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At least 19 recordsLinked to original sources
PubMed1985

Antigen presentation in the rat. II. An Ia+ radiosensitive T cell can present antigen to primed Ia- T cells.

We demonstrated previously the presence of an Ia+ (OX-6+) antigen-presenting cell within the rat T cell fraction that is capable of presenting antigen to antigen-primed OX-6-T cells. This antigen-presenting cell (T-APC) reacted with the monoclonal antibodies W3/25 and W3/13, which is known to react mainly with rat T cells. Further characterization of the T-APC indicated that the cell also reacted with the monoclonal antibody OX-19, which is highly specific for rat T cells. Moreover, the antigen-presenting function of the T-APC was sensitive to treatment with mitomycin C or gamma-irradiation (2000 rad). Under similar conditions, antigen presentation by partially purified dendritic cells or macrophages was totally resistant to these treatments. The antigen-presenting activity of gamma-irradiated T-APC was not reconstituted by the addition of the lymphokines IL 1, IL 2, or Con A supernatants. Although unirradiated T-APC were able to stimulate an MLR response, this function was also sensitive to gamma-irradiation, whereas the MLR-stimulating ability of macrophages and dendritic cells was resistant to gamma-irradiation. These data indicate that Ia+ T cells from the rat are capable of presenting antigen to antigen-primed T lymphocytes and that, in contrast to antigen presentation by macrophages and dendritic cells, the function of T-APC is gamma-radiation sensitive.

Animals↗
PubMed2005

Presenting antigen presentation in living cells using biophysical techniques.

The combination of genetically encoded fluorescent probes and advanced microscopic techniques has dramatically propelled the understanding of cell biology. Highly complex reactions can now be studied in detail in a relatively cost-effective and easy manner and, perhaps most importantly, in the context of a single living cell. In the past decade, numerous reports have uncovered the localization of key molecules in virtually all cellular processes. However, there remains a need for more accurate determination of genuine protein-protein interactions and quantification of highly dynamic processes, which has resulted in the revival of several biophysical techniques. Recent applications of these techniques have deepened understanding of processes involved in antigen presentation to the immune system.

Antigen Presentation↗
PubMed1981

Antigen-reactive T clones. III. Low responder antigen-presenting cells function effectively to present antigen to selected T cell clones derived from (High Responder x Low Responder)F1 mice.

Long-term-cultured poly(Tyr, Glu)-poly-D,L,-Ala-poly-Lys [(T,G)-A--L]-reactive T cells and clones derived from (high responder x low responder)F1 [(C57BL/6 x A/J)F1] mice were shown to recognize (T,G)-A--L presented by cells from low responder strain A/J mice. The antigen-presenting determinant(s) that allowed recognition of (T,G)-A--L by such T cell clones was controlled by the I-A subregion of the major histocompatibility complex. These results suggest that there is no functional defect in the ability of low responder Ir gene products (I-A antigens) to associate with (T,G)-A--L for effective recognition by T cells. Although these results might tentatively be interpreted to suggest that Ir gene-controlled low responsiveness is due to the inability of the T cell to recognize the association between (T,G)-A--L and low responder I-A gene products, it is similarly possible that there might be a defect in the functional capabilities of low responder antigen-presenting cells to effectively process (T,G)-A--L into immunodominant epitopes.

Animals↗
PubMed2005

Polarized uterine epithelial cells preferentially present antigen at the basolateral surface: role of stromal cells in regulating class II-mediated epithelial cell antigen presentation.

