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V Colizzi

Publications and source records attributed to V Colizzi.

At least 145 records · Page 8Linked to original sources
PubMed1984

Non-specific inhibitor made by T acceptor cells inhibits both the afferent and efferent stage of the contact sensitivity reaction.

In the T suppressor circuit which affects contact sensitivity, the T acceptor cell (Tacc) armed with T suppressor factor (TsF) and then triggered by antigen and major histocompatibility complex products (I-J) releases non-specific inhibitor (nsINH). These non-specific inhibitor(s) affect both the efferent and afferent stage of the contact sensitivity reaction and were originally detected by the inhibition of the passive transfer of contact sensitivity. The nsINH also blocks the induction of contact sensitivity when given intravenously at the time of immunization but has no effect when given at the time of challenge. Similarly, it blocks proliferation in the regional lymph nodes induced by contact sensitizer in a dose-dependent fashion; it acts when given at the time of immunization but not 1 day later. This effect is antigen non-specific and H-2 unrestricted. The nsINH bears I-J determinants as shown by affinity chromatography on monoclonal antibody. The nsINH comes from the Tacc and is not a breakdown product of the TsF. This is shown by the fact that, when the Tacc and TsF have I-J of different genotypes, the genotype of the nsINH corresponds to that of the Tacc. Parallel measurements of inhibition of lymphoproliferation and of passive transfer show that the nsINH has a molecular weight of 50-60 Kd and a pI around 6.8 and suggest that similar or identical molecules block both the afferent and efferent stage of the contact sensitivity reaction.

Animals↗
PubMed1984

Suppressor cells induced by BCG release non-specific factors in vitro which inhibit DNA synthesis and interleukin-2 production.

Mice injected intravenously with a high dose (5 X 10(7) ) of BCG fail to develop delayed hypersensitivity to BCG and are described as anergic or unresponsive. Spleen cells from these mice release factors on culture which suppress DNA synthesis induced by concanavalin A in vitro. Cell separation experiments showed that both macrophages and T cells produce inhibitory factors. However, the macrophage factor has a molecular weight 10,000-30,000, while the T cell factor has a molecular weight of 50,000-70,000. Further evidence that these two factors are different is provided by the kinetics of their action. The T cell factor only acts when given within 12 hr of stimulation with concanavalin A, while the macrophage factor acts even when given at 48 hr. In the case of the T cell factor, the inhibition of DNA synthesis may be attributed to its ability to block the interleukin-2 production induced by Con A. As similar T cell and macrophage factors are produced in mice responding to simple chemically reactive haptenes (contact sensitizers), it is possible that a similar suppressor circuit is involved in the control of the response to contact sensitizers and in the production of unresponsiveness (anergy) in mice given large doses of BCG.

Animals↗
PubMed1984

Analysis of the T suppressor cell circuit which regulates contact sensitivity in mice infected with the virus of Newcastle disease.

The interaction between the virus of Newcastle disease (NDV) and the different cellular elements involved in the T suppressor cell circuit which regulates the expression phase of contact sensitivity has been investigated. NDV does not interfere with the production of the antigen-specific T suppressor factor (TsF) but inhibits its binding to T acceptor cells (Tacc). This cell when armed with TsF and exposed to the antigen corresponding to TsF releases a non-specific inhibitor of the transfer of contact sensitivity. More detailed analysis of the effect of NDV on the Tacc system showed that not only Tacc activity is impaired by NDV, but also the ability of antigen presenting cells (APC) to trigger Tacc armed with TsF is inhibited. The impairment of APC activity by NDV has been also investigated using another system, such as the induction of contact sensitivity by footpad cell transfer. The possibility that a virus-induced membrane modification might be responsible for the effect of NDV on the regulation of contact sensitivity is discussed.

Animals↗
PubMed1984

Equivalence of conventional anti-picryl T suppressor factor in the contact sensitivity system and monoclonal anti-NP TsF3: their final non-specific effect via the T acceptor cell.

