Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Suppressor Factors, Immunologic”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1994

[Immunologic suppressor factors in sera of patients with ovarian cancer].

The suppressive activity of immunologic suppressor factors (ISF) in the sera of 34 patients with ovarian cancer was investigated by using the lymphocyte proliferation and inhibition test. It was found that the sera of the preoperative patients could significantly suppress PHA-induced lymphocyte response, and that the suppression was dose-dependent. When the sera were diluted to 1 : 4,000, the suppressive activity could still be demonstrated. We also observed the suppressive activities in the sera of patients with cervical cancer, endometrial cancer, gastric cancer and lung cancer, and compared them with ovarian cancer patients. The observation showed that the suppressive activity in the sera of preoperative ovarian cancer patients was higher than that in the sera of gastric cancer or lung cancer patients. These results suggested that ISF played an important role in the development of ovarian cancer.

Adult↗
PubMed1988

Immunosuppression during viral oncogenesis. IV. Generation of soluble virus-induced immunologic suppressor molecules.

We describe herein functional attributes and generation of immunologic suppressor activity elaborated in response to oncogenic virus infection. Malignant rabbit fibroma virus-induced immunologic suppressor factor (VISF) is a T cell product produced in peak quantities by spleen cells taken from infected rabbits 7 days after infection in vivo. Its production does not appear to require macrophage participation. VISF is highly labile, 3.5 to 12 kDa, and capable of suppressing both B and T lymphocytic responses. Indomethacin and the cyclic nucleotides cAMP and cGMP inhibit its generation. VISF activity is neither antigen nor species specific. It suppresses murine and leporine immune responses to antigens unrelated to the inducing virus. Comparable suppressor activity may be induced by infecting an apparently non-functional rabbit T lymphoma line, RL-5, with malignant rabbit fibroma virus. VISF is principally a suppressor-inducer factor: in vitro, lymphocytes exposed to VISF do not show decreased immunologic responsiveness until 4 days of culture. VISF induces T suppressor cell activity when normal spleen cells are exposed briefly to VISF. Thus, immunosuppressive consequences of malignant fibroma virus infection are partially mediated by a small, non-specific T cell-derived suppressor lymphokine with unique functional characteristics. Non-specific immunologic dysfunction that often attends virus infections may reflect the activity of such factors in humans as well.

Animals↗
PubMed1983

Acceptor-suppressor T cell hybridoma with a receptor recognizing antigen-specific suppressor factor.

An acceptor hybridoma with a receptor that recognizes the keyhole limpet hemocyanin (KLH)-specific suppressor T cell factor (KLH-TsF) was established after the fusion of C57BL/6 splenic T cells enriched with KLH-coated petri dishes. The cloned hybridoma (34S-281) could be specifically activated by stimulation with the conventional KLH-TsF or monoclonal KLH-TsF from three different hybridomas in the absence of the relevant antigen (KLH) and it started to produce another factor that suppresses the antibody response against DNP-KLH in a KLH-specific fashion. The KLH specificity of the TsF was required for activation. The new factor was found not to bind the KLH but to be absorbed with the KLH-TsF-producing hybridoma. It is thus strongly suggested that the acceptor site has a complementary structure (antiidiotype) for the KLH-TsF. Moreover, the idiotypic determinant on KLH-TsF was found to have a structure similar to that on some of the anti-KLH antibodies, since the acceptor hybridoma was specifically killed by the conventional anti-KLH antibodies and complement. Drawing on the above results, the idiotype-antiidiotype network in the conventional antigen system is discussed.

Animals↗
PubMed1984

Presence of an antigenic determinant common to rat IgE-potentiating factor, IgE-suppressive factor, and Fc epsilon receptors on T and B lymphocytes.