To study Ag presentation in the female reproductive tract, DO11.10 TCR transgenic mice specific for the class II MHC-restricted OVA(323-339) peptide and non-transgenic BALB/c mice were used. We report here that freshly isolated uterine epithelial cells, uterine stromal, and vaginal APCs present OVA and OVA(323-339) peptide to naive- and memory T cells, which is reduced when cells are incubated with Abs to CD80 and 86. To determine whether polarized primary epithelial cells present Ags, uterine epithelial cells were cultured on cell inserts in either the upright or inverted position. After reaching confluence, as indicated by high transepithelial resistance (>2000 ohms/well), Ag presentation by epithelial cells incubated with memory T cells and OVA(323-339) peptide placed on the basolateral surface (inverted) was 2- to 3-fold greater than that seen with epithelial cells in contact with T cells and peptide on the apical surface (upright). In contrast, whereas freshly isolated epithelial cells process OVA, polarized epithelial cells did not. When epithelial cells grown upright on inserts were incubated with T cells and OVA(323-339) peptide, coculture with either hepatocyte growth factor or conditioned stromal medium increased epithelial cell Ag presentation (approximately 90% higher than controls). These studies indicate that uterine stromal cells produce a soluble factor(s) in addition to a hepatocyte growth factor, which regulates epithelial cell Ag presentation. Overall, these results demonstrate that polarized epithelial cells are able to present Ags and suggest that uterine stromal cells communicate with epithelial cells via a soluble factor(s) to regulate Ag presentation in the uterus.

Animals↗
PubMed1988

Antigen presentation, antigen-presenting cells and antigen processing.

To summarize, during the period under review there have been considerable advances in our understanding of how antigen is associated with MHC on the surface of a presenting cell. Basic rules which govern this association have been confirmed as including both the nature and the configuration of the antigen. Although the different processing pathways which generate the antigen-MHC complex have remained ill-defined, it is now much more clear what the optimum end point of such processing must be. As a result of these studies, several new questions can now be addressed in the field of antigen presentation. During the next few years it should become apparent why there should be such an unusual differential presenting cell requirement for T cells which are expressing a selected variable region of the T cell receptor and whether other T cells expressing different receptors have different optimum presentation requirements. It should become clear also whether different antigens have similar residues at the sides of the alpha helix which are important in MHC binding, and whether the sheet or helix models are more important in vivo. A rational explanation for dominance of alloreactivity has been proposed, and kinetic studies of self-MHC processing are essential to define this further. Furthermore the possibility of an antigen unmasking an MHC polymorphism (which in turn could influence presentation) will have to be considered seriously in the pathogenesis of auto-immunity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

IL-1 secretion and membrane IL-1 expression by neonatal spleen cells during soluble antigen presentation.

Antigen presentation and IL-1 production by neonatal spleen cells were studied in a murine model. The T-helper-cell line (D10-G4.1) (D10), which is specific for soluble antigen presented on syngeneic antigen-presenting cells and dependent on IL-1 for its proliferation, was used as an indicator cell for the ability of syngeneic neonatal or adult spleen cells to present antigen and produce IL-1. The antigen-presenting capacity of neonatal spleen cells is low as attested by D10 proliferation. During antigen presentation there is an augmentation of IL-1 production by the antigen-presenting spleen cell population. However, neonatal spleen cells do not respond to the same levels as do adult spleen cells. These reduced levels of secreted IL-1 cannot be attributed to a low potential for producing IL-1 as attested by the high levels of IL-1 made by these cells after induction by a crude IL-1 inducer factor (IL-1-IF) and by the stimulus of the IL-1-IF produced by D10 cells during antigen presentation by paraformaldehyde-fixed adult cells. The spontaneous expression of membrane IL-1 by neonatal cells is low. Membrane IL-1 levels on neonatal cells can be brought to adult levels by induction with IL-1-IF. Neonatal spleen cells have an impaired capacity to process and/or present soluble antigen. This impairment leads to a decreased stimulus of the T helper cell to produce inducer factors and thus a reduced level of IL-1 production by the neonatal cells during antigen presentation.

Age Factors↗
PubMed1998

Cathepsins B and D are dispensable for major histocompatibility complex class II-mediated antigen presentation.

Antigen presentation by major histocompatibility complex (MHC) class II molecules requires the participation of different proteases in the endocytic route to degrade endocytosed antigens as well as the MHC class II-associated invariant chain (Ii). Thus far, only the cysteine protease cathepsin (Cat) S appears essential for complete destruction of Ii. The enzymes involved in degradation of the antigens themselves remain to be identified. Degradation of antigens in vitro and experiments using protease inhibitors have suggested that Cat B and Cat D, two major aspartyl and cysteine proteases, respectively, are involved in antigen degradation. We have analyzed the antigen-presenting properties of cells derived from mice deficient in either Cat B or Cat D. Although the absence of these proteases provoked a modest shift in the efficiency of presentation of some antigenic determinants, the overall capacity of Cat B-/- or Cat D-/- antigen-presenting cells was unaffected. Degradation of Ii proceeded normally in Cat B-/- splenocytes, as it did in Cat D-/- cells. We conclude that neither Cat B nor Cat D are essential for MHC class II-mediated antigen presentation.