There is considerable confusion over whether the antigen-specific T suppressor factors (TsF) described by different authors are indeed equivalent. This paper investigates whether monoclonal TsF3, obtained from hybridomas derived from mice injected subcutaneously with NP derived spleen cells, is functionally equivalent to the conventional T suppressor factor, produced by mice injected intravenously with chemically reactive, water soluble haptene (picrylsulphonic acid and oxazolone thioglycolic acid). Comparison of monoclonal anti-NP TsF3 with conventional anti-picryl and anti-oxazolone T suppressor factor showed that both armed the non-specific T acceptor cell (Tacc) which was sensitive to cyclophosphamide and adult thymectomy. Moreover, non-specific inhibitor (nsINH) of the transfer of contact sensitivity was released when antigen, together with major histocompatibility complex products (MHC), reacted with conventional or monoclonal TsF on the surface of the non-specific T acceptor cell. The interaction of monoclonal TsF3 with antigen, which led to the release of NsINH, required the presence of MHC and was I-J restricted. However, there was no Igh-1 restriction. The equivalence of conventional anti-picryl and anti-oxazolone TsF has been demonstrated by arming the Tacc with a mixture of these two suppressor factors, and then triggering the release of nsINH with the mixed haptene 'picryl-oxazolone-lysine' which crosslinks separate molecules of TsF. A similar equivalence of conventional anti-oxazolone TsF and monoclonal anti-NP TsF3 was demonstrated using the mixed hapten 'NP-oxazolone-lysine' to trigger the release of nsINH. It was concluded that monoclonal TsF3 and conventional TsF were equivalent, and that both had an indirect mode of action through the non-specific T acceptor cell which led to the production of non-specific inhibitor.

Animals↗
PubMed1984

Candida albicans polysaccharide extract (MPPS) and PPD stimulate the production of interleukin-1 and lymphocyte proliferation.

Peripheral blood mononuclear cells (PBMC) were stimulated in vitro either with Candida albicans polysaccharide extract (MPPS) or with PPD. Both MPPS and PPD driven lymphocyte proliferation was strictly dependent on the presence of macrophages. In fact purified T cells failed to proliferate unless adherent cells were added. The ability of monocytes to produce interleukin-1 (IL-1) was then investigated. Both MPPS and PPD caused the release IL-1 into the culture supernatant, as measured in a direct thymocyte proliferative assay. MPPS and PPD also stimulated the production of IL-1 by the mouse macrophage like line P388D1. These data support the view that the antigen specific activation of human T cells by MPPS and PPD requires both antigen presentation and IL-1 production.

Animals↗
PubMed1983

Auto-anti-idiotypic antibodies inhibit T-cell-mediated hypersensitivity in BCG-infected mice.

It is shown that serum from mice heavily infected with BCG contains antibodies which block the cell transfer of delayed-type hypersensitivity (DTH) to purified protein derivative (PPD) when BCG-immune cells were preincubated in it. This suppressive activity is antigen specific in that the serum does not block the cell transfer of contact sensitivity to oxazolone. However, the suppressive activity is not antigen directed in that it is absorbed neither by PPD-coupled Sepharose beads nor by PPD-pulsed normal peritoneal exudate cells. On the other hand, the activity can be absorbed to BCG-immune T cells and eluted from a Sepharose column conjugated with affinity-purified mouse anti-PPD antibodies. The possibility that antireceptor antibodies arise during the BCG infection and regulate DTH reaction is discussed.

Animals↗
PubMed1983

Regulation of the development of plaque-forming cells to bromelain-treated syngeneic mouse erythrocytes in bone marrow cell cultures.

The development of plaque-forming cells (PFC) to bromelain-treated syngeneic mouse red blood cells (Br-MRBC) was studied in bone marrow cell (BMC) cultures. It was found that the number of marrow PFC to Br-MRBC does not show the typical spontaneous increase observed in spleen cell (SPC), or peritoneal cell (PC) cultures. The number of anti-Br-MRBC PFC was markedly increased by lipopolysaccharide (LPS), even in conditions in which cell proliferation was blocked by mitomycin C, suggesting the presence of high numbers of Br-MRBC-specific precursor cells, potentially capable of differentiating into autoantibody-producing cells, in the marrow. Moreover, the low levels of anti-Br-MRBC PFC were further reduced in the presence of concanavalin A (Con A). The addition of Con A-activated BMC to BMC, SPC, or PC cultures actively suppressed the development of anti-Br-MRBC PFC. Con A-activated BM suppressor cells were found to be Thy 1.2-negative, Ig-negative, nonadherent cells. A possible role for the BM suppressor cell in tolerance to self antigens is discussed.

