Journal articles: 'Antigen Presenting Cell'

1

Knight, Stella C., and Andrew J. Stagg. "Antigen-presenting cell types." Current Opinion in Immunology 5, no. 3 (June 1993): 374–82. http://dx.doi.org/10.1016/0952-7915(93)90056-x.

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Spillane, Katelyn M., and Pavel Tolar. "B cell antigen extraction is regulated by physical properties of antigen-presenting cells." Journal of Cell Biology 216, no. 1 (December 6, 2016): 217–30. http://dx.doi.org/10.1083/jcb.201607064.

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Antibody production and affinity maturation are driven by B cell extraction and internalization of antigen from immune synapses. However, the extraction mechanism remains poorly understood. Here we develop DNA-based nanosensors to interrogate two previously proposed mechanisms, enzymatic liberation and mechanical force. Using antigens presented by either artificial substrates or live cells, we show that B cells primarily use force-dependent extraction and resort to enzymatic liberation only if mechanical forces fail to retrieve antigen. The use of mechanical forces renders antigen extraction sensitive to the physical properties of the presenting cells. We show that follicular dendritic cells are stiff cells that promote strong B cell pulling forces and stringent affinity discrimination. In contrast, dendritic cells are soft and promote acquisition of low-affinity antigens through low forces. Thus, the mechanical properties of B cell synapses regulate antigen extraction, suggesting that distinct properties of presenting cells support different stages of B cell responses.

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Erb, P., M. Kennedy, P. Wassmer, and G. Huegli. "Antigen-presenting cells and T cell activation." Agents and Actions 19, no. 5-6 (December 1986): 266–68. http://dx.doi.org/10.1007/bf01971224.

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Gonnella, P. A., and D. W. Wilmore. "Co-localization of class II antigen and exogenous antigen in the rat enterocyte." Journal of Cell Science 106, no. 3 (November 1, 1993): 937–40. http://dx.doi.org/10.1242/jcs.106.3.937.

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The role of class II major histocompatibility antigens in classical antigen-presenting cells has been described (Unanue (1984) Annu. Rev. Immunol. 2, 395–428; Watts and McConnell (1987) Rev. Immunol. 5, 461–475). Whether enterocytes, which also express class II antigens, can act as antigen-presenting cells in vivo is not known. One pre-requisite for a role for enterocytes in antigen presentation is an interaction between exogenous antigen and class II antigens. Our results demonstrate that class II antigen and exogenous antigen absorbed from the gastrointestinal tract are co-localized within endocytic compartments and along the basolateral membranes of enterocytes.

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Fishman, Michael A., and Alan S. Perelson. "Modeling T Cell-Antigen Presenting Cell Interactions." Journal of Theoretical Biology 160, no. 3 (February 1993): 311–42. http://dx.doi.org/10.1006/jtbi.1993.1021.

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Horna, Pedro, Alex Cuenca, Fengdong Cheng, Jason Brayer, Hong-Wei Wang, Ivan Borrello, Hyam Levitsky, and Eduardo M. Sotomayor. "In vivo disruption of tolerogenic cross-presentation mechanisms uncovers an effective T-cell activation by B-cell lymphomas leading to antitumor immunity." Blood 107, no. 7 (April 1, 2006): 2871–78. http://dx.doi.org/10.1182/blood-2005-07-3014.

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AbstractBone marrow-derived antigen-presenting cells (APCs) play a central role in the induction of tolerance to tumor antigens expressed by B-cell lymphomas. Here we show that in vivo disruption of this APC-mediated tolerogenic mechanism unveils an intrinsic ability of malignant B cells to efficiently present tumor antigens to antigen-specific CD4+ T cells, resulting in a strong antitumor effect. This intrinsic antigen-presenting ability of malignant B cells is, however, overridden by tolerogenic bone marrow-derived APCs, leading instead to T-cell unresponsiveness and lack of antitumor effect. These results highlight the concept that therapeutic strategies aimed at enhancing the antigen-presenting function of B-cell lymphomas might not succeed unless the tolerogenic mechanisms mediated by bone marrow-derived APCs are disrupted in the first place.

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Raimondi, Giorgio, Ivan Zanoni, Stefania Citterio, Paola Ricciardi-Castagnoli, and Francesca Granucci. "Induction of Peripheral T Cell Tolerance by Antigen-Presenting B Cells. II. Chronic Antigen Presentation Overrules Antigen-Presenting B Cell Activation." Journal of Immunology 176, no. 7 (March 17, 2006): 4021–28. http://dx.doi.org/10.4049/jimmunol.176.7.4021.

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8

Apple, R. J., P. L. Domen, A. Muckerheide, and J. G. Michael. "Cationization of protein antigens. IV. Increased antigen uptake by antigen-presenting cells." Journal of Immunology 140, no. 10 (May 15, 1988): 3290–95. http://dx.doi.org/10.4049/jimmunol.140.10.3290.

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Abstract Cationization of BSA generates a molecule that mounts antibody responses of increased magnitude and duration and induces T cell proliferation at concentrations 500 times less than native BSA (nBSA). To explain the alteration in immunogenic properties of this Ag, the uptake of nBSA and cationized BSA (cBSA) by splenic APC has been investigated. T cell proliferation assays were conducted with nBSA and cBSA preparations with varying degrees of substitution. An inverse correlation between the degree of cationization and the amounts of Ag needed for optimal T cell reactivity was observed. To determine whether affinity for APC resulted in an increased uptake of cBSA, splenic APC were incubated with nBSA or cBSA for varying amounts of time. Comparisons were made at each time point between untreated Ag-pulsed APC (Ag uptake) and paraformaldehyde-fixed Ag-pulsed APC (processed Ag). Proliferation of T cells primed with nBSA or cBSA increased in proportion to the amount of time of APC exposure to high concentrations of nBSA, first appearing after a 2-h pulse and peaking at 8 h. Conversely, untreated APC needed only a 30-min cBSA exposure to induce either nBSA- or cBSA-primed T cell proliferation, indicating a rapid uptake of cBSA. Comparisons with proliferation induced by paraformaldehyde-fixed cBSA APC indicate that nBSA T cells recognize a lag phase-processed form of cBSA, whereas a majority of cBSA T cells recognize either a rapidly processed form of cBSA, or a membrane-processed cBSA molecule without a classical lag phase processing event. When monensin was used as an inhibitor of fluid phase pinocytosis in splenic APC, the presentation of nBSA was inhibited by 85%, but the presentation of cBSA was inhibited by only 20%. These results imply that nBSA enters the cell by fluid phase pinocytosis, whereas cBSA enters by a nonspecific adsorptive mechanism. The different modes of cellular entry for the two molecules, nBSA and cBSA, resulting in a rapid uptake of cBSA, may have important ramifications on T cell activation and immunoregulation.