Polyclonal antibodies against purified IgE-potentiating factor were prepared in guinea pigs, and mouse monoclonal antibodies were prepared against inactive IgE-binding factor from a T cell hybridoma. The polyclonal antibodies and two of the monoclonal antibodies bound the IgE-potentiating factor, the IgE suppressive factor, and the inactive IgE-binding factor. The results indicate that the three IgE-binding factor molecules share a common antigenic determinant. The polyclonal antibodies and the monoclonal antibody bound intracellular IgE-binding factors that did not have affinity for either lentil lectin or peanut agglutinin, which suggests that the antibodies were directed against the peptide portion of IgE-binding factors. Pretreatment of Fc epsilon R+ T hybridoma cells and Fc epsilon R+ B cells with either the monoclonal or the polyclonal anti-IgE-binding factor (anti-IgE-bF) antibody prevented rosette formation of the cells with IgE-coated erythrocytes, whereas the same treatment failed to affect rosette formation of Fc gamma R+ cells with IgG-coated erythrocytes. Specific binding of the guinea pig anti-IgE-bF antibodies to Fc epsilon R on both B and T cells was confirmed by immunofluorescence. The results indicate that Fc epsilon R on B and T cells share a common antigenic determinant with IgE-binding factors. The F(ab')2 fragments of the guinea pig anti-IgE-bF induced the expression of Fc epsilon R on Fc gamma R+ lymphocytes and the formation of IgE-binding factors. The capacities of not only IgE, but also anti-IgE-bF, to induce both Fc epsilon R expression and IgE-binding factor formation indicate that Fc epsilon R on lymphocytes, rather than IgE, transmit the signal for the formation of IgE-binding molecules.

Animals↗
PubMed1981

Antigen- and receptor-driven regulatory mechanisms. VII. H-2-restricted anti-idiotypic suppressor factor from efferent suppressor T cells.

Azobenzenearsonate (ABA)-specific T cell-derived suppressor factor (TsF1) from A/J mice was used to induced second-order suppressor T cells (Ts2). Comparison of suppressor T cells induced by antigen (Ts1) with Ts2 induced by TsF1 revealed that Ts1 were afferent suppressors active only when given at the time of antigen priming, and not thereafter, whereas Ts2 could act when transferred at any time up to 1 d before antigen challenge for a delayed-type hypersensitivity response. This was true even when the recipient could be shown to be fully immune before transfer of Ts2, thus defining these cells as efferent suppressors. The anti-idiotypic specificity of the Ts2 was demonstrated by the ability of Ts to bind to idiotype (cross-reactive idiotype [CRI])-coated Petri dishes. A soluble extract from Ts2 (TsF2) was also capable of mediating efferent suppression that was functionally antigen- (ABA) specific. Comparison of TsF1 with this new factor, TsF2, revealed that both lack Ig-constant-region determinants, possess H-2-coded determinants, and show specific binding (to ABA and to CRI+-Ig, respectively). TsF1 acts in strains that differ with respect to H-2 and background genes, whereas TsF2 shows H-2- and non-H-2-linked genetic restrictions. This existence of H-2 restriction of TsF2 activity suggests that the apparent discrepancies in studies of H-2 restriction of TsF may be a result of the analysis of two separate classes of TsF, only one of which shows genetically restricted activity, thus unifying several models of suppressor cell activity.

Animals↗
PubMed1990

Comparative studies on FcR (FcRII, FcRIII, and FcR alpha) functions of murine B cells.

Distribution of FcR II, FcRIII, and FcR alpha on murine splenic B cells was examined by using FITC-labeled heat-aggregated IgG of each subclass and IgA. Almost 60 to 80% of B cells expressed both FcRII and FcRIII. However, FcR alpha was expressed on only a small proportion (6%) of B cells that co-expressed FcRII. By inhibition assays with the use of cold IgG of each subclass and IgA in addition to anti-FcRII mAb (2.4G2), it was found that IgG1, IgG2a, and IgG2b utilized the same receptor (FcRII), whereas IgG3 and IgA bound only to their unique receptors, FcRIII and FcR alpha, respectively. Immune complexes IC prepared by IgG1, IgG2a, IgG2b, and IgA anti-TNP mAb with TNP-coupled SRBC inhibited the polyclonal Ig secretion and proliferative responses of B cells stimulated with either IL-4 or LPS. The inhibition of B cell activation was associated with the blockade of the membrane depolarization. Moreover, IC prepared by these antibodies caused production of suppressive B cell factor (SBF) as is the case with rabbit IgG antibody to SRBC, and SBF thus prepared regulated antibody responses in an isotype-nonspecific manner. In contrast, no inhibition for these responses or production of SBF was attained by the IC of IgG3 antibody. We concluded that FcRII and FcR alpha mediates a suppressive signal for B cells by acting on the initial step of activation, whereas FcRIII lacks this activity.

Animals↗
PubMed1987

In vitro modulation of antigen-primed T cells by a glycosylation-inhibiting factor that regulates the formation of antigen-specific suppressive factors.