Animals↗
PubMed1989

The induction of intercellular adhesion molecule 1 (ICAM-1) expression on human fetal astrocytes by interferon-gamma, tumor necrosis factor alpha, lymphotoxin, and interleukin-1: relevance to intracerebral antigen presentation.

Antigen presentation reactions are dependent upon the expression of the class II major histocompatibility antigens (MHC), the T-cell receptor, and the presented antigen. Recent studies demonstrate that such processes also require the presence of adhesion molecules such as lymphocyte functional antigen 1 (LFA-1) and its cell surface ligand, intercellular adhesion molecule 1 (ICAM-1). It has been suggested that the brain astrocyte can function as a facultative antigen presenting cell (APC). This hypothesis is based upon the ability to induce the expression of the class II MHC antigens on astrocytes, and on their ability to present myelin basic protein to encephalitogenic T-cells in vitro. The best in vivo data showing that astrocytes serve as intracerebral APCs is the finding that astrocytes in multiple sclerosis plaques are DR+ (class II MHC in human). However, it still remains to be resolved whether the in vivo expression of the MHC antigens in disease states is instrumental to antigen presentation mechanisms or whether these cell surface glycoproteins are expressed secondary to brain immune responses. If astrocytes function as immunocompetent APCs within the brain, it would seem that they would also be able to express molecules important for intercellular adhesion. Here, we present the first data that indicates that human astrocytes are capable of expressing ICAM-1 in response to cytokines that either induce or upregulate the expression of DR. In essence, cytokines derived from different cell types seem to exert similar pleiotropic effects on the modulation of MHC and ICAM-1 expression on astrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Antigen-Presenting Cells↗
PubMed1995

Presentation of antigen by B cell subsets. V. Effect of interleukin 7 (IL-7) and interleukin 10 (IL-10) on phenotype and antigen presenting function of immature B cells.

In this communication we demonstrate that B cells from CBA/N mice with x chromosome-linked immunodeficiency and B cells from newborn mice, that have very limited ability to present antigen to antigen-specific T cells lines, acquire this function following preincubation with IL-7 or IL-10. These interleukins do not affect the antigen presenting function of B cells from normal, adult CBA mice. Incubation of B cells from xid and newborn mice with IL-7 or IL-10 but not with IL-2 induces expression of Lyb-5 marker on these cells. The study shows that the property of IL-7 and IL-10 to induce antigen presenting cell (APC) activity in immature B cells is associated with appearance of Lyb-5 antigen on these cells.

Animals↗
PubMed2002

A closer look at proteolysis and MHC-class-II-restricted antigen presentation.

Antigen presentation by MHC class II molecules relies on the action of endocytic proteases, which are differentially expressed in antigen-presenting cells and are regulated by different components of the immune system. Endocytic enzymes process and convert exogenous antigens into peptidic determinants capable of interaction with MHC class II molecules. Chemical and genetic tools have recently been developed to study the role of lysosomal proteases in antigen presentation.

Animals↗
PubMed2003

Lysosomal cysteine proteases regulate antigen presentation.

Antigen presentation by both classical MHC class II molecules and the non-classical MHC class I-like molecule CD1D requires their entry into the endosomal/lysosomal compartment. Lysosomal cysteine proteases constitute an important subset of the enzymes that are present in this compartment and, here, we discuss the role of these proteases in regulating antigen presentation by both MHC class II and CD1D molecules.

Animals↗
PubMed1998

A critical, invariant chain-independent role for H2-M in antigen presentation.

Antigen presentation by MHC class II (class II) is facilitated by the accessory molecules, invariant chain (Ii) and H2-M. Ii associates with class II during biosynthesis and promotes transport of class II to Ag-loading compartments. One function of H2-M is the removal of Ii fragments from MHC class II. We have previously demonstrated that Ii-deficient mice, unlike class II-deficient mice, are resistant to L. major infection. In the present study, we found that H2-M-deficient (H2-M0) mice were susceptible to progressive infection with L. major. The dispensability of Ii for control of L. major allowed genetic analysis of whether H2-M functions by association with or independently of Ii. In contrast to Ii-deficient (Ii0) mice, Ii0H2-M0 mice were as susceptible to L. major as H2-M0 mice. Thus, H2-M has an essential, Ii-independent function during presentation of microbial pathogens.

