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PubMed1993

Modulation of leukosialin (sialophorin, CD43 antigen) on the cell surface of human hematopoietic cell lines induced by cytokins, retinoic acid and 1,25(OH)2-vitamin D3.

Cell surface expression of leukosialin (sialophorin, CD43 antigen) on human neoplastic hematopoietic cell lines K-562, U-937, HL-60 and REH was determined with the aid of a new CD43 monoclonal antibody (Bra7G) by the immunochemical (radioimmunoprecipitation, immunoblotting) and immunocytofluorometric techniques. Interferon-gamma and TNF-alpha were utilized as the "physiological" inducers of differentiation-associated markers. The "non-physiological" inducer phorbol ester PMA induced down-regulation of leukosialin cell surface expression on immature erythroid-myeloid leukemia cell line K-562, but up-regulation of CD43 antigen on the promyelocyte leukemia cell line HL-60 and, to a lesser extent on the monocyte-like U-937 and CALLA+ ALL cell line REH. Retinoic acid down-regulated leukosialin on both U-937 monocyte-like cells and the CALLA+ ALL cell line REH. In contrast to these data, interferon-gamma, TNF-alpha, retinoic acid and 1,25(OH)2-vitamin D3 induced the up-regulation of leukosialin in a promyelocytic leukemia cell line HL-60.

Antigens, CD↗

PubMed1993

Current status of immunologic recurrent pregnancy loss.

Normal mammalian pregnancy is confronted with a great number of self (autoimmune) and foreign (alloimmune) antigens that modulate the immune system of the mother. When maternal immune response is affected, recurrent pregnancy loss can result. Recurrent pregnancy loss affects 2% to 5% of reproducing couples. Half of these failures can be explained by genetic, hormonal, infectious, and anatomic factors. Eighty percent of the unexplained failures are proposed to have an immunologic cause. HLA typing, mixed lymphocytotoxic antibody tests, mixed lymphocyte culture reactions, lupus anticoagulant tests, and antiphospholipid antibody determination are methods used to study and differentiate between auto- and alloimmune response. Experimental therapies, including leukocyte immunization, seminal plasma suppositories, intravenous immunoglobulin, aspirin and prednisone, and heparin, have been tried to manage this condition. Results of randomized placebo-controlled clinical trials will aid in the choice of treatment for recurrent pregnancy loss. New assays to diagnose auto- and alloimmune factors in recurrent pregnancy loss are being investigated.

Abortion, Habitual↗

PubMed1996

Coexistence of superficial pemphigus and psoriasis.

We describe a case of the coexistence of psoriasis and pemphigus erythematosus. The coexistence of these two diseases may be more than coincidental: the effects of one immune-mediated skin disease may influence the occurrence of another. Possible mechanisms include antigen modification, altered regulation of T-cell activity, and plasminogen activator abnormalities.

Anti-Inflammatory Agents↗

PubMed1994

Simultaneous expression of thyroid peroxidase and human leukocyte antigen-DR by human thyroid cells: modulation by thyrotropin, thyroid-stimulating antibody, and interferon-gamma.

