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PubMed1984

Modulation of the expression of Tac antigen (T-cell growth factor response) on human thymocytes.

This study shows that anti-Tac antibody does not bind to human thymocytes unless they are activated. Human thymocytes could be induced to express Tac antigen (TCGF receptor) on their cell surface by Concanavalin A. B lymphoblastoid cells or 12-O-tetradecanoylphorbol 13-acetate alone did not induce TCGF receptors, but they did exert a very marked synergistic effect with Concanavalin A. This observation is consistent with our earlier finding that B lymphoblastoid cells secrete a factor which exerts a synergistic effect on the induction of lymphokine secretion by thymocytes and T-cells. The early expression of Tac antigen was independent of thymocyte proliferation. Anti-Tac antibody (10(-3)) inhibited the expression of TCGF receptors and late proliferation of thymocytes. TCGF did not reverse this inhibition nor did it prevent the binding of Tac antibody, but it enhanced the expression of Tac antigen.

Child↗
PubMed1984

The modulation of expression of polypeptide surface antigens on developing schistosomula of Schistosoma mansoni.

Five low m.w. polypeptide antigens are expressed on the surface of freshly transformed schistosomula of Schistosoma mansoni, and were reproducibly identified by surface labeling with 125I by using IODOGEN and immunoprecipitating with immune mouse sera. These molecules have approximate m.w. of 38,000, 32,000, 20,000, 17,000, and 15,000. They correspond to antigens recognized previously by lactoperoxidase-catalyzed iodination. Analysis of the surface of developing schistosomulum demonstrated that the 38,000 and 17,000 dalton antigens were lost from the parasite surface during 48 hr of in vitro culture. This process was not dependent on the presence of host serum. The two antigens were not lost due to shedding into the culture medium but were apparently sequestered to a site where they were no longer available for surface labeling. The 32,000, 20,000, and 15,000 dalton antigens, however, remained exposed on the schistosomulum surface for up to 2 days of in vitro culture. The expression of two new antigens was also induced by culture in vitro: a doublet of approximately 45,000 daltons and an antigen of approximately 11,000 daltons. The expression of the former was dependent on the presence of serum. These results demonstrate that the development of the schistosomula surface is a complex process, with events both dependent and independent of the presence of serum. In addition, the expression of polypeptide antigens is not coordinated, and antigens are lost, retained, or appear on the schistosomulum surface during the early stages of maturation.

Animals↗
PubMed1982

Modulation of C2 biosynthesis by antigen-antibody complexes.

Antigen-antibody complexes prepared with BSA and immunoadsorbent purified anti-BSA enhance C2 production by human monocytes in culture. The ratio of antigen to antibody was found to influence the degree of enhancement of C2 synthesis. Complexes prepared with F(ab)2 had no effect on C2 synthesis, suggesting that the effect was mediated via the Fc receptor. Enhanced C2 production by antigen-antibody complexes was reversibly inhibited by cycloheximide (2.5 micrograms/ml). In contrast to complexes heat-aggregated rabbit IgG inhibited C2 production. The biological relevance of these findings is discussed.

Animals↗
PubMed1996

Modulation by IL-10 of antigen-induced IL-5 generation, and CD4+ T lymphocyte and eosinophil infiltration into the mouse peritoneal cavity.