Animals↗
PubMed1983

Nonspecific inhibitor of DNA synthesis elaborated by T acceptor cells. I. Specific hapten- and I-J-driven liberation of an inhibitor of cell proliferation by Lyt-1-2+ cyclophosphamide-sensitive T acceptor cells armed with a product of Lyt-1+2+-specific suppressor cells.

Lyt-1+2+ hapten-specific T suppressor cells (Ts) from mice injected and then painted with picryl or oxazolone derivatives produce hapten-specific T suppressor factors (TsF) in vitro. Stimulation by painting with contact sensitizer (which need not be specific) gives rise to Lyt-1-2+, I-J+, cyclophosphamide-sensitive T acceptor cells (Tacc). When the Tacc population is armed with TsF and then is exposed to specific antigen in the context of I-J-controlled determinants (antigen-presenting, haptenized spleen cells and Ts sharing the same I-J subregion), a nonspecific inhibitor of DNA synthesis (nsINH) appears in the supernatant. This inhibitor suppresses the primary DNA synthetic response to concanavalin A, lipopolysaccharide, and alloantigens in both syngeneic and allogeneic lymphocytes. The nsINH is only effective when added to lymphocyte cultures less than 8 hr after the stimulation with concanavalin A. The nsINH, however, affects neither primary nor secondary cytotoxicity in vitro. These data suggest the mouse immune system is capable of selective regulation of the response to specific antigen by the production of nonspecific soluble suppressor factor(s).

Animals↗
PubMed1983

The role of I-J in the suppressor T-cell circuit which influences the effector stage of contact sensitivity: antigen together with syngeneic I-J region determinants induces and activates T suppressor cells.

One of the T suppressor circuits induced by picrylsulphonic acid includes the T suppressor cell (Ts-eff) which acts at the efferent stage of the contact sensitivity reaction and produces antigen-specific T suppressor factor (TsF). This factor does not act directly but arms a T acceptor cell (Tacc). This Tacc liberates a non-specific inhibitor when it is armed with TsF and then exposed to picrylated cells sharing the I-J genotype of the source of the TsF. This paper investigates the role of I-J region gene products in this T suppressor circuit. Two approaches were used. Syngeneic CBA (H-2k) lymphocytes were separated into I-J+ and I-J- cells by treatment with anti-I-Jk serum followed by panning on anti-immunoglobulin plates. The cells were then picrylated and used as a source of antigen. Alternatively, B10.A congeneic mice syngeneic (5R) or allogeneic (3R) with CBA at the I-J locus were picrylated and used similarly. The main findings were as follows. (i) The intravenous injection of picrylated I-J+ spleen cells but not a similar number of I-J- cells induced Ts-eff which blocked the transfer of contact sensitivity. Picrylated unseparated cells syngeneic, but not allogeneic, at the I-J locus were also effective. (ii) It is known that the lymphocytes of mice injected wit picrylsulphonic acid and then re-exposed to antigen by painting with picryl chloride liberate TsF in vitro. The re-exposure to antigen can be replaced by the intravenous injection of picrylated I-J+ cells or by cells syngeneic at the I-J locus the day before harvesting the spleen cells. (iii) The release of non-specific inhibitor by Tacc armed with TsF requires exposure to picrylated I-J+ cells or cells syngeneic at the I-J locus. The requirement for antigen on a cell bearing syngeneic I-J suggests that antigen together with I-J is an activation signal in this T-cell circuit. The simplest explanation is that the receptor of the pristine Ts and of the mature Ts-eff is similar to T suppressor factor.

Animals↗
PubMed1983

Enhancement of the spontaneous development of autoreactive B cells by PPD in mouse peritoneal cell cultures.

The effect of tuberculin purified protein derivative (PPD) on the development of plaque-forming cells (PFC) against bromelain-treated syngeneic mouse red blood cells (Br-MRBC) was studied in peritoneal cell cultures. The finding that PPD enhances the development of PFC to Br-MRBC, even under conditions where cell division is blocked by mitomycin C treatment, suggests that cell proliferation does not represent a necessary prerequisite for differentiation of precursor cells into autoantibody-forming cells.