Major histocompatibility class II molecules human leukocyte antigen-DR (HLA-DR) are abnormally expressed by human thyroid cells (HTC) in autoimmune thyroid glands. The simultaneous expression of HLA-DR and organ-specific autoantigens such as thyroid peroxidase (TPO) by HTC might enable these cells to function as antigen-presenting cells, thus perpetuating the autoimmune process. The aim of the present study was to clarify the interplay of endocrine (TSH) and immune [TSab or interferon-gamma (IFN gamma)] factors on the expression of HLA-DR and TPO in HTC. Thyrocytes were cultured with supernatants of T-cells cloned from the infiltrate of Hashimoto's glands, human recombinant IFN gamma, TSab, or TSH. These factors were added either alone or in different combinations and sequences. HLA-DR and TPO were identified in HTC by a double indirect immunofluorescence technique, using a monoclonal anti-HLA-DR antibody and human serum containing anti-TPO antibody, respectively. IFN gamma, either recombinant or produced by T-cell clones, induced HLA-DR appearance in thyrocytes, whereas TSH or TSab stimulated TPO expression. The appearance of HLA-DR induced by IFN gamma was accompanied by a progressive reduction of TPO despite stimulation by TSH or TSab. This decline reached a nadir after 9-10 days in different primary cultures. During this period, a percentage of cells ranging from 10-40% simultaneously expressed HLA-DR and TPO on their surface and in the cytoplasm. The inhibition of TPO expression and the appearance of HLA-DR induced by IFN gamma were rapidly reverted when TSH or TSab was substituted for interleukin in the culture medium and vice versa. We conclude that 1) the expression of TPO or HLA-DR in thyroid cells is a dynamic phenomenon that is differently influenced by TSH, TSab, and IFN gamma. It is the interplay of these factors in different follicles and during different periods of time that determines the expression of TPO alone, HLA-DR alone, or both molecules together in the same thyroid cell; 2) during exposure to TSH (or TSab) and IFN gamma, TPO and HLA-DR can be expressed simultaneously by thyroid cells for up to 7 days; and 3) the modulation of HLA-DR and TPO by supernatants of T-cells cloned from Hashimoto's glands is reproduced by IFN gamma alone.

Antibodies, Monoclonal↗

PubMed1985

Expression of the microsomal antigen on the surface of continuously cultured rat thyroid cells is modulated by thyrotropin.

The thyroid microsomal antigen, commonly implicated in thyroid autoimmune diseases, is not confined to cytoplasm, but is also present on the surface of human thyroid cells in primary culture. In this study, a strain of differentiated rat thyroid cells (FRTL5) grown in continuous culture was used to investigate the relationship between functional status of the thyroid cell and expression of microsomal antigen on its surface. Sera from eight patients with Hashimoto's thyroiditis, one with idiopathic hypothyroidism, and three with hyperthyroid Graves' disease were selected for the presence of microsomal antibody, but undetectable thyroglobulin antibody. One additional serum sample from a patient with Graves' disease, which was negative for both thyroid antibodies was used. Sera from eight normal subjects were used as controls. Indirect immunofluorescence was applied to FRTL5 cells that were viable or fixed with acetone in order to expose intracellular antigens. When FRTL5 cells were cultured in Coon's medium containing TSH (300 microU/ml), positive indirect immunofluorescence surface staining was observed with sera containing microsomal antibody, but not with control sera or with the Graves' serum negative for microsomal antibody. A rough correlation was found between the intensity of the surface fluorescence and microsomal antibody titer. After acetone treatment, microsomal antibody-positive sera produced typical cytoplasmic staining. When FRTL5 cells were cultured in the absence of TSH, disappearance of the surface fluorescence and reduction of the cytoplasmic microsomal antigen occurred. Readdition of TSH progressively restored both the surface and cytoplasmic microsomal antigen. The present data indicate that the thyroid microsomal antigen is represented on the surface of FRTL5 cells, and its expression is modulated by TSH.

Animals↗

PubMed1990

Antigen-induced T-cell changes: modulation by pharmacologic agents.

To determine the effect of pharmacologic modulation of alterations of peripheral blood T-cell subsets caused by antigen-induced bronchoconstriction, we administered albuterol immediately after antigen-induced bronchoconstriction in a double-blind to protocol to 12 atopic asthmatic subjects. We also administered cromolyn sodium before antigen to 7 of the same subjects. Peripheral blood T-cell subset composition (CD4, CD8, Ia) of a highly purified T-cell preparation was determined before, 24, 48, 72, and 168 h after bronchoconstriction. We found that placebo inhalation immediately after antigen-induced bronchoconstriction did not affect subsequent peripheral blood T-cell subset changes (decrease in CD4+ and increase in Ia+ T lymphocytes). In contrast, inhaled albuterol abolished these T-cell subset changes. Although cromolyn sodium significantly decreased the severity of antigen-induced bronchoconstriction, it did not affect T-cell subset composition changes at the dosage used. We conclude that albuterol can ablate T-cell subset changes associated with antigen-induced bronchoconstriction. Cromolyn sodium ameliorates bronchoconstriction, but has no affect on T-cell subset composition changes. This implies that T-cell changes and bronchoconstriction caused by antigen inhalation are mediated through different pathways.

