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Journal articles on the topic 'Antigen-specific immune responses'

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Published: 10 December 2022
Last updated: 28 January 2023

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1

Lillard, James W., Prosper N. Boyaka, Dennis D. Taub, and Jerry R. McGhee. "RANTES Potentiates Antigen-Specific Mucosal Immune Responses." Journal of Immunology 166, no. 1 (January 1, 2001): 162–69. http://dx.doi.org/10.4049/jimmunol.166.1.162.

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2

Gratama, Jan W., Florian Kern, Fabrizio Manca, and Mario Roederer. "Measuring Antigen-Specific Immune Responses, 2008 update." Cytometry Part A 73A, no. 11 (October 22, 2008): 971–74. http://dx.doi.org/10.1002/cyto.a.20655.

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3

Pira, Giuseppina Li, Florian Kern, Jan Gratama, Mario Roederer, and Fabrizio Manca. "Measurement of antigen specific immune responses: 2006 update." Cytometry Part B: Clinical Cytometry 72B, no. 2 (2007): 77–85. http://dx.doi.org/10.1002/cyto.b.20186.

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4

Rastogi, Deepa, Chaodong Wang, Xia Mao, Cynthia Lendor, Paul B. Rothman, and Rachel L. Miller. "Antigen-specific immune responses to influenza vaccine in utero." Journal of Clinical Investigation 117, no. 6 (June 1, 2007): 1637–46. http://dx.doi.org/10.1172/jci29466.

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5

Trollmo, C., S. Gudmundsson, N. Feltelius, S. Rogberg, G. Smedegard, and L. Klareskog. "Sulphasalazine inhibits human antigen-specific immune responses in vivo." Annals of the Rheumatic Diseases 66, no. 4 (September 19, 2006): 481–85. http://dx.doi.org/10.1136/ard.2006.059881.

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6

Woodham, Andrew W., Ross W. Cheloha, Jingjing Ling, Mohammad Rashidian, Stephen C. Kolifrath, Maia Mesyngier, Joao N. Duarte, et al. "Nanobody–Antigen Conjugates Elicit HPV-Specific Antitumor Immune Responses." Cancer Immunology Research 6, no. 7 (May 23, 2018): 870–80. http://dx.doi.org/10.1158/2326-6066.cir-17-0661.

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7

Facciabene, Andrea, Luigi Aurisicchio, and Nicola La Monica. "Baculovirus Vectors Elicit Antigen-Specific Immune Responses in Mice." Journal of Virology 78, no. 16 (August 15, 2004): 8663–72. http://dx.doi.org/10.1128/jvi.78.16.8663-8672.2004.

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ABSTRACT To characterize the induction of antigen-specific immune response mediated by baculovirus, vectors expressing the E2 glycoprotein of hepatitis C virus or the carcinoembryonic antigen (CEA) under the control of the cytomegalovirus immediate-early promoter-enhancer were constructed. Additionally, a baculovirus vector encoding the E2 glycoprotein (Bac-G-E2) and expressing vesicular stomatitis virus glycoprotein (VSV-G) in the viral envelope was generated by inserting the VSV-G coding sequence downstream of the polyhedrin promoter. Mice were subjected to intramuscular, intranasal, or subcutaneous inoculations with Bac-E2 and the cellular immune response was monitored by ELISPOT and intracellular staining. Additionally, humoral response was monitored by titrating anti-E2 antibodies. Induction of a measurable anti-E2 T-cell response was observed only after intramuscular injection and was predominantly CD8+ specific. The immunogenic properties of baculovirus as vaccine vector were not restricted to E2 because a CEA-specific CD4+ T-cell response was observed upon intramuscular injection of Bac-CEA. Interestingly, the Bac-G-E2 vector was shown to be a more efficient immunogen than Bac-E2, in view of the 10-fold difference in the minimal dose required to elicit a measurable T-cell response upon intramuscular injection. Induction of inflammatory cytokines such as gamma interferon, tumor necrosis factor alpha, and interleukin-6 was detected as early as 6 h postinjection of Bac-G-E2. Most importantly, both vectors elicited CD8+ T cells with effector function capable of lysing target cells loaded with a hepatitis C virus-specific epitope. Additionally, enhanced NK cytolytic activity was detected in immunized mice. Thus, these results further demonstrate that baculovirus may be considered a useful vector for gene therapy.
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8

Kapp, Kerstin, Jochen Maul, Arwed Hostmann, Pamela Mundt, Jan C. Preiss, Arlett Wenzel, Andreas Thiel, Martin Zeitz, Reiner Ullrich, and Rainer Duchmann. "Modulation of systemic antigen-specific immune responses by oral antigen in humans." European Journal of Immunology 40, no. 11 (October 19, 2010): 3128–37. http://dx.doi.org/10.1002/eji.201040701.