BDF1 [(C57BL/6 X DBA/2)F1] mice were primed with alum-absorbed ovalbumin, and their spleen cells were cultured with ovalbumin to activate antigen-primed T cells. The activated T cells were then propagated in interleukin 2-containing medium in the presence or absence of affinity-purified glycosylation-inhibiting factor (GIF). Upon incubation with ovalbumin-pulsed macrophages, T cells propagated in the absence of GIF produced IgE-potentiating factor and glycosylation-enhancing factor. In contrast, T cells propagated in the presence of GIF produced IgE-suppressive factor and GIF. The ovalbumin-primed T cells propagated in the presence of GIF constitutively produced the 13-kDa GIF that lacked affinity for ovalbumin. However, stimulation of the same T cells with ovalbumin-pulsed macrophages resulted in the production of 80- and 35-kDa GIF that had affinity for ovalbumin. Both the antigen-specific GIF and nonspecific GIF from the activated BDF1 T cells had I-Jb determinants. Since the ovalbumin-specific GIF is derived from Lyt-2+, I-J+ ovalbumin-specific suppressor T cells and suppresses the anti-hapten antibody response to dinitrophenyl-coupled ovalbumin, the results strongly suggest that the presence of GIF during the propagation of antigen-primed T cells facilitates the generation of antigen-specific suppressor T cells.

Animals↗
PubMed2006

ILT3+ ILT4+ tolerogenic endothelial cells in transplantation.

T cells can recognize allogeneic major histocompatibility complex (MHC) antigens by two distinct routes: either directly as intact molecules or indirectly as processed peptides presented by syngeneic antigen-presenting cells (APC). The graft endothelium plays an important role in rejection eliciting and serving as a target of T cells activated via the direct and/or indirect allorecognition pathway. Recent evidence demonstrates, however, that endothelial cells are also endowed with the capacity to downregulate alloreactivity inducing tolerogenic responses. Similar to professional APC (such as dendritic cells), endothelial cells express high levels of inhibitory receptors (ILT3 and ILT4 in humans and PIR-B in rodents) and low levels of costimulatory and adhesion molecules upon interaction with allospecific CD8 T suppressor cells or exposure to inhibitory cytokines. Because of the importance of endothelial cells in the activation and control of T cell reactivity, understanding of their biology is crucial for the development of new strategies for induction of transplantation tolerance and treatment of cancer, chronic infection, and autoimmunity.

Antigen-Presenting Cells↗
PubMed2002

B6 strain Ly49I inhibitory gene expression on T cells in FVB.Ly49IB6 transgenic mice fails to prevent normal T cell functions.

Inhibitory Ly49 receptors expressed on NK cells provide a mechanism for tolerance to normal self tissues. The immunoregulatory tyrosine-based inhibitory motifs present in some Ly49s are able to transmit an inhibitory signal upon ligation by MHC class I ligands. In our system, as well as others, mice transgenic for inhibitory Ly49 receptors express these receptors on both NK and T cells. FVB (H2(q)) mice transgenic for the B6 strain Ly49I (Ly49I(B6)) express the inhibitory Ly49 receptor on the surface of both T and NK cells. Although Ly49I functions to prevent NK-mediated rejection of H2(b) donor bone marrow cells in this transgenic mouse strain, the T cells do not appear to be affected by the expression of the Ly49I transgene. FVB.Ly49I T cells have normal proliferative capabilities both in vitro and in vivo in response to the Ly49I ligand, H2(b). In vivo functional T cell assays were also done, showing that transgenic T cells were not functionally affected. T cells in these mice also appear to undergo normal T cell development and activation. Only upon stimulation with suboptimal doses of anti-CD3 in the presence of anti-Ly49I is T cell proliferation inhibited. These data are in contrast with findings in Ly49A, and Ly49G2 receptor transgenic models. Perhaps Ly49I-H2(b) interactions are weaker or of lower avidity than Ly49A-H-2D(d) interactions, especially in T cells.

Animals↗
PubMedDate not supplied

Multiple sclerosis. I. The immune pathogenetic hypothesis.

Animal models indicate that chronic relapsing demyelinating diseases of the central nervous system (CNS) can be induced both by certain viruses and by sensitization to myelinic antigens. Epidemiological data (studies on emigrants and on so-called "Multiple Sclerosis (MS) epidemics") suggest that an environmental transmissible agent, acting on a genetic substrate, could play a role in the pathogenesis of the disease. The transmissible agent could be a virus. Data to this effect are insufficiently indicative, but the hypothesis has been recently put forward that it could be antigenically related to the lymphotropic viruses (HTLV). The transmissible agent could act either by desegregating myelinic antigens or by inducing an alteration of the immune system with a reduction of T lymphocyte suppressor activity. There appears to be rapid and intense activated T lymphocyte "traffic" across the blood-brain barrier in patients affected with MS. Cells specifically sensitized to the unknown antigen find within the CNS other cells able to perpetuate presentation of the antigen (HLA-DR+ astrocytes and endothelial cells, not present in normal brain) and then activate the macrophages which in turn begin immuno-mediated phagocytosis of the healthy myelin. Aspecific immune cells are also recruited into CNS where seem to abnormally proliferate (possibly owing to reduced suppressor activity) producing antibodies against various viral or cerebral antigens which are not clearly related to the pathogenesis of the disease (production of intra-CNS "nonsense" antibodies and synthesis of the oligoclonal immunoglobulin bands seen at the cerebrospinal fluid electrophoresis.)

