolone produce antigen-specific T-helper factor. This is detected by its ability to increase the contact sensitivity response to the injection of small numbers of haptenized spleen cells into the footpads of naive recipients. The production of this T-helper factor is inhibited by the injection of spleen cells from mice given water-soluble, chemically reactive hapten such as picrylsulphonic (trinitrobenzenesulphonic) acid--an agent which induces unresponsiveness. The cells which inhibit the production of T-helper factor are antigen-specific T-suppressor cells. They are sensitive to cyclophosphamide given before the injection of picrylsulphonic acid, but are unaffected by adult thymectomy. In this respect, they resemble the family of Ts-aff which inhibit the development of contact sensitivity, specific antigen-induced lymph node proliferation and the specific IgG response, and differ from the T-suppressor efferent cell (Ts-eff) which acts at the expression stage of the contact sensitivity reaction. These results are fully compatible with the view that the Ts-aff inhibits the development of contact sensitivity by blocking the production of antigen-specific T-helper factor.

Animals↗
PubMed1985

In vivo activity of interleukin-2: conversion of a stimulus causing unresponsiveness to a stimulus causing contact hypersensitivity by the injection of interleukin-2.

The intravenous injection of hapten-modified (picrylated) cells causes unresponsiveness. When conventional or recombinant interleukin-2 (IL-2) is also injected, strong contact sensitivity occurs. This IL-2 is effective when given 7 hr after the injection of the picrylated cells or 2 days later, but has no effect when given beforehand. It is suggested that picrylated cells given intravenously fail to induce contact sensitivity secondary to a failure of IL-2 production, and that IL-2 may be one of the second signals which converts a 'tolerogenic' stimulus into an immunogenic stimulus.

Animals↗
PubMed1985

A non-specific inhibitor produced by Candida albicans activated T cells impairs cell proliferation by inhibiting interleukin-1 production.

Human T lymphocytes cultured in vitro for 5 days with Candida albicans purified polysaccharide (MPPS) produce and antigen non-specific inhibitor (nsINH) which blocks cell proliferation when added at the beginning of the culture. The antigen presenting function of antigen pulsed adherent cells (macrophages) is significantly impaired by incubation in nsINH. Further analysis shows that nsINH blocks the production of interleukin-1 both from human mononuclear cells stimulated with lipopolysaccharide. Furthermore, the production of interleukin-2 (IL-2) is also suppressed when MPPS stimulated cells are cultured in presence of nsINH. However nsINH does not affect the appearance of IL-2 responsive cells as the addition of gibbon IL-2 to the culture fully reverses the suppressive effect of nsINH on blast transformation.

Antigens, Fungal↗
PubMed1985

Monocyte subsets in the production of inhibitory factor by Candida albicans-activated human T cells.

Macrophages are essential for the proliferative response of human T lymphocytes to a purified polysaccharide extract from Candida albicans (MPPS). The role of macrophages as antigen-presenting cells in the production of an antigen non-specific inhibitory factor (nsINH) by MPPS-activated T cells was also investigated. Fc receptor positive (FcR+) or negative (FcR-) plastic-adherent mononuclear cells were used as MPPS-presenting cells, and the results show that the FcR- subset is mainly responsible for the release of nsINH from activated T cells.

Antigen-Presenting Cells↗
PubMed1984

Immunoregulation of lysozyme-specific suppression. I. Induction and suppression of delayed-type hypersensitivity to hen egg-white lysozyme.

Subcutaneous immunization with hen egg-white lysozyme (HEL) in complete Freund's adjuvant induces, both in antibody responder and nonresponder mice, a classical delayed-type hypersensitivity (DTH) reaction evaluated as footpad swelling. This response can be specifically transferred to naive recipients by Lyt-1+2- T cells and passive transfer is restricted by genes mapping in or to the left of the I-A region of the H-2 complex. Fine antigenic specificity analysis shows that HEL-primed T cells mediating DTH recognize ring-necked pheasant egg-white lysozyme, a lysozyme closely related to HEL, but fail to respond to human lysozyme, differing from HEL at 40% amino acid residues. Complete cross-reactivity between native and denaturated (reduced and carboxymethylated) HEL is exhibited by T cells involved in the DTH response. Subcutaneous injection of HEL coupled to spleen cells is also able to induce antigen-specific and genetically restricted DTH responses whereas the same cells administered by i.v. or i.p. route induce predominantly suppressor T cell activation. These suppressor T cells specifically inhibit the induction phase of DTH reactivity to HEL.

Animals↗