Sensitized BALB/c mice challenged i.p. with 1 microgram of OVA showed IL-5 release in the peritoneal lavage fluid, which peaked at 6 h and decreased thereafter. This was followed by a massive eosinophil accumulation, which started at 6 h and reached a plateau between 24 and 48 h. The i.p. injection of recombinant murine (rm) IL-10 (0.01-0.1 microgram/cavity) along with OVA reduced IL-5 release at 6 h and allergic eosinophilia at 6, 24, and 48 h. rmIL-10 also blocked in vitro IL-5 generation by sensitized peritoneal cells cultured in the presence of OVA. The inhibitory effect of rmIL-10 on Ag-induced eosinophilia and IL-5 release was suppressed by pretreatment of the animals with 1 mg/mouse of a neutralizing anti-mIL-10 mAb. Flow cytometric analysis revealed an increase in the number of CD4+ and CD8+ T lymphocytes and in the number of CD25+/CD4+ cells in the peritoneal lavage fluid collected 24 and 48 h after challenge, respectively; these numbers were reduced significantly by the administration of 0.1 microgram of rmIL-10. Finally, rmIL-10 failed to modify the anti-CD3-induced IL-5 release in vivo in the peritoneal cavity and in vitro from purified spleen CD4+ T lymphocytes. This suggests that rmIL-10 acts indirectly, by deactivating APC, rather than directly on T cell activation. These findings indicate that rmIL-10 displays anti-allergic activity in sensitized BALB/c mice by preventing Ag-induced CD4+ T lymphocyte and eosinophil accumulation as well as IL-5 release in the peritoneal cavity.

Animals↗
PubMed2006

The tick protective antigen, 4D8, is a conserved protein involved in modulation of tick blood ingestion and reproduction.

The gene that encodes the tick protective antigen, 4D8, was cloned from 10 species belonging to 6 genera, and the nucleotide and amino acid sequences were analyzed. 4D8 nucleotide and protein sequences were conserved among these tick species with identity/similarity between 65-98 and 60-98%, respectively. The function of 4D8 was characterized by RNA interference (RNAi) in five tick species. After the ticks were allowed to feed, degeneration of gut, salivary glands and reproductive tissues was observed, and tick survival, weight and oviposition were significantly reduced. 4D8 RNAi effected >90% reduction in oviposition in all tick species tested. Because of the critical role that 4D8 plays during tick feeding and oviposition, which ultimately results in the reduction of tick progeny, we proposed the generic name "subolesin" (Latin, suboles: offspring, progeny) for tick 4D8 proteins and subA for the subolesin-encoding gene.

Amino Acid Sequence↗
PubMed1999

Establishment of a human thymic myoid cell line. Phenotypic and functional characteristics.

The subset of myoid cells is a normal component of the thymic stroma. To characterize these cells, we immortalized stromal cells from human thymus by using a plasmid vector encoding the SV40 T oncogene. Among the eight cell lines obtained, one had myoid characteristics including desmin and troponin antigens. This new line was designated MITC (myoid immortalized thymic cells). These cells expressed both the fetal and adult forms of muscle acetylcholine receptor (AChR) at the mRNA level, as well as the myogenic transcription factor MyoD1. alpha-Subunit AChR protein expression was detected by flow cytometry and the AChR was functional in patch-clamp studies. In addition, AChR expression was down-modulated by myasthenia gravis sera or by monoclonal antibody anti-AChR on MITC line similarly to TE671 rhabdomyosarcoma cells, making the MITC line an interesting tool for AChR antigenic modulation experiments. Finally, the MITC line expressed LFA-3, produced several cytokines able to act on T cells, and protected total thymocytes from spontaneous apoptosis in vitro. These results are compatible with a role of thymic myoid cells in some steps of thymocyte development. Therefore MITC line appears to be a useful tool to investigate the physiological role of thymic myoid cells.

Antigenic Modulation↗
PubMed1988

Effect of interferon-gamma on HLA class II antigen expression and sensitivity to prostaglandin E1 by normal and leukemic myeloid progenitors.