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Lechler, R. I., M. A. Norcross, and R. N. Germain. "Qualitative and quantitative studies of antigen-presenting cell function by using I-A-expressing L cells." Journal of Immunology 135, no. 5 (November 1, 1985): 2914–22. http://dx.doi.org/10.4049/jimmunol.135.5.2914.

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Abstract I-A-expressing transfected murine L cells were analyzed as model antigen-presenting cells. Four features of accessory cell function were explored: antigen processing, interaction with accessory molecules (LFA-1, L3T4), influence of Ia density, and ability to stimulate resting, unprimed T lymphocytes. I-A+ L cells could present complex protein antigens to a variety of T cell hybridomas and clones. Paraformaldehyde fixation before but not subsequent to antigen exposure rendered I-A+ L cells unable to present intact antigen. These results are consistent with earlier studies that made use of these methods to inhibit "processing" by conventional antigen-presenting cells. The ability of anti-L3T4 antibody to inhibit T cell activation was the same for either B lymphoma or L cell antigen-presenting cells. In striking contrast, anti-LFA-1 antibody, which totally blocked B lymphoma-induced responses, had no effect on L cell antigen presentation, measured as interleukin 2 (IL 2) release by T hybridomas, proliferation, IL 2 release, or IL 2 receptor upregulation by a T cell clone. I-A+ L cell transfectants were found to have a stable level of membrane I-A and I-A mRNA, even after exposure to interferon-gamma-containing T cell supernatants. In agreement with earlier reports, a proportional relationship between the (Ia) X (Ag) product and T cell response was found for medium or bright I-A+ cells. However, dull I-A+ cells had a disproportionately low stimulatory capacity, suggesting that there may be a threshold density of Ia per antigen-presenting cell necessary for effective T cell stimulation. Finally, I-A-bearing L cells were shown to trigger low, but reproducible primary allogeneic mixed lymphocyte responses with the use of purified responder T cells, indicating that they are capable of triggering even resting T cells. These studies confirm the importance of antigen processing and I-A density in antigen-presenting cell function, but raise questions about the postulated role of the LFA-1 accessory molecule in T cell-antigen-presenting cell interaction. They also illustrate the utility of the L cell transfection model for analysis and dissection of antigen-presenting cell function.

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Rossjohn, Jamie, Stephanie Gras, John J. Miles, Stephen J. Turner, Dale I. Godfrey, and James McCluskey. "T Cell Antigen Receptor Recognition of Antigen-Presenting Molecules." Annual Review of Immunology 33, no. 1 (March 21, 2015): 169–200. http://dx.doi.org/10.1146/annurev-immunol-032414-112334.

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Natkanski, Elizabeth, Wing-Yiu Lee, Bhakti Mistry, Antonio Casal, Justin E. Molloy, and Pavel Tolar. "B Cells Use Mechanical Energy to Discriminate Antigen Affinities." Science 340, no. 6140 (May 16, 2013): 1587–90. http://dx.doi.org/10.1126/science.1237572.

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The generation of high-affinity antibodies depends on the ability of B cells to extract antigens from the surfaces of antigen-presenting cells. B cells that express high-affinity B cell receptors (BCRs) acquire more antigen and obtain better T cell help. However, the mechanisms by which B cells extract antigen remain unclear. Using fluid and flexible membrane substrates to mimic antigen-presenting cells, we showed that B cells acquire antigen by dynamic myosin IIa–mediated contractions that pull out and invaginate the presenting membranes. The forces generated by myosin IIa contractions ruptured most individual BCR-antigen bonds and promoted internalization of only high-affinity, multivalent BCR microclusters. Thus, B cell contractility contributes to affinity discrimination by mechanically testing the strength of antigen binding.

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Arora, Pooja, and Steven Porcelli. "Identification of the physiological antigen presenting cell for glycolipid antigens." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 146.19. http://dx.doi.org/10.4049/jimmunol.198.supp.146.19.

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Abstract A major subset of T cells that recognize complexes formed by the binding of glycolipids to CD1d are called invariant natural killer T (iNKT) cells. Unlike conventional T cells that need to proliferate and differentiate to become activated effector T cells, iNKT cells exist as an effector population and start responding rapidly after glycolipid recognition. The prototypical iNKT stimulatory antigen is synthetic α-galactosylceramide (αGC), initially designated as KRN7000. Administration of this antigen in vivo results in the production of cytokines associated with both T helper type 1 (Th1) or type 2 (Th2) responses. Several variants of this antigen having different fatty acyl- and phytosphinganine chains have been synthesized and polarize the response towards a predominance of either Th1 or Th2 cytokines, and are therefore described as Th1- or Th2-biasing analogues. It is not clear how the Th1- or Th2-bias in iNKT mediated response is induced, although selective presentation by distinct cell types has been proposed as a possible mechanism. By visualizing glycolipid antigen presentation directly with monoclonal antibodies specific for complexes of αGC bound to CD1d, we showed that the CD8αPosDEC-205Pos dendritic cells were the major APCs in the spleen for a range of αGC analogues, irrespective of their chemical structures and cytokine biasing activities. We found that DCs presenting Th1-biasing agonists upregulated ligands for stimulatory NK receptor molecules, while Th2-agonist presenting cells showed a marked upregulation of ligands for inhibitory receptors. Furthermore, modulation of accessory immune proteins was dependent on CD1d, suggesting direct cell-cell interactions between DC and iNKT cells.

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Joglekar, Alok, Michael Troy Leonard, John Jeppson, Michael T. Bethune, and David Baltimore. "T Cell Antigen Discovery using Signaling and Antigen-presenting Bifunctional Receptors (SABRs)." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 181.9. http://dx.doi.org/10.4049/jimmunol.200.supp.181.9.