Animals↗
PubMed1995

Single-cell observation of calcium signals in T cells and antigen-presenting cells during antigen presentation.

Intracellular calcium ion mobilization in T-cell hybridomas and antigen-presenting cells (APC) during the interaction was observed using confocal fluorescence microscopy. No calcium signal was detected in non-activated T-cell hybridomas by antigen presentation. However, in activated T-cell hybridomas, intracellular calcium ion concentration rapidly increased by antigen presentation and thereafter apoptosis was induced. On the contrary, during the interaction with T-cell hybridomas, calcium signal was induced in APCs irrespective of the activation of T-cell hybridomas. Chemical modification of APCs with 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide, which is known to induce T-cell unresponsiveness during antigen presentation, inhibited cap formation of surface MHC class II molecules and suppressed calcium signals during the interaction with T-cell hybridomas.

Animals↗
PubMed2003

Influence of stage of the reproductive cycle and estradiol on thymus cell antigen presentation.

The objective of this study was to determine whether thymus cells present antigen and if endocrine balance influences antigen presentation. We report here that antigen presenting cells (APC) from the thymus glands of male and female rats, when incubated with ovalbumin (OVA)-specific T cells and OVA, are functionally able to present antigen via MHC class II. To determine whether antigen presentation in the thymus is under hormonal control, tissues from female rats at different stages of the estrous cycle were analyzed. Antigen presentation was higher at estrus and proestrus than that seen at diestrus when estradiol levels are low. Estradiol given to ovariectomized animals for 3 days stimulated antigen presentation by adherent thymus cells compared to saline controls. Flow cytometry studies indicated that the adherent thymus cell preparations consisted of DC, T cells, B cells and cells of the myeloid lineage all of which expressed MHC class II, as did a small population of non-leukocytes. Antibody neutralization studies indicated that thymus cell antigen presentation involves the expression of transmembrane proteins B7.1 and B7.2. These studies demonstrate that sex hormones play a central role in regulating antigen presentation in the thymus.

Animals↗
PubMed1996

Enhancing effects of (2S,3S,4R)-1-O-(alpha-D-galactopyranosyl)-2-(N-hexacosanoylamino) -1,3,4-octadecanetriol (KRN7000) on antigen-presenting function of antigen-presenting cells and antimetastatic activity of KRN7000-pretreated antigen-presenting cells.

(2S,3S,4R)-1-O-(alpha-D-galactopyranosyl)-2-(N-hexacosanoylamino)- 1,3, 4-octadecanetriol (KRN7000), with an alpha-galactosylceramide structure, is an immunomodulator showing potent antimetastatic activities. In an in vitro study, KRN7000 potently stimulated proliferation and enhanced natural killer activity in spleen cells from BALB/c euthymic mice, but not BALB/c athymic (nu/nu) mice, suggesting that T cells play an important role in these activities. To study the detailed immunostimulatory mechanisms of KRN7000, syngeneic mixed leukocyte reactions were then performed using dendritic cell-enriched fractions (DCEFs) from spleens of BALB/c euthymic and athymic mice. In these studies, KRN7000 enhanced the antigen-presenting cell activities of the DCEFs. In addition, marked production of interleukin-2 and interferon-gamma in BALB/c euthymic mice was observed following treatment with KRN7000 in vitro and in vivo. Because of these strong immunostimulating effects of KRN7000, its antimetastatic effects were also evaluated. Adoptively transferred KRN7000-treated DCEF markedly prolonged the survival time of mice bearing B16 pulmonary metastases. These results demonstrate that KRN7000 may be useful for cancer therapy not only as an antitumor agent but also as an activator of antigen-presenting cells such as dendritic cells, which can be used for adoptive cellular therapy.

Adjuvants, Immunologic↗
PubMed1998

Class II MHC/peptide complexes on T cell antigen-presenting cells: agonistic antigen recognition inhibits subsequent antigen presentation.