Chronic myelogenous leukemia (CML) granulo-monocyte committed progenitors (CFU-GM) are markedly less sensitive than normal progenitors to the inhibitory action of prostaglandin E (PGE). This phenomenon has been ascribed to their abnormal expression of HLA class II (mainly DR) determinants. Since interferon gamma (IFN-gamma) is a potent inducer of the expression of HLA class II (DR and to a lesser extent DQ) antigens, we have sought to determine the extent to which this agent can modulate both the antigenic pattern of normal and leukemic progenitors and their sensitivity to PGE 1. 72-h preincubation of normal and CML bone marrow cells with or without IFN-gamma does not significantly change DR and DQ expression by CFU-GM. Pre-incubation for 72 h with and without IFN-gamma produces the following changes in PGE 1 sensitivity: (1) normal CFU-GM lose some sensitivity to PGE 1. This is only marginally counteracted by the presence of IFN-gamma. (2) CML CFU-GM, preincubated with IFN-gamma regain a significant sensitivity to high concentrations of PGE 1. Our data confirm the expression of DR molecules on normal and leukemic progenitors. They also show that, although incubation with IFN-gamma for 72 h in a liquid culture system does not significantly affect the expression of HLA class II molecules by progenitor cells, it may increase their sensitivity to PGE, particularly in the case of CML CFU-GM. Thus expression of HLA class II antigens and sensitivity to PGE may be dissociated.

Alprostadil↗
PubMed1989

Nedocromil sodium inhibits IgE- and IgG-related antigen-induced contraction in guinea-pig trachea.

The effects of nedrocromil sodium and disodium cromoglycate were studied on the anaphylactic contraction of guinea-pig trachea in two models of active sensitization (IgE and IgG models). The influence of epithelial removal on the effects of nedocromil sodium and disodium cromoglycate was examined because several studies have shown that the epithelial layer can modulate agonist- or antigen-induced contractile responses. Disodium cromoglycate (10(-4) M) and nedocromil sodium (10(-4) M) provided significant protection against antigen-induced contractions of guinea-pig tracheal smooth muscle in the IgG model. But only nedocromil sodium had an effect at this concentration in the IgG model and was also effective at 10(-5) M in the epithelium-denuded tracheal strips. At this concentration, disodium cromoglycate lost its protective effect. Comparison with the results obtained with FPL-55712, AA-861 and mepyramine suggested that these drugs affect histamine and particularly leukotriene synthesis and/or release by mast cells or other immunocompetent cells. These findings indicate that nedocromil sodium inhibits the IgE- and IgG-related antigen-induced contraction in guinea-pig airways, whereas disodium cromoglycate inhibits only the IgG-related processes. This study supports the hypothesis that these drugs modulate antigen-induced mediator synthesis and/or release from immunocompetent cells.

Airway Resistance↗
PubMed1990

Modulation of tPA, PAI-1 and PAI-2 antigen and mRNA levels by EGF in the A431 cell line.

It has been reported that EGF treatment enhances uPA but not tPA in the A431 epidermoid carcinoma cell line. To determine whether the absence of tPA modulation by EGF could be due to the action of inhibitors, we assayed tPA, PAI-1, PAI-2 and tPA/PAI-1 complexes by immunological assays and zymography in A431 serum-free medium. We found that, under conditions in which EGF had no effect on tPA activity, tPA antigen increased with a concomitant rise of tPA/PAI-1 complexes, indicating the action of an inhibitor. Both tPA antigen and tPA/PAI-1 complexes were modulated by EGF in a time and concentration dependent manner. tPA/PAI-1 complex levels were lower than tPA levels, suggesting the presence of other inhibitors. Immunological assays detected PAI-2 in addition to PAI-1 and showed a time and dose response to EGF. Modulation of tPA and the anti-activators by the growth factor was confirmed by identification of the corresponding transcripts with cDNA probes. We conclude that the net plasminogen activator activity in A431 cells is the result of a balance between activators and inhibitors.

DNA↗
PubMed1993

In vitro induction of basal keratinocyte MY7 antigen expression in cutaneous T-cell lymphoma is associated with response to interferon-alfa therapy.