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Abstract Checkpoint inhibitors, cancer vaccines, and adoptive cell therapy exploit T cell mediated immune responses to cancers. Discovering the exact antigens targeted by T cell responses is important for their efficacy. Antigen discovery for ‘orphan’ T cells or TCRs has been a challenging prospect due to high number of possible pMHC specificities. Several current approaches to decipher antigen specificities require prior knowledge of antigen sequences, are unable to scale up, or require production of soluble TCRs. To overcome these drawbacks, we have developed chimeric receptors called Signaling and Antigen-presenting Bifunctional Receptors (SABRs) that allow identification of antigen-presenting cells. SABRs present display pMHC on their extracellular domain, which is recognized by an orphan TCR. Upon recognition, SABRs initiate signaling in the presenting cell using a CD3zeta signaling domain. We transduced reporter cells with SABRs presenting HLA-A2-restricted epitopes from MelanA and NY-ESO-1, and co-incubated them with target cells expressing their cognate TCRs, which resulted in signal transduction only upon correct pMHC-TCR pairing, allowing the presenting cells to express GFP. Second, we showed that SABRs displaying independently expressed peptide and MHC could function similarly. These receptors could present pulsed peptides or endogenously expressed proteins, allowing the uncoupling of peptide and MHC, while retaining their signaling capability. We are currently testing the use of SABR-based antigen libraries to identify novel antigenic specificities targeted by T cells in cancers, infectious diseases, and autoimmune diseases.

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Fisher, R. I., J. Cossman, V. Diehl, and D. J. Volkman. "Antigen presentation by Hodgkin's disease cells." Journal of Immunology 135, no. 5 (November 1, 1985): 3568–71. http://dx.doi.org/10.4049/jimmunol.135.5.3568.

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Abstract The L428 tumor cell line is a long-term tissue culture of Reed-Sternberg cells which was derived from the pleural effusion of a patient with Hodgkin's disease. The L428 cells express all known cell surface antigens, cytochemical staining, and cytologic features of freshly explanted Reed-Sternberg cells. In addition to the previously described HLA-DR cell surface antigens, the L428 cells are now demonstrated to express both DS and SB alloantigens. Thus, the L428 cells express all of the known subclasses of the human immune response genes that are located in the major histocompatibility complex. Furthermore, the L428 cells are capable of presenting soluble antigen to T cells in a genetically restricted fashion. T cell lines were established from normal donors previously immunized with tetanus toxoid. The T cells utilized were incapable of tetanus toxoid-induced proliferation unless antigen-presenting cells were added to the cultures. However, T cells from the two normal donors, which like the L428 cells expressed HLA-DR 5, demonstrated significant proliferative responses when cultured with tetanus toxoid and L428 cells. No proliferative response was observed when the L428 cells were used as antigen-presenting cells for a DR (4,-), DR (2,-) or DR (1,7) T cell line. The tetanus toxoid dose-response curve was similar regardless of whether autologous mononuclear leukocytes or L428 cells were used as antigen-presenting cells. The T cell proliferation induced by soluble antigen was also blocked by anti-HLA-DR antibody. Thus, functionally, Hodgkin's disease may be classified as a tumor of antigen-presenting cells.

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15

Hinke, Daniëla Maria, Tor Kristian Andersen, Ramakrishna Prabhu Gopalakrishnan, Lise Madelene Skullerud, Ina Charlotta Werninghaus, Gunnveig Grødeland, Even Fossum, Ranveig Braathen, and Bjarne Bogen. "Antigen bivalency of antigen-presenting cell-targeted vaccines increases B cell responses." Cell Reports 39, no. 9 (May 2022): 110901. http://dx.doi.org/10.1016/j.celrep.2022.110901.

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Meyer, Randall A., Joel C. Sunshine, Karlo Perica, Alyssa K. Kosmides, Kent Aje, Jonathan P. Schneck, and Jordan J. Green. "Biodegradable Nanoellipsoidal Artificial Antigen Presenting Cells for Antigen Specific T-Cell Activation." Small 11, no. 13 (January 12, 2015): 1519–25. http://dx.doi.org/10.1002/smll.201402369.

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Lem, V. M., M. F. Lipscomb, J. C. Weissler, G. Nunez, E. J. Ball, P. Stastny, and G. B. Toews. "Bronchoalveolar cells from sarcoid patients demonstrate enhanced antigen presentation." Journal of Immunology 135, no. 3 (September 1, 1985): 1766–71. http://dx.doi.org/10.4049/jimmunol.135.3.1766.

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Abstract The recognition of foreign antigens by T lymphocytes in association with lung antigen-presenting cells may be critical in the initiation of the mononuclear alveolitis and granuloma formation of pulmonary sarcoidosis. However, it has been shown that bronchoalveolar cells (BAC) from normal volunteers function poorly as antigen-presenting cells. Therefore, the ability of sarcoid BAC to serve as accessory cells for antigen-dependent autologous T cell proliferation, as measured by tritiated thymidine uptake, was compared with that of normal BAC. Although irradiated sarcoid BAC supported antigen-induced T cell proliferation, normal BAC did so poorly (p less than 0.005). Because it has been shown that sarcoid BAC produce more interleukin 1 (IL 1) than normal BAC, it was considered that the enhancement of antigen-induced proliferative responses could result from an increased amount of IL 1, and that contaminating monocytes in the peripheral blood T cell preparations displayed the antigen for T cell recognition. Therefore, it was necessary to establish that antigen-induced T cell responses required HLA-D region compatibility between the sarcoid BAC and T lymphocytes. BAC from sarcoid patients stimulated antigen-specific proliferation in T cells lines matched for at least one HLA-D-region antigen, but failed to stimulate T cell lines that were unmatched for both antigens. This finding indicates that cells in bronchoalveolar lavage fluids from sarcoid patients were fully capable of acting as antigen-presenting cells. The identification of antigen-presenting cells in the lungs of patients with sarcoidosis together with the previous findings of activated T cells, enhanced IL 1 production, and spontaneous interleukin 2 release in sarcoid patients is compatible with the hypothesis that local cell-mediated immunity is involved in the pathogenesis of pulmonary sarcoidosis.

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Hari, Aswin, and Yan Shi. "Plasma Membrane Interactions that determine Antigen Presentation by Antigen-Presenting Cells (106.20)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 106.20. http://dx.doi.org/10.4049/jimmunol.188.supp.106.20.

