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J Marcinkiewicz

Publications and source records attributed to J Marcinkiewicz.

At least 73 records · Page 4Linked to original sources
PubMed1990

Further studies on the regulation of lymphokine biosynthesis in contact sensitivity.

Contact sensitivity (CS) results from a series of cellular interactions involving CD4+ T cells and macrophages. We have studied the production of lymphokines by T cells from mice immunized by contact sensitization and by a variety of stimuli leading to CS or tolerance to CS. Primed T cells from mice immunized for CS are predominantly of the TH1 type. Conversely, a failure in the activation of these antigen-specific TH1 cells is a key step in the induction of tolerance to CS. Spleen cells from tolerant mice can suppress the production of lymphokines from primed cells, both in an adoptive transfer system and when mixed with effector cells in vitro. The relative importance of lymphokine competition, prostaglandin production by adherent cells, and other mechanisms underlying this suppression is discussed.

Animals↗
PubMed1990

Cell-mediated immunity: role of IL-3 and IL-6 in the regulation of contact sensitivity reaction.

Delayed type hypersensitivity reaction (DTH) consists of a sequential cascade of steps depending on different types of T cells, as well as mast cells, endothelial cells and macrophages. Recently it has been shown that CD4+ TH1 lymphocytes ("inflammatory type") play a central role in DTH reaction. Activated TH1 cells produce a characteristic pattern of cytokines: IL-2, IL-3, TNF-beta, IFN-gamma. Using the contact sensitivity (CS) reaction on mice as a model system, the role of cytokines in the regulation of DTH is presented, particularly the significance of IL-3 and IL-6. The recent data can be interpreted to show that IL-6 released by activated macrophages (APC cells) in the induction phase of the CS reaction probably stimulate CD8+ T suppressor cells. These in turn inhibit the production of IL-2 and IL-3 by CD4+ TH1 cells followed by a state of unresponsiveness.

Animals↗
PubMed1989

Antigen processing: current issues, exceptional cases (Thy 1 alloantigen, MHC class-II-restricted cytolytic T cells), and implications for vaccine development.

A dogmatic view of antigen processing is presented in outline, followed by a survey of unresolved issues in the subject. The activity of Thy 1 as an alloantigen, and allospecific MHC Class-II-restricted cytolytic T cells offer examples of exceptional cases of antigen presentation. Implications for the design of vaccines are drawn.

Animals↗
PubMed1989

Antigen-specific inhibition of IL-2 and IL-3 production in contact sensitivity to TNP.

The production of IL-2 and IL-3 by T cells from mice which had been contact sensitized to TNP and/or tolerized by intravenous injections of TNBS was assayed. Contact sensitization rapidly primes T cells, so that they respond to in vitro restimulation with haptenated syngeneic cells by producing IL-2 and IL-3. This production is strongly inhibited, in an antigen-specific manner, in tolerized mice. At least part of this inhibition can be attributed to the action of suppressor T cells that act by preventing the activation of lymphokine production in vitro. Lymphokine production thus closely parallels the in vivo delayed-type hypersensitivity (DTH) reaction in this system.

Animals↗
PubMed1988

Immunoregulatory role of Ig isotypes. I. Induction of contrasuppressor T cells for contact sensitivity responses by antibodies of the IgM, IgG1, and IgG3 isotypes.

A profound state of specific tolerance for the contact sensitivity reaction can be produced by i.v. exposure to hapten on the surface of syngeneic macrophages. When the same haptenated cells are incubated with specific antibody to form cell-bound Ag-antibody complexes, i.v. injection induces immunity rather than tolerance. We observe that such cell-bound Ag-antibody complexes induce not only effector cells for contact sensitivity but also hapten-specific contrasuppressor T (Tcs) cells, which are capable of rendering effector cells resistant to the inhibitory effects of Ts cells. Whereas the induction of the effector cells of contact sensitivity by cell-bound complexes required I region compatibility between the injected cells and the recipient, the induction of Tcs cells showed no genetic restriction. On the other hand, induction of contrasuppression required intact Fc on the complexed antibody, inasmuch as F(ab')2 fragments of specific antibody did not induce immunity. In addition, Tcs cells could also be induced by Ag-antibody complexes on opsonized TNP-mouse RBC treated with anti-TNP antibody. Immunity induced by cell-bound Ag-antibody complexes was observed only when antibodies of the IgM, IgG3, or IgG1 isotypes are used to generate the complexes. Further studies demonstrated that the Tcs cells induced in this way displayed the phenotype of Tcs cells described in other systems (Lyt-1+,2- I-J+, Vicia villosa lectin-adherent) and released a hapten-specific contrasuppressor factor. These studies indicate that Tcs cells can be induced independently of other T cells (such as the effector cells of contact sensitivity) and are likely to be responsible for some of the immunoregulatory effects of cell-bound Ag-antibody complexes. The role of antibody isotype in the induction of Tcs cells is discussed.

Adjuvants, Immunologic↗
PubMed1988

Sex differences in regulation of contact sensitivity reaction in mice. 1. Influence of sex on the generation of contrasuppressor and afferent suppressor cells.