BACKGROUND: Normal basal cell keratinocytes express an antigen recognized by monoclonal antibody MY7. This expression is lost in cutaneous T-cell lymphoma (CTCL) and may be reinduced under interferon-alfa-2a therapy. We investigated whether similar modulation of MY7 antigen could be obtained in vitro and determined the relationship between in vitro modulation and clinical response. SUBJECTS: We studied MY7 expression by basal cell keratinocytes in reconstituted skin specimens from 10 patients with CTCL and from skin specimens from five control patients and determined its modulation by interferon-alfa-2a and interleukin 1 using the indirect immunofluorescence technique. Concurrently, clinical examination and in vivo immunologic study on cutaneous biopsy specimens were carried out for these 10 patients before and while receiving interferon-alfa-2a therapy. RESULTS: In vitro studies showed that in five control specimens MY7 expression by basal cells was constant without modulation by interferon-alfa-2a or interleukin 1. Two of 10 CTCL specimens spontaneously expressed MY7 antigen while an additional five did so after incubation with interferon-alfa-2a and the last three never did. CONCLUSION: The three patients with CTCL for whom no MY7 expression was observed in reconstituted skin studies were "poor responders" to interferon-alfa-2a therapy. The five patients with CTCL for whom in vitro MY7 expression was induced by interferon-alfa-2a were responders. For the last two patients, results were variable. Thus, in vitro MY7 antigen is expressed in normal basal cell keratinocytes, absent in CTCL basal cell keratinocytes, but can be induced by interferon-alfa-2a. Moreover this in vitro modulation appears to be possibly correlated with interferon-alfa efficacy in vivo.

Antigens, CD↗
PubMed2000

Antigen presenting cells expressing Fas ligand down-modulate chronic inflammatory disease in Fas ligand-deficient mice.

We assessed the effect of modified antigen presenting cells (APCs) expressing high levels of Fas ligand (APC-FasL) on post-viral chronic inflammatory disease. FasL-deficient B6-gld/gld mice infected with murine cytomegalovirus (MCMV) cleared the virus from their lungs, kidneys, and livers within 2 weeks of infection. However, inflammation persisted in these organs for more than 8 weeks, with a chronically increased T-cell response to MCMV-infected APCs and production of autoantibodies. Administration of APC-AdFasL at 4 weeks suppressed this inflammation and diminished the T-cell response and autoantibody production. APC-AdFasL that had been transfected with ultraviolet-irradiated MCMV were more effective than uninfected APC-AdFasL in ameliorating the chronic inflammation. APC-AdFasL migrated preferentially to the spleen, where they triggered apoptosis of lymphocytes in the marginal zone of the spleen. These results confirm that Fas-mediated apoptosis is not required for clearance of virus, but is required for down-modulation of the virally induced chronic inflammatory response. This organwide effect of APC-AdFasL appears to be mediated by elimination of activated T lymphocytes in the spleen before their emigration to the target organs.

Adenoviridae↗
PubMed2002

Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) as modulators of both innate and adaptive immunity.

The structurally related neuropeptides VIP and PACAP are released within the lymphoid organs following antigenic stimulation, and modulate the function of inflammatory cells through specific receptors. In activated macrophages, VIP and PACAP inhibit the production of pro-inflammatory agents (cytokines, chemokines, and nitric oxide), and stimulate the production of the anti-inflammatory cytokine IL-10. These events are mediated through the VIP/PACAP effects on de novo expression or nuclear translocation of several transcription factors, i.e., NFkappaB, CREB, c-Jun, JunB, and IRF-1. The in vivo administration of VIP/PACAP results in a similar pattern of cytokine and chemokine modulation, which presumably mediates the protective effect of VIP/PACAP in septic shock. In addition, VIP/PACAP reduce the expression of the co-stimulatory molecules B7.1/B7.2, and the subsequent stimulatory activity of macrophages for T-helper cells. In T-cells expressing specific VIP/PACAP receptors, VIP and PACAP inhibit the expression of FasL through effects on NFkappaB, NFAT, and Egr2/3. The reduction of FasL expression has several biological consequences: inhibition of antigen-induced cell death in CD4 T-cells, inhibition of the FasL-mediated cytotoxicity of CD8 and CD4 effectors against direct and bystander targets, and promotion of long-term memory Th2 cells, through a positive effect on the survival of Th2, but not Th1, effectors. The various biological effects of VIP and PACAP are discussed within the range of a general anti-inflammatory model.