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Abstract Antigen presentation is a critical process in host defense for initiating adaptive immune responses. The APC loads peptides derived from antigens onto major histocompatibility complex (MHC) molecules and exports them to the surface for T cells sampling. If the primary interaction between an APC and T cell is successful, i.e. the TCR binds an appropriate MHC-peptide complex, this leads to an adaptive immune response. Peptide antigens are presented on two types of MHC molecules, MHC I and MHC II via several distinct processing pathways. In turn, the MHC molecule dictates which type of T cell can be activated and thereby the nature of the adaptive immune response. Therefore, antigen loading onto MHC molecules is a critical determinant of the adaptive immune responses. Exogenous antigens can be presented on MHC I and II molecules. Antigen processing mechanisms have been elucidated in great detail, but the fundamental reason behind why an antigen is directed into a specific pathway is not known. One of the foremost aims for this project is to determine why particulate antigens are presented more often on MHC I and why soluble antigens are more efficiently presented on MHC II, by deciphering the interactions of plasma membrane with particulate versus soluble antigen. This fundamental sensing mechanism of the human body when elucidated can help in generating an antiviral response in diseases like HIV and in field of preventative medicine.

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St Louis, J. D., J. A. Lederer, and A. H. Lichtman. "Costimulator deficient antigen presentation by an endothelial cell line induces a nonproliferative T cell activation response without anergy." Journal of Experimental Medicine 178, no. 5 (November 1, 1993): 1597–605. http://dx.doi.org/10.1084/jem.178.5.1597.

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The ability of endothelial cells to activate helper T (Th) cells by antigen presentation was studied using the murine endothelial cell line SVEC4-10 and antigen-specific murine T cell clones. SEVEC4-10 cells constitutively express vascular cell adhesion molecule 1 but not intercellular adhesion molecule 1. Interferon gamma (IFN-gamma) treatment of these cells induced class II major histocompatibility complex (MHC) expression and antigen-presenting capabilities, but did not alter surface integrin expression. IFN-gamma-treated SVEC4-10 cells were competent at mediating antigen-dependent cytokine production and proliferation of a Th2 clone. In contrast, endothelial antigen presentation to Th1 cells did not stimulate T cell proliferation. The addition of MHC mismatched spleen cells as a source of costimulatory molecules resulted in the ability of the endothelial cells to stimulate Th1 cell proliferation in an antigen-specific manner. The failure of the endothelial cell line alone to support Th1 cell proliferation correlated with the failure to stimulate interleukin 2 (IL-2) gene expression. T cell exposure to the endothelial cells plus antigen resulted in upregulation of IL-2 receptors and an enhanced response to subsequent antigen presentation by splenic antigen-presenting cells. Despite the lack of functional costimulators for IL-2 expression, antigen presentation by the endothelial cell line did not induce Th1 cell anergy, indicating that costimulator deficiency for IL-2 expression is not obligatorily linked to anergy induction. Thus, endothelial cells are capable of presenting antigens to helper T lymphocytes, but stimulate only partial T cell responses. These partial responses may serve to selectively stimulate transmigration of antigen-specific T cells and may enhance functional responses upon subsequent, extravascular antigen exposure.

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Dahotre, Shreyas N., Anna M. Romanov, Fang‐Yi Su, and Gabriel A. Kwong. "Synthetic Antigen‐Presenting Cells for Adoptive T Cell Therapy." Advanced Therapeutics 4, no. 8 (March 18, 2021): 2100034. http://dx.doi.org/10.1002/adtp.202100034.

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21

Delabie, Jan, Wing C. Chan, Dennis D. Weisenburger, and Chris De Wolf-peeters. "The Antigen-Presenting Cell Function of Reed-Sternberg Cells." Leukemia & Lymphoma 18, no. 1-2 (January 1995): 35–40. http://dx.doi.org/10.3109/10428199509064920.

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22

Gogolák, P., B. Réthy, A. Horváth, G. K. Tóth, E. Buzás, L. Cervenák, G. László, and É. Rajnavölgyi. "Differential T cell activation regulated by antigen presenting cells." Immunology Letters 56 (May 1997): 267. http://dx.doi.org/10.1016/s0165-2478(97)86067-1.

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Perica, Karlo, Andrés De León Medero, Malarvizhi Durai, Yen Ling Chiu, Joan Glick Bieler, Leah Sibener, Michaela Niemöller, et al. "Nanoscale artificial antigen presenting cells for T cell immunotherapy." Nanomedicine: Nanotechnology, Biology and Medicine 10, no. 1 (January 2014): 119–29. http://dx.doi.org/10.1016/j.nano.2013.06.015.

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GogolÃ¡k, P. "Differential T cell activation regulated by antigen presenting cells." Immunology Letters 56, no. 1-3 (May 1997): 267. http://dx.doi.org/10.1016/s0165-2478(97)87905-9.

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Ju, Shyr-Te, Rosemarie H. DeKruyff, and Martin E. Dorf. "Inducer T-cell-mediated killing of antigen-presenting cells." Cellular Immunology 101, no. 2 (September 1986): 613–24. http://dx.doi.org/10.1016/0008-8749(86)90171-1.

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Jensen, P. E. "Stable association of processed antigen with antigen-presenting cell membranes." Journal of Immunology 143, no. 2 (July 15, 1989): 420–25. http://dx.doi.org/10.4049/jimmunol.143.2.420.

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Abstract Th cells recognize a processed form of Ag in association with class II histocompatibility molecules expressed on the surface of APC. The physical nature of the cell surface association of physiologically processed Ag was investigated by using membranes isolated from Ag-pulsed APC. Such membranes were sufficient to directly activate class II-restricted T cell hybridomas without further Ag processing. T cell-stimulating activity remained after treatment of membranes in harsh conditions, including pH 4.0, pH 9.0, high salt, and chaotropic solvents. Activity was lost after exposure to pH 2.0 or protease. The capacity of pH 2.0 (but not protease) treated membranes to present artificially processed, peptide Ag to T cells suggests that exposure to pH 2.0 results in the selective dissociation of processed Ag from membranes. Similar results were obtained in parallel experiments with peptide-pulsed membranes. No qualitative differences were found between physiologically processed Ag and peptide Ag with respect to their remarkably stable association with the APC plasma membrane.

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de Waal Malefyt, R., J. Haanen, H. Spits, M. G. Roncarolo, A. te Velde, C. Figdor, K. Johnson, R. Kastelein, H. Yssel, and J. E. de Vries. "Interleukin 10 (IL-10) and viral IL-10 strongly reduce antigen-specific human T cell proliferation by diminishing the antigen-presenting capacity of monocytes via downregulation of class II major histocompatibility complex expression." Journal of Experimental Medicine 174, no. 4 (October 1, 1991): 915–24. http://dx.doi.org/10.1084/jem.174.4.915.