Antibodies, Monoclonal↗
PubMed1993

Binding of the two polypeptide chains of dengue virus-induced suppressor cytokine to its receptor isolated from macrophages.

Dengue type 2 virus (DV)-induced suppressor cytokine (SF) is composed of two polypeptide chains (alpha and beta) and has a receptor on macrophages (M phi), which has been purified. The present study was undertaken to study the binding of the two polypeptide chains of SF to M phi and its purified receptor (SF-R) protein. It was observed that both alpha and beta-chains of SF, purified by high performance liquid chromatography (HPLC), bound to M phi cell, but only alpha-chain bound to SF-R protein. Only H-2A positive M phi bound SF. Anti-H-2Ak mAb blocked the binding of SF to M phi but had no effect on binding of SF to SF-R. Both anti-SF-antiserum and anti-SF-R-antiserum blocked the binding of SF to M phi. The binding of the beta-chain of SF to M phi was blocked by anti-H-2Ak mAb while the anti-SF-R-antiserum blocked the binding of alpha-chain on M phi. Thus, the alpha-chain of SF binds to SF-R and the beta-chain binds to H-2A determinants on M phi.

Animals↗
PubMed1990

Transforming growth factor-beta and cellular immune responses in synovial fluids.

Mononuclear cells in synovial fluids (SF) from patients with rheumatoid arthritis and other arthropathies are characterized by functional and phenotypic changes, including impaired mitogen responsiveness and inverted ratios of CD4+/CD8+ T lymphocytes. This is related to previously described activities in synovial fluids that inhibit proliferation of lymphocytes induced by mitogens and cytokines. The present study examines the relationship of these activities and transforming growth factor beta (TGF-beta), which is now known as the most potent endogenous inhibitor of lymphocyte function. It is shown that most of the activity in SF that inhibits IL-1-induced thymocyte or T cell proliferation is neutralized by a specific antibody to TGF-beta. Analysis of the SF in the CCL64 assay, a standard test for TGF-beta, showed a close correlation between the levels of immunosuppressive activity and TGF-beta. SF contain spontaneously active inhibitors of T cell function and this is caused by the presence of active TGF-beta. Higher titers are found after transient acidification, which is known to activate the latent form of TGF-beta. Characterization of the TGF-beta isoforms showed that most of the material in SF is TGF-beta 2. Analysis of TGF-beta effects on T cell subsets demonstrated that it completely inhibits proliferation of CD4+ cells whereas at the same concentrations of purified or rTGF-beta CD8+ cells are only inhibited by maximally 31.1%. SF also preferentially inhibit CD4+ Th cell proliferation and this effect is neutralized by antibody to TGF-beta. Collectively these results indicate that the presence of TGF-beta accounts for most of the immunosuppressive activities in SF and that this factor may be responsible for functional and phenotypic changes of SF lymphocytes.

Arthritis, Rheumatoid↗
PubMed1986

Binding of human EPF to receptors on PMBC as a first signal of pregnancy immunomodulation.

The interaction between human early pregnancy factor (EPF) and a specific receptor present on human peripheral blood mononuclear cells (PMBC) has been assessed. EPF was radioiodiated by the lactoperoxidase method to a high specific activity, and the [125I]EPF obtained bound in a specific and saturable manner to the receptors on PBMC. Saturation of the binding sites occurred at 10(-9) M. There were 6600 specific binding sites per cell in cells partially purified from pregnant women and fewer in those from non-pregnant women. Unlabelled EPF was capable of competing for binding sites with [125I]EPF, while the binding of [125I]EPF was not inhibited by human chorionic gonadotrophin. A new assay was used that permits the culture of PBMC and the detection of the surface IgG expression in the same microplate. With this method the influence in vitro of human EPF on lymphocyte expression was tested. The results demonstrated a specific inhibition of surface IgG expression of PBMC using a very low concentration of EPF (10 pg/ml).

Binding, Competitive↗