Previous studies have shown that tolerogenic anti-CD4 (W3/25) and anti-LFA-1 mAb (LRTC1) which block T cell activation paradoxically enhance T cell-mediated antigen presentation. Lasting T cell APC (T-APC) activity requires and initial exposure of T cells to these mAb in the presence of professional APC and antigen. This study revealed a central mechanism regulating the duration of T-APC activity. T cell recognition of class II MHC complexes of T-APC catalyzed a rapid decay in the presentation of agonistic antigens, whereas partial agonistic signals decayed at a shower rate. Likewise, blockade of agonistic T-T cell autorecognition by these mAb led to the persistence of agonistic MHC/antigen on T-APC. The best predictor of T-APC activity was related to the ability of clonal T cells to respond to antigen presented by neighboring T cells. Strong responders were inefficient T-APC, whereas inefficient responders were strong T-APC. Addition of irradiated myelin basic protein (MBP0-specific responders to T-APC cultures specifically inhibited the subsequent presentation of MBP but not conalbumin, and vice versa. T-APC presentation of antigen to responder T cells also resulted in reduced surface expression of class II MHC I-A glycoproteins on T-APC. These findings indicate that agonistic recognition of antigen of T-APC specifically inhibits subsequent presentation of that antigen, whereas antagonistic MHC/antigen complexes are preserved for an enduring T-APC activity.

Animals↗
PubMed1986

Antigen presentation by human antigen-presenting cells to antigen-specific xenogeneic murine T cells.

Successful antigen presentation by xenogeneic human antigen-presenting cells (APC) to stimulate the proliferation of antigen-specific, keyhole limpet hemocyanin (KLH)-specific, ovalbumin (OVA)-specific, and purified protein derivative of Mycobacterium tuberculosis (PPD)-specific murine T cells was observed. Evidence indicating a direct cell interaction between antigen-specific murine T cells and xenogeneic human APC was given by experiments using antigen-specific murine T cell clones. The OVA-specific B10.S(9R) T cell line (9-0-A1) and PPD-specific B10.A(4R) T cell line (4-P-1) were stimulated by both xenogeneic human APC and murine APC from syngeneic or I-A compatible strains, while the PPD-specific human T cell line (Y-P-5) was stimulated by autologous human APC but not by murine APC. Anti-HLA-DR monoclonal antibodies (MoAb) blocked the xenogeneic human APC-antigen-specific murine T cell clone interaction. Thus, human xenogeneic APC can stimulate antigen-specific murine T cells through HLA-DR molecules in the same manner as syngeneic murine APC do through Ia molecules coded for by the I region of the H-2 complex, while murine APC failed to present antigen to stimulate human antigen-specific T cells.

Animals↗
PubMed2003

Dendritic cells constitutively present self antigens in their immature state in vivo and regulate antigen presentation by controlling the rates of MHC class II synthesis and endocytosis.

Dendritic cells (DCs) change their antigen-presenting properties during maturation. Immature DCs efficiently capture antigens, but are reported to be impaired in their processing and presenting capacity. Upon an encounter with an inflammatory stimulus, DCs undergo a maturation process that leads to efficient presentation of antigens captured at the time of activation, but precludes processing of antigens encountered at later time points. The mechanisms that underlie these developmental changes are controversial. Thus, it is unclear whether immature DCs can present self antigens, and which are the checkpoints that regulate antigen presentation in immature and mature DCs. We have characterized these mechanisms using DCs derived directly from lymphoid organs. Immature lymphoid organ DCs constitutively presented self peptides bound to major histocompatibility complex class II (MHCII) molecules, but these MHCII-peptide complexes were degraded quickly after their transient expression on the cell surface. During maturation, MHC II endocytosis was down-regulated, so that newly generated MHC II-peptide complexes accumulated on the plasma membrane. Simultaneously, MHC II synthesis was down-regulated, thus preventing the turnover of the MHC II-peptide complexes that accumulated early during maturation. Our results demonstrate that immature DCs constitutively present self antigens in the lymphoid organs and characterize the molecular basis of the capacity of DCs to provide "antigenic memory" in vivo.

Animals↗