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Interleukin 10 (IL-10) and viral IL-10 (v-IL-10) strongly reduced antigen-specific proliferation of human T cells and CD4+ T cell clones when monocytes were used as antigen-presenting cells. In contrast, IL-10 and v-IL-10 did not affect the proliferative responses to antigens presented by autologous Epstein-Barr virus-lymphoblastoid cell line (EBV-LCL). Inhibition of antigen-specific T cell responses was associated with downregulation of constitutive, as well as interferon gamma- or IL-4-induced, class II MHC expression on monocytes by IL-10 and v-IL-10, resulting in the reduction in antigen-presenting capacity of these cells. In contrast, IL-10 and v-IL-10 had no effect on class II major histocompatibility complex (MHC) expression on EBV-LCL. The reduced antigen-presenting capacity of monocytes correlated with a decreased capacity to mobilize intracellular Ca2+ in the responder T cell clones. The diminished antigen-presenting capacities of monocytes were not due to inhibitory effects of IL-10 and v-IL-10 on antigen processing, since the proliferative T cell responses to antigenic peptides, which did not require processing, were equally well inhibited. Furthermore, the inhibitory effects of IL-10 and v-IL-10 on antigen-specific proliferative T cell responses could not be neutralized by exogenous IL-2 or IL-4. Although IL-10 and v-IL-10 suppressed IL-1 alpha, IL-1 beta, tumor necrosis factor alpha (TNF-alpha), and IL-6 production by monocytes, it was excluded that these cytokines played a role in antigen-specific T cell proliferation, since normal antigen-specific responses were observed in the presence of neutralizing anti-IL-1, -IL-6, and -TNF-alpha mAbs. Furthermore, addition of saturating concentrations of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha to the cultures had no effect on the reduced proliferative T cell responses in the presence of IL-10, or v-IL-10. Collectively, our data indicate that IL-10 and v-IL-10 can completely prevent antigen-specific T cell proliferation by inhibition of the antigen-presenting capacity of monocytes through downregulation of class II MHC antigens on monocytes.

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Antal, Dóra, Shahrzad Alimohammadi, Péter Bai, Attila Gábor Szöllősi, and Magdolna Szántó. "Antigen-Presenting Cells in Psoriasis." Life 12, no. 2 (February 3, 2022): 234. http://dx.doi.org/10.3390/life12020234.

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Psoriasis is classically considered a chronic inflammatory skin disorder, however the identification of autoantigens in its pathogenesis established it as a T cell mediated autoimmune disease. As such professional antigen-presenting cells (APCs) are key players in the development of lesions. APCs in the skin include dendritic cells, Langerhans cells and monocytes/macrophages. In addition, epidermal keratinocytes and dermal mast cells are also endowed with antigen-presenting capacity. Skin APCs have central role in the maintenance of cutaneous immune homeostasis, as well as in initiating and sustaining inflammation under pathologic conditions. In this review we discuss the functional specialization of human skin APCs that promote T cell activation and adaptive immune response during psoriasis initiation and onset.

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Harryvan, Tom J., Sabine de Lange, Lukas J. A. C. Hawinkels, and Els M. E. Verdegaal. "The ABCs of Antigen Presentation by Stromal Non-Professional Antigen-Presenting Cells." International Journal of Molecular Sciences 23, no. 1 (December 23, 2021): 137. http://dx.doi.org/10.3390/ijms23010137.

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Professional antigen-presenting cells (APCs), such as dendritic cells and macrophages, are known for their ability to present exogenous antigens to T cells. However, many other cell types, including endothelial cells, fibroblasts, and lymph node stromal cells, are also capable of presenting exogenous antigens to either CD8+ or CD4+ T cells via cross-presentation or major histocompatibility complex (MHC) class II-mediated presentation, respectively. Antigen presentation by these stromal nonprofessional APCs differentially affect T cell function, depending on the type of cells that present the antigen, as well as the local (inflammatory) micro-environment. It has been recently appreciated that nonprofessional APCs can, as such, orchestrate immunity against pathogens, tumor survival, or rejection, and aid in the progression of various auto-immune pathologies. Therefore, the interest for these nonprofessional APCs is growing as they might be an important target for enhancing various immunotherapies. In this review, the different nonprofessional APCs are discussed, as well as their functional consequences on the T cell response, with a focus on immuno-oncology.

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Johnson, Daniel T., Jiarong Zhou, Ashley V. Kroll, Ronnie H. Fang, Ming Yan, Crystal Xiao, Xiufen Chen, Justin Kline, Liangfang Zhang, and Dong-Er Zhang. "Acute myeloid leukemia cell membrane-coated nanoparticles for cancer vaccination immunotherapy." Leukemia 36, no. 4 (November 29, 2021): 994–1005. http://dx.doi.org/10.1038/s41375-021-01432-w.

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AbstractCancer vaccines are promising treatments to prevent relapse after chemotherapy in acute myeloid leukemia (AML) patients, particularly for those who cannot tolerate intensive consolidation therapies. Here, we report the development of an AML cell membrane-coated nanoparticle (AMCNP) vaccine platform, in which immune-stimulatory adjuvant-loaded nanoparticles are coated with leukemic cell membrane material. This AMCNP vaccination strategy stimulates leukemia-specific immune responses by co-delivering membrane-associated antigens along with adjuvants to antigen-presenting cells. To demonstrate that this AMCNP vaccine enhances leukemia-specific antigen presentation and T cell responses, we modified a murine AML cell line to express membrane-bound chicken ovalbumin as a model antigen. AMCNPs were efficiently acquired by antigen-presenting cells in vitro and in vivo and stimulated antigen cross-presentation. Vaccination with AMCNPs significantly enhanced antigen-specific T cell expansion and effector function compared with control vaccines. Prophylactic vaccination with AMCNPs enhanced cellular immunity and protected against AML challenge. Moreover, in an AML post-remission vaccination model, AMCNP vaccination significantly enhanced survival in comparison to vaccination with whole leukemia cell lysates. Collectively, AMCNPs retained AML-specific antigens, elicited enhanced antigen-specific immune responses, and provided therapeutic benefit against AML challenge.

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Berkower, Ira, and Howard Z. Streicher. "The Mononuclear Phagocyte as Antigen-Presenting Cell." Pediatric Annals 16, no. 5 (May 1, 1987): 395–401. http://dx.doi.org/10.3928/0090-4481-19870501-07.

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Murtaugh, Michael P., and Dennis L. Foss. "Inflammatory cytokines and antigen presenting cell activation." Veterinary Immunology and Immunopathology 87, no. 3-4 (September 2002): 109–21. http://dx.doi.org/10.1016/s0165-2427(02)00042-9.