Administration, Inhalation↗

PubMed1982

Activation and immunoregulation of antigen-specific human b lymphocyte responses: multifaceted role of the monocyte.

The multifaceted role of the monocyte in the induction and modulation of antigen-specific antibody responses by human B cells was delineated. Monocytes were absolutely required for the induction of specific antibody responses to both TT and KLH in an antigen-induced in vitro assay. Monocytes were also required for the PWM induction of specific antibody in immunized subjects. Pulsing monocytes with specific antigen or with PWM consistently stimulated proliferation of T cells in absence of added antigen and could also stimulate specific antibody synthesis although less consistently. Stimulation of specific antibody responses with antigen required fewer numbers of monocytes than did stimulation of specific antibody responses with PWM. Polyclonal antibody synthesis induced by PWM was also dependent on monocytes. However, polyclonal antibody synthesis induced by supraoptimal concentrations of antigen was usually optimal in the absence of monocytes and was actually suppressed when increased numbers of monocytes were added to monocyte-depleted cultures. Monocyte supernatants could not replace the absolute requirements for monocytes in the induction of specific antibody synthesis. However, monocyte supernatants could profoundly modulate the antigen-specific as well as the polyclonal Ig response of lymphocytes to either antigen or PWM stimulation in a manner closely resembling monocytes themselves. Thus, we demonstrated that monocytes and their products play a critical role in the activation and immunoregulation of antigen-specific antibody responses of human B cells.

Antibody Formation↗

PubMed1981

The sympathetic nervous system modulates antibody response to thymus-independent antigens.

Sympathetic nerve endings were destroyed with 6-hydroxydopamine (6-OHDA) and the response to thymus-dependent and -independent antigens compared in 6-OHDA-treated and control mice. A significantly enhanced plaque-forming cell response to 2 thymus-independent antigens was observed in the 6-OHDA-treated mice; in contrast the response to a thymus-dependent antigen was normal. The findings point to selective modulation of antibody response by the sympathetic nervous system.

Animals↗

PubMed1995

Idiotypic modulation of the antibody response of mice to Echinococcus granulosus antigens.

In this work we analysed the modulation of the antibody response to Echinococcus granulosus antigens via anti-idiotype (Ab2) administration. In a first set of experiments, we determined the antibody response to hydatid cyst fluid antigen (HCFA) of mice immunized with Ab2. Results showed that Ab2 elicited anti-HCFA antibodies in mice that had never been exposed to HCFA before. Moreover, that response was characterized by booster effect, avidity maturation and an inverse correlation between avidity and Ab2 dose. We infected these mice and measured the titre and avidity of anti-HCFA antibodies during 250 days of infection. Lack of avidity maturation was the most important feature observed, suggesting that the parasite (either protoscolex or cyst) could modulate the antibody response of its host. In a second set of experiments, we investigated the presence of regulatory anti-idiotypes in the Ab2 preparation. In this context we treated neonates with different doses of Ab2, immunized them with HCFA 12 weeks later and determined their anti-HCFA titres. A specific and Ab2 dose-dependent suppression of the response to HCFA was observed, suggesting the existence of regulatory anti-idiotypes in the Ab2 preparation. Although this Ab2 could be involved in the regulation of the anti-HCFA response, other anti-idiotypes could also be involved. Our results show that it may be possible to improve the avidity of the anti-HCFA response via the administration of the anti-idiotype Ab. However, the live parasite could successfully revert this effect by mechanisms not yet characterized.

Animals↗

PubMed1990

Modulation of the HLA class II antigen at a molecular level by maternal serum.