Animals↗
PubMed1982

Impairment of cell-mediated immunity in Pseudomonas aeruginosa pyelonephritis: lack of suppressor cell activity in vivo.

Bacterial pyelonephritis was induced in mice by direct microinoculation of Pseudomonas aeruginosa in the kidney. In the acute phase of P. aeruginosa pyelonephritis, a state of cell-mediated immunity impairment, evaluated both in vitro as lymphocyte reactivity to concanavalin A and in vivo as host versus graft reaction has been observed. Furthermore, delayed-type hypersensitivity to specific bacterial antigen has been detected only when the kidney infection was subsiding, i.e., 3 weeks after bacteria inoculation. When investigating the mechanism of such T-cell impairment, we were unable to transfer the immunodepression, suggesting that suppressor cells are not involved in vivo. The role of P. aeruginosa inhibition of cell-mediated immunity in the pyelonephritic host is discussed.

Animals↗
PubMed1982

Cell-mediated immunity and delayed-type hypersensitivity in Pseudomonas aeruginosa-infected mice.

In mice repeated systemic injections of Pseudomonas aeruginosa viable cells were able to induce a specific delayed-type hypersensitivity, which was evaluated as increase both in footpad swelling and in the weight of popliteal lymph nodes, after a challenge in the footpad. Unfractionated spleen cells or T lymphocyte-enriched spleen cells from sensitized donors were able to specifically transfer the delayed-type hypersensitivity to syngeneic recipients but failed to protect them against a lethal challenge with P. aeruginosa. In contrast, serum or B lymphocyte and macrophage-enriched spleen cells from the same donors were capable of transferring protective immunity but failed to induce any delayed-type hypersensitivity reaction in the recipients. These results clearly show that in systemic P. aeruginosa infections a dissociation between delayed-type hypersensitivity and acquired cellular resistance occurs.

Animals↗
PubMed1982

Evidence for autoantibody production associated with polyclonal B-cell activation by Pseudomonas aeruginosa.

Experimental infection of mice with Pseudomonas aeruginosa resulted in the polyclonal activation of B lymphocytes, as assessed by the spontaneous plaque-forming cell (PFC) response to trinitrophenyl and sheep erythrocytes. Additionally, a PFC response to bromelain-treated syngeneic erythrocytes (Br-MRBC) could be detected in infected mice, suggesting that P. aeruginosa infection might also induce activation of self-reactive B-cell clones and consequently lead to autoantibody production. Furthermore, in cultures of mouse peritoneal cells, heat-killed P. aeruginosa enhanced the development of anti-Br-MRBC PFC, even under conditions where cell division was blocked, suggesting that the in vitro P. aeruginosa-induced enhancement of anti-Br-MRBC PFC was essentially related to cell differentiation, cell division playing only a minor role. The mechanism of the in vivo and in vitro P. aeruginosa-induced activation of anti-Br-MRBC PFC are discussed.

Animals↗
PubMed1982

Urinary excretion of oxalate in renal failure.

The daily urinary excretion of oxalate has been found to be lower than normal in patients with renal failure and the decrease to be directly proportional to the impairment of renal function. It has also been found that the gut flora from uremic patients destroys oxalate 'in vitro' more efficiently than the gut flora from normal people. It is postulated that an adaptation occurs in the gut flora of uremics to 'metabolize' oxalate, and this enteric elimination may account for its decreased urinary excretion.

Humans↗
PubMed1982

LPS-induced enhancement of plaque-forming cell response to bromelain-treated syngeneic erythrocytes in mouse peritoneal cell cultures.

The effect of bacterial lipopolysaccharide (LPS) on the development of plaque-forming cells (PFC) against bromelain-treated syngeneic mouse red blood cells (Br-MRBC) was studied in peritoneal cell (PC) cultures. It was found that LPS enhances the development of PFC to Br-MRBC and increases DNA synthesis in PC cultures. The LPS-induced enhancement of PFC to Br-MRBC, however, does not appear to require cell proliferation, since it also occurred in PC cultures pretreated with mitomycin C. In addition, the LPS-induced B lymphocytes blastogenesis is under the control of macrophages, while cell differentiation of precursor B lymphocytes into cells actively producing antibodies against Br-MRBC is regulated by suppressor T lymphocytes.

Animals↗