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Basu, Sreyashi, and Toyoshi Matsutake. "Heat shock protein–antigen presenting cell interactions." Methods 32, no. 1 (January 2004): 38–41. http://dx.doi.org/10.1016/s1046-2023(03)00189-0.

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Goyvaerts, C., J. Dingemans, K. De Groeve, C. Heirman, E. Van Gulck, G. Vanham, P. De Baetselier, K. Thielemans, G. Raes, and K. Breckpot. "Targeting of Human Antigen-Presenting Cell Subsets." Journal of Virology 87, no. 20 (July 17, 2013): 11304–8. http://dx.doi.org/10.1128/jvi.01498-13.

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Campton, Kristina, Wanhong Ding, Zengmin Yan, Hiroaki Ozawa, Kristina Seiffert, Edward Miranda, Richard D. Granstein, Antonietta Lonati, and Stefan Beissert. "Tumor Antigen Presentation by Dermal Antigen-Presenting Cells." Journal of Investigative Dermatology 115, no. 1 (July 2000): 57–61. http://dx.doi.org/10.1046/j.1523-1747.2000.00014.x.

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Zlotnik, A., M. Fischer, N. Roehm, and D. Zipori. "Evidence for effects of interleukin 4 (B cell stimulatory factor 1) on macrophages: enhancement of antigen presenting ability of bone marrow-derived macrophages." Journal of Immunology 138, no. 12 (June 15, 1987): 4275–79. http://dx.doi.org/10.4049/jimmunol.138.12.4275.

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Abstract We have studied the effects of recombinant mouse interleukin 4 (IL 4) (previously known as B cell stimulatory factor 1) on the antigen-presenting ability of murine splenic B cells and bone marrow macrophages. Our assay is based on the induction of antigen-presenting ability in these cells after incubation with IL 4 for 24 hr. The presenting cells were then used to stimulate IL 2 production by antigen-specific, I-Ad-restricted T cell hybridomas, a response mainly dependent on the induction of Ia antigens. Consistent with our previously published data using partially purified natural IL 4, we show here that recombinant IL 4 (but not interferon-gamma (IFN-gamma) or IL 1) induces antigen-presenting ability in B cells. Recombinant IL 4 was also found to induce antigen-presenting ability in a cloned, bone marrow derived-macrophage cell line (14M1.4), and in normal bone marrow-derived macrophages. These macrophage populations also respond to IFN-gamma showing enhanced antigen-presenting ability (mediated by increased Ia antigen expression). A small but significant increase in Ia antigen expression was also detected in 14M1.4 macrophages induced with IL 4. However, additional analysis suggested that the effect of IL 4 on 14M1.4 is different from that of IFN-gamma, because IL 4 (but not IFN-gamma) is able to maintain the viability and increase the size of and metabolic activity of bone marrow macrophages. However, IL 4 may not affect all macrophages because the macrophage cell line P388D1, which responds to IFN-gamma, failed to show enhanced antigen-presenting function after stimulation with IL 4. These observations indicate that IL 4, a lymphokine previously considered to be B cell lineage specific, has effects on macrophages and may be involved in their activation.

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Selby, Dale M., Debra F. Singer, Robert W. Anderson, John E. Coligan, Jennifer J. Linderman, and Roderick Nairn. "Antigen-Presenting Cell Lines Internalize Peptide Antigens via Fluid-Phase Endocytosis." Cellular Immunology 163, no. 1 (June 1995): 47–54. http://dx.doi.org/10.1006/cimm.1995.1097.

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Feng, Xiangru, Jiaxue Liu, Weiguo Xu, Gao Li, and Jianxun Ding. "Tackling autoimmunity with nanomedicines." Nanomedicine 15, no. 16 (July 2020): 1585–97. http://dx.doi.org/10.2217/nnm-2020-0102.

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Tolerogenic immunotherapy aims to blunt pathogenic inflammation without affecting systemic immunity. However, the anti-inflammatory drugs and immunosuppressive biologics that are used in the clinic usually result in nonspecific immune cell suppression and off-target toxicity. For this reason, strategies have been developed to induce antigen-specific immune tolerance through the delivery of disease-relevant antigens by nanocarriers as a benefit of their preferential internalization by antigen-presenting cells. Herein, we discuss the recent advances in the nanotechnology-based antigen-specific tolerance approaches. Some of these designs are based on nanoparticles delivering antigens and immunoregulatory agents to modulate antigen-presenting pathways, while others directly target T cells via nanoparticle-based artificial antigen-presenting cells. These antigen-specific therapies are hoped to replace systemic immune suppression and provide long-term disease remission.

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Watkins, Elyse A., Jennifer T. Antane, Jaeda L. Roberts, Kristen M. Lorentz, Sarah Zuerndorfer, Anya C. Dunaif, Lucas J. Bailey, et al. "Persistent antigen exposure via the eryptotic pathway drives terminal T cell dysfunction." Science Immunology 6, no. 56 (February 26, 2021): eabe1801. http://dx.doi.org/10.1126/sciimmunol.abe1801.

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Although most current treatments for autoimmunity involve broad immunosuppression, recent efforts have aimed to suppress T cells in an antigen-specific manner to minimize risk of infection. One such effort is through targeting antigen to the apoptotic pathway to increase presentation of the antigen of interest in a tolerogenic context. Erythrocytes present a rational candidate to target because of their high rate of eryptosis, which facilitates continual uptake by antigen-presenting cells in the spleen. Here, we develop an approach that binds antigens to erythrocytes to induce sustained T cell dysfunction. Transcriptomic and phenotypic analyses revealed signatures of self-tolerance and exhaustion, including up-regulation of PD-1, CTLA4, Lag3, and TOX. Antigen-specific T cells were incapable of responding to an adjuvanted antigenic challenge even months after antigen clearance. With this strategy, we prevented pathology in a mouse experimental autoimmune encephalomyelitis model. CD8+ T cell education occurred in the spleen and was dependent on cross-presenting Batf3+ dendritic cells. These results demonstrate that antigens associated with eryptotic erythrocytes induce lasting T cell dysfunction that could be protective in deactivating pathogenic T cells.

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Reske-Kunz, A. B., K. Reske, and E. Rüde. "Cloned murine Ia+ BK-BI-2.6.C6 T cells function as accessory cells presenting protein antigens to long-term-cultured antigen-specific T cell lines." Journal of Immunology 136, no. 6 (March 15, 1986): 2033–40. http://dx.doi.org/10.4049/jimmunol.136.6.2033.