Adjuvants, Immunologic↗
PubMed1999

Autoreactive CD4+ T cells protect from autoimmune diabetes via bystander suppression using the IL-4/Stat6 pathway.

Targeted immune regulation can be achieved by use of tissue-specific T cells and offers the potential for organ-specific suppression of destructive autoimmune processes. Here, we report the generation and characterization of insulin B chain-specific "autoreactive" CD4+ regulatory T cells that locally suppress diabetogenic T cell responses against an unrelated self-antigen (viral transgene) in a virus-induced model for type 1 diabetes. Interleukin 4 (IL-4) is essential for prevention of diabetes since regulatory T cells cannot be induced in the absence of IL-4 or stat6 (IL-4 signaling pathway). Our observations demonstrate that autoreactive regulatory T cells can suppress autoreactive destructive T cell activity of differential antigenic specificity locally in the pancreatic draining lymph node, probably via cytokine-mediated modulation of antigen-presenting cells.

Administration, Oral↗
PubMed1983

An in vivo model for measuring antigen-induced SRS-A-mediated bronchoconstriction and plasma SRS-A levels in the guinea-pig.

1 Pharmacological modulation of antigen-induced anaphylaxis in actively sensitized guinea-pigs with intravenously administered indomethacin (10 mg/kg), pyrilamine (2.0 mg/kg) and propranolol (0.1 mg/kg) resulted in a delayed onset, slowly developing bronchoconstriction indicative of a slow-reacting substance of anaphylaxis (SRS-A) response. 2 Measurements of pulmonary mechanics on the drug-pretreated animals challenged with ovalbumin demonstrated a more prominent effect on dynamic compliance than resistance. This is consistent with the more potent effects of SRS-A on peripheral rather than central airways. 3 The slowly developing bronchoconstriction obtained after treatment with indomethacin, pyrilamine and propranolol was inhibited by the standard SRS-A antagonist, FPL 55712 and the SRS-A synthesis inhibitors, phenidone, BW 755C and nordihydroguaiaretic acid. 4 Plasma SRS-A levels were determined in guinea-pigs following antigen challenge. The appearance of SRS-A in the plasma preceded the onset of bronchoconstriction and SRS-A levels remained elevated throughout its development. Coincident with the inhibition of bronchoconstriction by the SRS-A synthesis inhibitor, phenidone, was a dose-dependent reduction in plasma SRS-A. The intravenous ED50 in each case was 4 mg/kg. 5 This model of antigen-induced SRS-A-mediated bronchoconstriction should prove useful for the in vivo evaluation and development of therapeutics which regulate the synthesis of SRS-A.

Animals↗
PubMed1989

Restricted expression of an early myeloid and monocytic cell surface antigen defined by monoclonal antibody M195.

A mouse monoclonal IgG2a antibody, M195, with reactivity restricted to early myeloid cells, acute non-lymphoid leukemia cells (ANLL), and monocytic cells is described. The antibody was derived from a mouse immunized with live human leukemic myeloblasts. Specificity of binding of mAb M195 was determined by protein-A red blood cell rosetting assays, immunoabsorption, radioimmunoassays with iodine-125 labeled M195 IgG and F(Ab)'2, and complement cytotoxicity with live human cells and cell lines representing a broad range of lineages and tissues. Antigen expression was restricted to myeloid and monocytic leukemia cell lines and a fraction of mature adherent monocytes. Mature myeloid cells, T and B cells, erythrocytes, and platelets were negative. The antigen was not expressed on adult human tissues in immunoperoxidase and immunofluorescence assays. Blocking antigen was not found in the serum of patients with ANLL. Ten thousand sites per cell were expressed on myeloid or monocytic leukemia cell lines and 5000 sites per cell on mature monocytes. M195 IgG bound to its antigen target with an avidity of 3 x 10(9) liters/mol and induced rapid modulation of the antigen. M195 IgG was able to effectively kill cells with rabbit or guinea pig complement, but not human complement. The antibody did not mediate antibody dependent cellular cytotoxicity. The molecular nature of the target antigen remains unknown but it appears to be carried on the CD33 protein p67. Because of its restricted distribution on myelomonocytic cells, mAb M195 may be useful in studying myeloid differentiation, in the clinical diagnosis of ANLL, in purging of bone marrow of ANLL, and/or in monoclonal antibody therapy in vivo.