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9

Nagafuchi, Shinya, Satoshi Hachimura, Mamoru Totsuka, Takeshi Takahashi, Masao Goto, Takaji Yajima, Tamotsu Kuwata, Sonoko Habu, and Shuichi Kaminogawa. "Dietary Nucleotides Can Up-Regulate Antigen-Specific Th1 Immune Responses and Suppress Antigen-Specific IgE Responses in Mice." International Archives of Allergy and Immunology 122, no. 1 (2000): 33–41. http://dx.doi.org/10.1159/000024356.

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10

Yang, De, Yuri Postnikov, Yana Li, Poonam Tewary, Gonzalo de la Rosa, Dennis Kliman, Takashi Furusawa, Michael Bustin, Feng Wei, and Joost Oppenheim. "High mobility group nucleosome-binding protein 1 acts as an alarmin critical for the induction of immune response (113.7)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 113.7. http://dx.doi.org/10.4049/jimmunol.186.supp.113.7.

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Abstract Alarmins, defined as endogenous mediator(s) capable of promoting the recruitment and activation of antigen-presenting cells (APCs) including dendritic cells (DCs), can potentially promote immunity, however, their essential contribution to the induction immune responses remain to be demonstrated. Here we report the identification of HMGN1 as a novel alarmin that is critical to the induction of antigen-specific immune response. HMGN1 induced DC maturation and recruitment of APCs and activated NF-κB and multiple MAPKs, in a MyD88-dependent manner. HMGN1 promoted antigen-specific immune response upon co-administration with an antigen. Furthermore, knockout of HMGN1 in mice greatly reduced antigen-specific antibody and T cell responses upon intraperitoneal immunization with an antigen using LPS as an adjuvant. The impaired ability of HMGN1 KO mice to mount antigen-specific immune responses was accompanied by both deficient DC recruitment at sites of immunization and reduced production of inflammatory cytokines. Bone marrow chimera experiments revealed that HMGN1 derived from non-leukocytes played a more critical role in the induction of antigen-specific antibody and T cell responses. Thus, HMGN1 acts as a novel alarmin critical for the induction of adaptive immune response.
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11

Greiner, Jochen Marlies, Vanessa Schneider, Hubert Schrezenmeier, Susanne Hofmann, and Marlies Götz. "Enhanced Stimulation of Antigen-Specific Immune Responses Against NPM1-Mutated AML." Blood 138, Supplement 1 (November 5, 2021): 1292. http://dx.doi.org/10.1182/blood-2021-146875.

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Abstract Nucleophosmin1 (NPM1) is one of the most frequently mutated genes in AML, is often associated with a favorable prognosis and seems to be a suitable target structure for immunotherapeutic approaches. Other groups and ours described specific immune responses of CD8-positive T cells against immunogenic epitopes derived from the mutational region of NPM1 in AML patients (pts). In this extended immunological study, we investigated immune responses against the mutational epitope of NPM1 but also against other LAA in NPM1 mut compared to NPM1 wt pts. 30 AML pts were analyzed using FACS analysis, tetramer staining and colony forming immunoassays (CFI). 15 NPM1 mut and 15 NPM1 wt pts were investigated in CFI to detect CTL mediated immune responses against leukemic progenitor/stem cells (LPC/LSC). We also added immune checkpoint inhibitors to investigate whether these immune responses could be enhanced. Against the LAA PRAME-P3, WT1 and RHAMM-R3 we detected similar frequencies of T cell responses in CFI in NPM1 mut compared to NPM1 wt pts. Antigen specific immune responses were detected in CFI by comparing growth of patient cells alone with growth by addition of antigen specific CTL and calculating colony reduction. Comparing NPM1 mut/NPM1 wt pts many had an immune response to LAA, more than 50% of the pts in both cohorts exhibited an immune response against all epitopes. In NPM1 wt pts no responses were found against the NPM1 epitope as expected, whereas NPM1 mut patients showed a high frequency of immune responses in 10/15 NPM1 mut AML pts (67%) in CFI a reduction of colonies was detected. With the addition of anti-PD1 antibody to CFI we detected an increase of immune responses. For the LAA responses were similar comparing NPM1 mut/NPM1 wt. Compared to LAA, the epitope NPM1 showed a particularly strong immune response when the antibody anti-PD1 was added. All 15 NPM1 mut pts showed an immune response with anti-PD1, with a median reduction of colonies of 47%. 7 of 15 NPM1 mut pts showed a strong immune response against LPC/LSC in CFI with more than 50% reduction of colonies. The data suggest that especially NPM1 mut patients are suitable candidates for antibody therapy with the PD1 antibody. Combination with another immunotherapy such as an NPM1 specific vaccine would be a possibility. Even though no advantage in therapy with the anti-PD1 antibody has yet been shown in the overall AML collective, this therapy could be an option for patients with NPM1 mutated AML. Disclosures Greiner: Bristol Myers Squibb: Other: Unspecified Relationship. Schneider: AbbVie: Current Employment. Schrezenmeier: Novartis: Honoraria; Apellis: Honoraria; Sanofi: Honoraria; Alexion, AstraZeneca Rare Disease: Honoraria, Other: Travel support, Research Funding; Roche: Honoraria.
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12

Candando, Kathleen, Masahiro Kamata, Evgueni Kountikov, Jacquelyn M. Lykken, Ayumi Yoshizaki, Tomomitsu Miyagaki, and Thomas Tedder. "Regulatory B10 cells control immune responses via antigen-specific pathways." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 125.8. http://dx.doi.org/10.4049/jimmunol.196.supp.125.8.