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Abstract A variant clone, BK-BI-2.6.C6, was derived from the murine bovine insulin-reactive T cell line BK-BI-2.6 with helper/amplifier phenotype. Variant cells have lost reactivity to insulin, but have acquired constitutive IL 2 receptor expression, growing in IL 2-containing medium without feeder cells. In contrast to their ancestor line, variant cells synthesize and express I-A and I-E region-dependent class II molecules as indicated by metabolic radiolabeling, immunoprecipitation with subregion-specific monoclonal antibodies and two-dimensional (2D) gel electrophoresis (1D isoelectric focusing, 2D SDS-PAGE). BK-BI-2.6.C6 cells can act as accessory cells, presenting the protein antigens bovine insulin and ovalbumin to antigen-dependent long-term cultured T cell lines BK-BI-1.2 and BK-OVA-1 in the context of I-A restriction elements. Antigen recognition on presenting BK-BI-2.6.C6 accessory cells resulted in highly efficient IL 2 production. However, in contrast to splenic antigen-presenting cells, BK-BI-2.6.C6 cells did not initiate antigen-specific [3H]thymidine incorporation by the T cell lines tested. Further study of accessory function of Ia+ T cell clones might provide insight into processes regulating T cell responses to antigen.

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Jakubzick, Claudia, Shaihk Atif, Sophie Gibbings, Michelle Nelsen, Ronald Gill, Ross Kedl, and Philippa Marrack. "Double-edged sword: self-acquiring Batf3-dependent dendritic cell required for anti-tumor immunity and graft rejection (APP3P.104)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 113.5. http://dx.doi.org/10.4049/jimmunol.194.supp.113.5.

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Abstract One of the major obstacles for the graft acceptance of tissue and organs is the mismatch of major and minor histocompatibility (H) antigens. Minor H antigens are peptides derived from polymorphic proteins and presented by antigen-presenting cells on major histocompatibility complex (MHC) molecules. Here we hypothesized that the self-acquiring, cross-presenting Batf3-dependent dendritic cell (DC) is responsible for minor-antigen graft rejection. Using three models of minor-antigen graft rejection: 1) male antigen 2) non-sex complex minor antigen and 3) skin organ transplant, we demonstrate that Batf3-dependent DCs are responsible for minor-antigen graft rejection. However, in the presence of a TLR7 ligand, the requirement for Batf3-dependent DCs is bypassed by shifting the functionality of Batf3-independent DCs to elicit minor-antigen graft rejection. Overall our study identifies the DC subtype responsible for minor-antigen graft rejection.

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George-Chandy, Annie, Kristina Eriksson, Michael Lebens, Inger Nordström, Emma Schön, and Jan Holmgren. "Cholera Toxin B Subunit as a Carrier Molecule Promotes Antigen Presentation and Increases CD40 and CD86 Expression on Antigen-Presenting Cells." Infection and Immunity 69, no. 9 (September 1, 2001): 5716–25. http://dx.doi.org/10.1128/iai.69.9.5716-5725.2001.

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ABSTRACT Cholera toxin B subunit (CTB) is an efficient mucosal carrier molecule for the generation of mucosal antibody responses and/or induction of systemic T-cell tolerance to linked antigens. CTB binds with high affinity to GM1 ganglioside cell surface receptors. In this study, we evaluated how conjugation of a peptide or protein antigen to CTB by chemical coupling or genetic fusion influences the T-cell-activating capacity of different antigen-presenting cell (APC) subsets. Using an in vitro system in which antigen-pulsed APCs were incubated with antigen-specific, T-cell receptor-transgenic T cells, we found that the dose of antigen required for T-cell activation could be decreased >10,000-fold using CTB-conjugated compared to free antigen. In contrast, no beneficial effects were observed when CTB was simply admixed with antigen. CTB conjugation enhanced the antigen-presenting capacity not only of dendritic cells and B cells but also of macrophages, which expressed low levels of cell surface major histocompatibility complex (MHC) class II and were normally poor activators of naive T cells. Enhanced antigen-presenting activity by CTB-linked antigen resulted in both increased T-cell proliferation and increased interleukin-12 and gamma interferon secretion and was associated with up-regulation of CD40 and CD86 on the APC surface. These results imply that conjugation to CTB dramatically lowers the threshold concentration of antigen required for immune cell activation and also permits low-MHC II-expressing APCs to prime for a specific immune response.

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Spillane, Katelyn M., and Pavel Tolar. "B Cell Antigen Extraction is Regulated by Physical Properties of Antigen Presenting Cells." Biophysical Journal 112, no. 3 (February 2017): 126a. http://dx.doi.org/10.1016/j.bpj.2016.11.701.

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Pierobon, Paolo, and Ana-Maria Lennon-Duménil. "To use or not to use the force: How B lymphocytes extract surface-tethered antigens." Journal of Cell Biology 216, no. 1 (December 20, 2016): 17–19. http://dx.doi.org/10.1083/jcb.201612043.

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Using an exquisite cell imaging approach based on DNA nanosensors, Spillane and Tolar (2016. J. Cell Biol. https://doi.org/10.1083/jcb.201607064) explore how the physical properties of antigen-presenting cell surfaces affect how B cells internalize surface-tethered antigens. Soft and flexible surfaces promote mechanical force-mediated antigen extraction, whereas stiff surfaces lead to enzyme-mediated antigen release before subsequent internalization.

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Townsend, Sarah E., and Christopher C. Goodnow. "Abortive Proliferation of Rare T Cells Induced by Direct or Indirect Antigen Presentation by Rare B Cells In Vivo." Journal of Experimental Medicine 187, no. 10 (May 18, 1998): 1611–21. http://dx.doi.org/10.1084/jem.187.10.1611.

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Antigen-specific B cells are implicated as antigen-presenting cells in memory and tolerance responses because they capture antigens efficiently and localize to T cell zones after antigen capture. It has not been possible, however, to visualize the effect of specific B cells on specific CD4+ helper T cells under physiological conditions. We demonstrate here that rare T cells are activated in vivo by minute quantities of antigen captured by antigen-specific B cells. Antigen-activated B cells are helped under these conditions, whereas antigen-tolerant B cells are killed. The T cells proliferate and then disappear regardless of whether the B cells are activated or tolerant. We show genetically that T cell activation, proliferation, and disappearance can be mediated either by transfer of antigen from antigen-specific B cells to endogenous antigen-presenting cells or by direct B–T cell interactions. These results identify a novel antigen presentation route, and demonstrate that B cell presentation of antigen has profound effects on T cell fate that could not be predicted from in vitro studies.