It is well known that humoral and cell-mediated immune responses are better in females than in males. Females also develop autoimmunity more easily than males. Contact sensitivity, one of the forms of cell-mediated immunity, is controlled at the afferent and efferent phases by complex interactions of regulatory T cells. Our present experiments indicate that T suppressor afferent (Ts-aff) and T contrasuppressor cells (Tcs) are generated in the mouse in a sex-dependent fashion. These two types of regulatory cells are induced by antigen-antibody complexes containing various immunoglobulin isotypes. Females require fewer antigen (Ag)-IgG1 complexes to produce Tcs cells, but more Tcs cells after antigenic stimulation in females tips the balance toward better immune responsiveness. It remains to be established whether the peculiarities in generation of regulatory cells in female mice are relevant to the pathogenesis of autoimmune diseases which predominantly affect females.

Animals↗
PubMed1985

Effect of surgical trauma (gastrectomy) on cell-mediated and humoral responses in mice.

Gastrectomy in mice affects the cell-mediated (CMI) and humoral immunity in a diverse fashion, such as CMI (contact sensitivity reaction) is severely impaired and antibody response is enhanced. Both effects are transient and disappear several days after surgery. While suppression of contact sensitivity is mediated by non-specific Ly 1-2+, L-J+ suppressor T cells generated by surgical stress, the mechanisms of enhancement of antibody response is unknown. We assume that the split unresponsiveness induced by surgical trauma has a clear survival advantage. Increased antibody production is the major defence mechanism against bacterial infections, while decrease of CMI prevents autoimmune response against altered (damaged) self structures.

Animals↗
PubMed1985

Influence of anatomic localization and extent of surgical trauma on immune responses in mice.

The humoral immune response to SRBC and contact sensitivity (CS) reaction to picryl chloride and oxazolone was studied in traumatized mice (laparotomy, gastrectomy, leg amputation). While depression of CS was observed after leg amputation and gastrectomy, laparotomy had no effect. On the other hand, laparotomy and gastrectomy evoked stimulation of anti-SRBC antibody production, whereas leg amputation significantly reduced the humoral response. Results are discussed in relation to postulated role of trauma in the modulation of immune response regarding the anatomic localization and extent of surgical procedure.

Amputation, Surgical↗
PubMed1984

The induction of oxazolone-specific T suppressor afferent cells in mice by hapten-modified isologous IgG.

Injection of isologous 4(ethoxymethylene)-2-phenyl-oxazolin-5-one (oxazolone; OX)-substituted thymocytes or OX-labeled IgG (OX-IgG) into mice produces specific unresponsiveness in which immunization with homologous (OX), but not heterologous (picryl chloride), hapten on the skin does not result in significant contact sensitization. However, while injection of OX-substituted thymocytes triggers suppressor cells which inhibit the effector stage of contact sensitivity reaction, OX-IgG induces cells which suppress exclusively the afferent stage of reaction. In contrast to OX-IgG, OX-substituted F(ab')2 fragments, IgM, and albumin are ineffective. T suppressor afferent cells have Ly-2 and I-J surface markers and their precursors are resistant to cyclophosphamide treatment and adult thymectomy. We assume that T suppressor afferent cells recognize antigen in conjunction with intact IgG molecules, although the exact mechanism is unclear.

Animals↗
PubMed1984

Induction of "allogeneic effect"-like reaction by syngeneic TNP-modified lymphoid cells.

TNP-substituted SRBC-immune spleen cells, when injected into cyclophosphamide-treated recipients, are recognized by T lymphocytes and produce, in the presence of specific antigen (SRBC), significantly more PFC than nonsubstituted cells. Labeling of immune B cells is more important in producing the augmented responses than is the labeling of immune T cells. TNP determinant has to be bound directly to the transferred immune cells to produce enhanced antibody responses, as when recipients were injected with non-substituted immune cells and TNP-substituted non-immune cells simultaneously, no increase in PFC number was noted (lack of a bystander effect). When recipients were rendered tolerant to TNP, two separate effects were observed, dependent on the mode of inducing unresponsiveness. In mice which were treated with TNP over an extended period of time, lack of recognition of TNP was demonstrated, such that TNP-substituted cells failed, when transferred, to produce an augmented response. When a short-term tolerogenic regime was used, the adoptively transferred TNP-labeled cells gave a very poor response (greater than 95% inhibition) due to in vivo suppression and/or killing. These results, together with the lack of influence of tolerance induced to unrelated hapten (DNP or OX), confirm the antigen specificity of the phenomenon. The reaction observed by us shows a striking resemblance with, but not identical to, the "allogeneic effect" produced by MHC encoded alloantigens. Our results extend the list of analogous immune reactions induced by MHC encoded alloantigens and TNP-derivatized self.

Animals↗
PubMed1984

Production of antigen-specific contrasuppressor cells and factor, and their use in augmentation of cell-mediated immunity.