Animals↗
PubMed1999

Lack of interleukin 10 regulation of antigen presentation-associated molecules expressed on colonic epithelial cells.

BACKGROUND: Colonic epithelial cells may behave as antigen-presenting cells. Interleukin 10 (IL-10) is known to play a major role in the intestinal immune system; however, it remains to be determined whether human intestinal epithelial cells express IL-10 receptor, and whether this cytokine modulates their expression of antigen presentation-associated molecules. METHODS: The binding of biotinylated IL-10 was studied in SW 1116, HT-29 and T84 human colonic epithelial cell lines and freshly isolated normal colonic epithelial cells. Reverse transcription-polymerase chain reaction was also performed to detect IL-10 receptor mRNA. The effect of IL-10 on antigen presentation associated molecules was assessed by flow cytometry. RESULTS: Biotinylated IL-10 bound to SW 1116, HT-29, T84, and normal colonic epithelial cells. IL-10 receptor mRNA was detected in SW 1116 and normal epithelial cells. SW 1116 and HT-29 cells expressed MHC class I and ICAM-1, but not CD80, and SW 1116 constitutively expressed HLA-DR. Interferon-gamma up-regulated HLA-DR and ICAM-1 expression on both cells, whereas lipopolysaccharide increased ICAM-1 expression only on SW 1116. IL-10 failed to modulate these antigens, even after stimulation by lipopolysaccharide or interferon-gamma. Moreover, these molecules decreased IL-10 binding in both lines. CONCLUSION: The presence of IL-10 receptor on intestinal epithelial cells suggest that IL-10 may play a role in mucosal physiology, however its effect on the immune response remains to be determined.

Adenocarcinoma↗
PubMed1997

n-butyrate downregulates the stimulatory function of peripheral blood-derived antigen-presenting cells: a potential mechanism for modulating T-cell responses by short-chain fatty acids.

Modulation of proliferative T-cell responses by n-butyrate has been suggested to result from direct interference with cell cycle progression. Considering the important role of antigen-presenting cells (APC) in T-cell activation, we were particularly interested in studying the impact of n-butyrate on these cells. We demonstrated that pretreatment of human peripheral blood mononuclear cells (PBMC) or monocytes with this agent resulted in a dose- and time-dependent downregulation of their capability to stimulate T-cell responses with a similar pattern of inhibition when this agent was present throughout the culture period. Pretreatment with n-butyrate was effective in preventing both alloresponses and T-cell proliferation to immobilized anti-CD3 monoclonal antibody (mAb) suggesting alteration of costimulatory function. Flow cytometric analysis revealed that interferon-gamma (IFN-gamma)-induced upregulation of B7-1 expression on monocytes was profoundly inhibited by n-butyrate. Furthermore, this agent significantly suppressed the expression of intercellular adhesion molecule-1 (ICAM-1) or lymphocyte function-associated antigen-3 (LFA-3). In contrast, constitutive as well as cytokine-induced expression of B7-2 was enhanced by n-butyrate. Additionally, in monocytes, but not in T cells, treatment with n-butyrate led to significant alteration of membrane integrity owing to apoptotic cell death. Our findings indicate that modulation of T-cell responses by n-butyrate could also result from altered APC function, possibly as a consequence of downregulating distinct adhesion and/or costimulatory receptors as well as of inducing apoptosis. A potential clinical relevance of short-chain fatty acids for reducing T-cell-mediated immune reactions via modulating APC function is speculated.

Antigen-Presenting Cells↗