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Vojtech, Lucia N., Sean Hughes, Claire Levy, Alexandria Taber, Fernanda Calienes, and Florian Hladik. "Exosomes in human semen impair antigen-presenting cell function and decrease antigen-specific T cell responses." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 136.14. http://dx.doi.org/10.4049/jimmunol.196.supp.136.14.

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Abstract Exposure to semen is the primary route of transmission for many sexually transmitted infections. Accumulating evidence suggests that components in semen directly impair leukocytes, which could compromise the protective efficacy of vaccine-induced immune responses in the mucosa. Exosomes, small microvesicles with immunomodulatory functions, are present at an average concentration of 2.2 × 1013 particles per ejaculate (n = 18). These seminal exosomes (SE) efficiently and rapidly entered peripheral and vaginal dendritic cells (DCs), whereas T cell uptake was poor. In PBMC cultures, SE impaired memory T cell function, reducing the production of TNF-alpha, IL-2 and/or IFN-gamma in response to virus-derived peptides an average of 60% for CD4+ T cells and 48% for CD8+ T cells, in a dose-responsive manner (n = 6). Reduction of cytokine production by memory CD8+ T cells was reduced to a greater extent for protein antigens as compared to peptide antigens, implying that antigen-presenting cell function was impaired by the presence of SE. Exposing only DCs, as opposed to bulk PBMCs, to SE also blocked subsequent CD8+ memory T cell activation, reducing the proportion of cells making cytokines by 22% (n = 5 donors). Expression of CD107a, a marker of cytotoxic T cell degranulation, was decreased by 42% in PBMC cultures exposed to SE and superantigen (n=4). SE also impaired vaginal T cell cytokine and degranulation responses to superantigen. Thus, SE likely inhibit antigen-specific T cell responses by impairing antigen-presenting cell function. Understanding how programmed immune responses are altered by the presence of semen is important to developing the next generation of vaccine and preventative treatments against sexually transmitted disease

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Falo, L. D., B. Benacerraf, L. Rothstein, and K. L. Rock. "Cerulenin is a potent inhibitor of antigen processing by antigen-presenting cells." Journal of Immunology 139, no. 12 (December 15, 1987): 3918–23. http://dx.doi.org/10.4049/jimmunol.139.12.3918.

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Abstract Cerulenin is an antibiotic that inhibits eukaryotic lipid and sterol synthesis and blocks lipid modification of proteins. The effect of cerulenin on the ability of accessory cells to present antigen to T cells was investigated. This antibiotic strongly inhibits the ability of accessory cells to present antigen to murine T-T hybrids. This effect is observed for multiple distinct antigens including L-glutamic acid60-L-alanine30-L-tyrosine10, bovine insulin, L-glutamic acid56-L-lysine35-L-phenylalanine9, and ovalbumen. Presentation by both macrophage and B lymphoblastoid cell lines is inhibited. The ability to effectively pulse these cells with antigen is inhibited but not the ability of these same cells to present antigen that they have previously processed. Furthermore, this inhibition is selective as it can occur without significant inhibition of the antigen-presenting cell protein or DNA synthesis. Cerulenin does not inhibit antigen uptake or catabolism as assessed with labeled antigen. By these criteria this drug is shown to interfere with an antigen-processing step. The ability of cerulenin to block processing was compared with other known inhibitors. Although cerulenin was effective with all antigens tested, at least one inhibitor was not. Taken together, these results suggest that the effect of cerulenin may define a distinct step in antigen processing and provides evidence that some other processing events are not universally required. The ability of cerulenin to interfere with antigen processing is discussed in the context of the known actions of this antibiotic and events of antigen processing and presentation.

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Lees, Jason R., Saule Nurmukhambetova, Yong Chan Kim, Ai-Hong Zhang, and David W. Scott. "Using transgenic expression of a MHC Class II/peptide restricted T cell receptor in mature CD8+ T cells to target auto-antigen decorated antigen presenting cells for destruction." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 139.11. http://dx.doi.org/10.4049/jimmunol.196.supp.139.11.

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Abstract CD4+ T cells are thought to be necessary for MS neuroinflammation, coordinating the destructive immune response following recognition of central nervous system (CNS) antigens in the context of MHC class II molecules on professional antigen presenting cells (APC). Recognition of CNS antigens within the CNS is required to drive CD4 re-activation and subsequent production of cytokines and chemokines crucial to the recruitment of secondary immune effector cells. This CD4+ T cell driven recruitment in turn results in induction of immune pathology while also priming APC to enhance future T cell-APC interactions. Recent studies in cancer immunotherapy have defined protocols for inducing expression of chimeric antigen-specific T cell receptors (CAR) in mature CD8 T cells for the purpose of inducing destruction of antigen bearing cells, apparently without modulating the underlying effector profile of the transduced T cell (i.e., CD8 cells are still cytotoxic through perforin and granzymes). Here we detail the use of defined MHC class II/peptide restricted T cell receptor expression in mature CD8 T cells in an effort to target for destruction MHC class II expressing professional antigen presenting cells containing CNS antigen while sparing MHC II negative neurons and oligodendrocytes. Crucially, an effective antigen elimination strategy would not only modulate the cognate antigen recognized by the transgenic TCR but, given the propensity of APC to present multiple antigens derived from the same phagocytized material, should also impact uncharacterized CNS antigen epitopes. This study examines a novel potential therapeutic modality for its efficacy in neuroinflammation. Supported by NMSS pilot grant PP3361.

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Yewdall, Alice W., Scott B. Drutman, Felecia Jinwala, Keith S. Bahjat, and Nina Bhardwaj. "CD8+ T Cell Priming by Dendritic Cell Vaccines Requires Antigen Transfer to Endogenous Antigen Presenting Cells." PLoS ONE 5, no. 6 (June 16, 2010): e11144. http://dx.doi.org/10.1371/journal.pone.0011144.

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Sopori, M. L., D. A. Cohen, S. Cherian, R. S. Perrone, and A. M. Kaplan. "Antigen presentation in the rat. II. An Ia+ radiosensitive T cell can present antigen to primed Ia- T cells." Journal of Immunology 134, no. 3 (March 1, 1985): 1369–73. http://dx.doi.org/10.4049/jimmunol.134.3.1369.

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Abstract 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.

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Journal articles on the topic 'Antigen Presenting Cell'

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