The recent immunological literature has described the existence of a retroplacental serum factor being responsible for the downregulation of the MHC Class II antigen expression. In this report, the same property has been found in peripheral maternal serum. The HLA Class II modulating activity is however diminished in the presence of peripheral maternal serum as compared to retroplacental serum suggesting that the IA like inhibiting factor is released at the fetomaternal interface. After a three-day incubation period of unrelated lymphocytes in a maternal serum pool, it was shown that the HLA Dr., the HLA Dp., and more significantly, the HLA Dq. molecules were modulated. When third party lymphocytes were stimulated by Candidine or unrelated mononuclear cells in the presence of retroplacental serum, only the cellular subpopulation belonging to the CD4+ subset showed an HLA Dq. downregulation. The molecular constituents of the MHC Class II antigen expression characterizing cells belonging to other subsets remained unchanged. When the same stimulation assay was performed in the presence of a control medium (nulliparous serum), no changes concerning the MHC Class II molecular constituents were observed. When unrelated mononuclear cells were PHA stimulated in the presence of maternal and nulliparous serums, the HLA Dq. expression of the CD8+ subset showed a significant downregulation in the maternal serum mediated stimulation assay as compared to the control stimulation test. The molecular expression of the HLA Class II antigen related to the other subpopulations (CD4+, CD3+) stimulated by a mitogenic lectin remained unchanged. It is suggested that these molecular MHC Class II modulations are due to a factor included in the maternal IgG reaction. Retroplacental IgG contains the highest concentration of this factor.

Down-Regulation↗

PubMed1991

Modulation of the HLA class II antigen at a molecular level by maternal serum among cord blood cells and unrelated lymphocytes.

A retroplacental serum factor responsible for the downregulation of the MHC class II antigen expression has been described [1]. We found that maternal serum had the same property. The HLA class II modulating activity is however diminished in the presence of maternal serum as compared to retroplacental serum suggesting that the IA like inhibiting factor is released at the fetomaternal interface. After a 3-day incubation period of unrelated lymphocytes and mononuclear cord blood cells in a maternal serum pool, it was shown that the HLA Dr, the HLADp, and more significantly, the HLADq molecules were modulated. This phenomenon was more pronounced among cord blood cells. When third party lymphocytes and mononuclear cord blood cells were stimulated by Candidine or unrelated mononuclear cells in the presence of retroplacental serum, only the cellular subpopulation belonging to the CD4+ subset showed an HLADq downregulation. The molecular constituents of the MHC class II antigen expression characterizing cells belonging to other subsets remained unchanged. When the same stimulation assay was performed in the presence of a control medium (nulliparous serum), we found no changes in the MHC class II molecular constituents. When unrelated mononuclear cells and mononuclear cord blood cells were PHA stimulated in the presence of maternal and nulliparous serum, the HLADq expression of the CD8+ subset showed a significant downregulation in the maternal serum mediated stimulation assay as compared to the control stimulation test. The molecular expression of the HLA class II antigen related to the other subpopulation (CD4+, CD3+) stimulated by a mitogenic lectin remained unchanged. It is suggested that these molecular MHC class II modulations are due to a factor included in the maternal IgG reaction. Retroplacental IgG contains the highest concentration of this factor.

Anti-Bacterial Agents↗

PubMedDate not supplied

Vagal sensitivity in intrinsic and allergic asthma.

In 20 intrinsic and 25 allergic asthmatic patients with active disease, vagal baroreflex sensitivity was assessed by use of the phenylephrine test, and vagal blockade effects on airways were measured by the response to intravenous atropine. For a given phenylephrine-induced increase in blood pressure, bradycardia was more marked in patients with intrinsic asthma than in those with allergic asthma. Intravenous atropine caused a similar spirometric improvement in both groups. It is suggested that: 1) an inverse relationship exists between vagal sensitivity and the allergic state in asthma; 2) antigenic related stimulation modulated by a low vagal tone and non-antigenic related stimuli with high tone modulation result in similar cholinergic discharges.