A single injection of TNP-labeled mouse gamma-globulin (TNP-IgG) can render the contact sensitivity response of mice resistant to suppressor cells (Tsc) and their biologically active cellfree products (TsF). Lyt-1 T cells of mice treated with TNP-IgG can protect the adoptive contact sensitivity response of immune cells from the antigen-specific suppressive effect produced by the addition of antigen-specific TsF or Tsc. When T cells of TNP-IgG-treated mice are put into culture, they produce an antigen-specific contrasuppressor factor (TcsF) that can replace the activity of the cells. When immune cells are preincubated in vitro with TcsF, they become refractory to Tsc and TsF added subsequently. The TcsF, however, has no ability to restore responsiveness to immune cells that had been previously exposed to TsF. The TcsF binds specifically to TNP, expresses an I-J-controlled determinant, and does not express standard determinants found on mouse Ig. The treatment that primes the contrasuppressor system to protect the contact sensitivity response also reportedly renders the antibody-producing system tolerant, (i.e., produces so called "split tolerance"). These results are discussed in light of the possibility that the contrasuppressor system can be responsible for so called isotype-specific immunity by rendering one arm of the immune system resistant to generalized suppressive mechanisms.

Animals↗
PubMed1983

Suppression of contact sensitivity to picryl chloride. Interaction between T suppressor auxiliary cells, suppressor factors and macrophages.

Immunization with picryl chloride generates cyclophosphamide resistant T immune cells (TDH) as well as cyclophosphamide sensitive T suppressor auxiliary cells (Ts-aux). T suppressor efferent cells do not inhibit effector phase of contact sensitivity in the absence of Ts-aux. These cells as well as macrophages adsorb TNP--T suppressor factor (TNP-TSF) and on these "armed" cells suppression may be transferred into recipients. Interactions between T-suppressor cells, their factors, Ts-auxiliary cells and macrophages are discussed.

Animals↗
PubMed1981

Inhibition of contact sensitivity by macrophages.

Lymphoid cells of mice injected with picrylsulphonic acid and then painted with picryl chloride produce a specific T suppressor factor (TSF) in vitro. This factor arms peritoneal exudate cells, which then produce a nonspecific factor which inhibits the transfer of contact sensitivity by immune cells incubated in it. An adherent, theta-negative cell, which is presumably a macrophage, is responsible. This justifies the use of the term macrophage suppressor factor. As a separate phenomenon, passive transfer cells lose their activity when incubated on high density monolayers of normal peritoneal exudate cells. However, this is not associated with the production of a supernatant factor. The inhibition of transfer when immune cells are incubated with specific TSF is unaffected by nylon wool filtration (which removes macrophages). This suggests that TSF is able to depress the passive transfer of contact sensitivity by a macrophage-independent process.

Animals↗
PubMed1980

Macrophage suppressor factor in contact sensitivity. Mechanisms of its release and action.

An antigen-specific suppressor factor (TSF) produced by mouse T lymphocytes prevents immune cells from conferring adoptive immunity on normal recipients. This TSF attaches easily to the macrophage surface, and these 'armed' macrophages in the presence of a corresponding antigen manufacture (in vitro) a non-specific macrophage suppressor factor (MSF) which impairs the activity of cells sensitized to homologous or heterologous antigens. Our experiments show that MSF is temperature- and trypsin-sensitive, and is not a prostaglandin. Its molecular weight is in the range of 10 kD. MSF is synthesized by macrophages de novo subsequent to triggering by TSF and antigen. MSF impairs only the activity of cells mediating contact sensitivity reaction (Ly 1) but has no influence on T-suppressor cells (Ly 23). The possibility that MSF is an enzyme is discussed.

Animals↗
PubMedDate not supplied

The effect of taurine chloramine on pro-inflammatory cytokine production by peripheral blood mononuclear cells isolated from rheumatoid arthritis and osteoarthritis patients.

OBJECTIVE: Pro-inflammatory cytokines play a critical role in the pathogenesis of RA. A natural oxidant, TauCl exerts anti-inflammatory activities. Here, the effects of Tau and TauCl on key pro-inflammatory cytokines--IL-1beta, IL-6 and TNF-alpha production by LPS-triggered peripheral blood mononuclear cells (PBMCs) isolated from RA and OA patients and healthy blood donors--were examined. METHODS: PBMCs were stimulated with LPS (24 h) in the presence of Tau or TauCl (200-400 microM). Cytokine production was measured in culture supernatants (secreted) and cells lysates (cell-associated) using specific ELISAs. RESULTS: Production of the secretedforms of IL-1beta and IL-6 was inhibited by TauCl with IC50 approximately equal to 250 microM and 300-400 microM respectively, in all investigated groups. In all cultures of PBMCs TauCl raised the TNF-alpha production at the low concentration (200 mM), while at the higher concentration (400 microM) either reduced it (55% of RA, 70% of OA patients and 55% of healthy donors) or exerted no effect (remainder of patients). Interestingly, Tau did not significantly affect any cytokine production. CONCLUSION: TauCl at high concentrations down-regulates pro-inflammatory cytokine production. However, the impact of TauCl on TNF-alpha production by PBMCs from RA is more limited than in cells isolated from OA patients.

Adult↗