Adult↗

PubMed1978

Peripheral human T cells sensitized in mixed leukocyte culture synthesize and express Ia-like antigens.

We have studied the modulation of Ia-like antigens on the surface membrane of human T cells responding in a one-way mixed leukocyte culture. A heterologous antiserum, (anti-p23,30), which is specific to HLA-D-related antigens and which is unreactive with normal peripheral T cells or thymocytes, was found to bind significantly to all T cells transformed in mixed leukocyte culture (MLC) as determined by indirect immunofluorescence on a fluorescence-activated cell sorter 1. Furthermore, cytotoxic T cells responsible for cell-mediated lympholysis were shown to react with anti-p23,30, whereas their unactivated progenitors did not. Immunoprecipitation and sodium dodecyl sulfate polyacrylamide gel electrophoresis of a radioactive 29,000 and 34,000 dalton complex from MLC-primed T cells labeled with [35S]methionine indicated that allosensitized T cells synthesized these HLA-D-related antigens.

Antigens, Surface↗

PubMed1999

Antigen-induced TCR-CD3 down-modulation does not require CD3delta or CD3gamma cytoplasmic domains, necessary in response to anti-CD3 antibody.

We studied cytotoxic T lymphocyte (CTL) clones expressing cytoplasmic domain-deleted CD3delta and CD3gamma chains. These cells retained efficient antigen-specific cytolysis. Because the cytoplasmic domains of native CD3delta and CD3gamma chains contain a dileucine-based and a tyrosine-based motif thought to be important for receptor endocytosis, we compared TCR-CD3 down-modulation on the CTL clones expressing or not these domains. We found that antigen-induced TCR-CD3 down-modulation was not dependent on either the CD3delta or CD3gamma cytoplasmic domains. This contrasts with phorbol ester- and anti-CD3 mAb (soluble or plastic-coated)-induced TCR-CD3 down-modulation, that are respectively dependent on CD3gamma and on either CD3delta or CD3gamma cytoplasmic domains, suggesting that differences may exist between the mechanisms of TCR-CD3 down-modulation in response to the three stimuli. TCR-CD3 down-modulation in response to antigen was demonstrated by confocal microscopy to be associated with TCRbeta chain internalization, whether CD3delta and CD3gamma were native or truncated. Inhibition by the protein tyrosine kinase inhibitor PP1 of TCR-CD3 down-modulation in response to antigen was also similar whether CD3delta and CD3gamma cytoplasmic domains were present or not. These properties of receptor down-modulation are discussed with respect to the requirements for TCR engagement on antigen-presenting cells.

Animals↗

PubMed1998

Adjuvant is the major parameter influencing the isotype profiles generated during immunization with a protein antigen, the Schistosoma mansoni Sm28-GST.

We have previously shown that immunization of mice with the vaccine candidate, the 28-kDa glutathione-S-transferase of Schistosoma mansoni (Sm28-GST), in alum or complete Freund's adjuvant, or with recombinant Salmonella typhimurium expressing Sm28-GST, induced type 2, mixed, or type 1 immune responses, respectively. In the present study we examined whether the genetic background, the dose and the route of antigen administration could modulate the profile of the immune response induced during these immunizations. Our results show that the nature of the adjuvant is the major factor that determines the profile of the response. Surprisingly, the genetic background did not influence the response, while the route of immunization, and to a lesser extent the dose of the antigen, weakly modulated the adjuvant-dependent orientation of the immune response.

Adjuvants, Immunologic↗

PubMed1992

Tumor antigen presentation by epidermal antigen-presenting cells in the mouse: modulation by granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha, and ultraviolet radiation.

I-A+ epidermal antigen-presenting cells (APCs, Langerhans cells) have been shown to present tumor-associated antigens (TAAs) and to induce tumor immunity in vivo. This study examined the effects of ultraviolet radiation (UVR) and the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha) on the ability of epidermal cells (ECs) to induce or to elicit immunity against the murine spindle cell tumor S1509a. Naive syngeneic mice were immunized three times at weekly intervals with ECs that had been cultured in GM-CSF for 18 h and then pulsed with TAA derived from S1509a. This resulted in protective immunity against subsequent tumor challenge, providing a model to study the conditions required for sensitization against TAAs by epidermal APCs. Culture of ECs in GM-CSF was required for induction of significant protective tumor immunity, and UV irradiation or incubation in TNF-alpha for 2 h after GM-CSF incubation abrogated the immunostimulatory effect of GM-CSF. However, unlike UVR, TNF-alpha did not significantly inhibit the induction of immunity when ECs were exposed to TNF-alpha before overnight incubation in GM-CSF, together with GM-CSF, or after pulsing with TAA, and anti-TNF-alpha antibody treatment did not abrogate the effects of UVR on this system. Furthermore, TNF-alpha incubation of ECs augmented their ability to elicit delayed-type hypersensitivity (DTH) and also enhanced elicitation of DTH by GM-CSF-cultured ECs, whereas UV-irradiation reduced it in a dose-dependent fashion. Taken together, these results demonstrate that GM-CSF, TNF-alpha, and UVR are significant regulators of tumor antigen presentation by epidermal APCs and that the effects of the cytokines examined differ with regard to induction or elicitation of immunity.

Animals↗

PubMed2002

Immunomodulatory effects of glatiramer acetate on superantigen- and mitogen-induced T-cell stimulation in vitro.

Glatiramer acetate (GA) interferes with antigen recognition and modulates cytokine secretion of T cells in an antigen-specific manner. Here we analysed the capacity of GA to modulate proliferative responses and cytokine secretion of peripheral blood mononuclear cells (PBMCs) in response to antigen-independent stimuli, i.e., phytohaemagglutinin (PHA) and staphylococcal enterotoxin B (SEB) stimulation in five healthy volunteers. A significant reduction of proliferative responses, as well as interferon-gamma (IFNalpha) and tumour necrosis factor-alpha (TNFalpha) secretion, was observed at concentrations of 200 microg/ml suggesting that GA may also exert immunomodulatory effects on mitogen- and superantigen-induced T-cell stimulation in vitro. However, since systemic GA concentrations of this magnitude are highly unlikely to occur in vivo the immunomodulatory effects observed here are not likely to contribute to the therapeutic mechanisms of action under physiological conditions.

Adult↗

PubMed1983

Noncovalently bonded subunits of 22 and 28 kd are rapidly internalized by T cells reacted with anti-Leu-4 antibody.

Using immunofluorescence analysis in a FACS or cytofluorograph, we monitored the density of four different human T cell surface molecules (Leu-1/OKT1, Leu-2/OKT5,8, Leu-3/OKT4, and Leu-4/OKT3) at different intervals of incubation at 37 degrees C with monoclonal antibodies that react with these structures. Leu-1 and Leu-2 are probable human homologues of the murine Lyt-1 and Lyt-2,3 antigens, respectively. Leu-3 is a 55 kd antigen that is restricted to Leu-2- (helper) T cells. Leu-4 is expressed by all peripheral T cells and has at least two components of 22 and 28 kd that have an undefined structural relationship. The ultimate degree of modulation of each antigen varied considerably. Modulation of Leu-4 was particularly striking, because this antigen disappeared completely from the cell membrane within 7 hr of culture with saturating concentrations of alpha Leu-4. After modulation of surface 125I-labeled T cells, Leu-4 was found in the detergent-solubilized cell lysate, but not in the cellfree supernatant, indicating that it was internalized. Our results also indicated that the internalized antigen-antibody complex existed in at least two forms: a) as an antigen-antibody complex having only the lower m.w. (22 kd) component bound to antibody, or b) as free antigen having the 28 kd chain in noncovalent association with the 22 kd moiety. These studies indicate that the Leu-4 structure is composed of at least two distinct chains that are noncovalently associated. The rapid modulation and structural properties of the Leu-4 complex are discussed in the context of its possible functions in T cell immunity.

Antibodies, Monoclonal↗