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Abstract B cells secrete antigen-specific antibodies during immune responses to neutralize pathogens and other threats. Despite this well-characterized pro-inflammatory B cell function, a rare subset of B cells (B10 cells) in both humans and mice are known to produce the inhibitory cytokine interleukin 10 (IL-10) and provide negative regulation of inflammation and T cell-dependent autoimmunity. B cell receptor (BCR)-derived signals are essential to regulatory B cell function as B10 cell suppression of disease is antigen-specific and requires cognate interactions with T cells. In addition, B10 cell development is blunted in mice with fixed BCR specificities, underscoring the key role that BCR signaling plays in the acquisition of B cell IL-10 competence. Given the importance of the BCR in both B10 cell development and function, we hypothesized that antigen-specific B10 cells are required for optimal disease suppression. Here we show by single-cell PCR that B10 cells derived from naive mice as well as from mice exposed to antigen express a diverse set of both heavy and light chain immunoglobulin genes that are predominantly without mutations. In addition, we demonstrate using IL-10 reporter mice that antigen-specific B10 cells are reliably expanded in vivo and that these antigen-specific B10 cells are required for optimal disease suppression upon adoptive transfer. Thus, B10 cells provide robust antigen-specific regulation of immune responses in vivo through diverse, unmutated BCRs.
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13

Yang, De, Yuri V. Postnikov, Yana Li, Poonam Tewary, Gonzalo de la Rosa, Feng Wei, Dennis Klinman, et al. "High-mobility group nucleosome-binding protein 1 acts as an alarmin and is critical for lipopolysaccharide-induced immune responses." Journal of Experimental Medicine 209, no. 1 (December 19, 2011): 157–71. http://dx.doi.org/10.1084/jem.20101354.

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Alarmins are endogenous mediators capable of promoting the recruitment and activation of antigen-presenting cells (APCs), including dendritic cells (DCs), that can potentially alert host defense against danger signals. However, the relevance of alarmins to the induction of adaptive immune responses remains to be demonstrated. In this study, we report the identification of HMGN1 (high-mobility group nucleosome-binding protein 1) as a novel alarmin and demonstrate that it contributes to the induction of antigen-specific immune responses. HMGN1 induced DC maturation via TLR4 (Toll-like receptor 4), recruitment of APCs at sites of injection, and activation of NF-κB and multiple mitogen-activated protein kinases in DCs. HMGN1 promoted antigen-specific immune response upon co-administration with antigens, and Hmgn1−/− mice developed greatly reduced antigen-specific antibody and T cell responses when immunized with antigens in the presence of lipopolysaccharide (LPS). The impaired ability of Hmgn1−/− mice to mount antigen-specific immune responses was accompanied by both deficient DC recruitment at sites of immunization and reduced production of inflammatory cytokines. Bone marrow chimera experiments revealed that HMGN1 derived from nonleukocytes was critical for the induction of antigen-specific antibody and T cell responses. Thus, extracellular HMGN1 acts as a novel alarmin critical for LPS-induced development of innate and adaptive immune responses.
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14

Tomiyama, Shunichi, Elizabeth M. Keithley, and Jeffrey P. Harris. "Antigen-Specific Immune Response in the Inner Ear." Annals of Otology, Rhinology & Laryngology 98, no. 6 (June 1989): 447–50. http://dx.doi.org/10.1177/000348948909800610.

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The specificity of inner ear immune responses was investigated by challenging each inner ear of presensitized animals with different antigens. Animals presensitized systemically with keyhole limpet hemocyanin (klh) and bovine serum albumin (BSA) were challenged with klh in the right and BSA in the left inner ears. Two weeks later perilymph anti-klh levels were increased significantly in the right inner ears compared to the levels in the left inner ears. In contrast, perilymph anti-BSA levels were increased significantly in the left inner ears compared to the levels in the right inner ears. These results suggested that the rise in perilymph antibody following inner ear antigen challenge was predominantly the result of an antigen-specific immune response in the inner ear and not simply the result of an increase in vascular permeability or serum contamination from the experimental procedure itself.
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15

Steinman, Lawrence. "The re-emergence of antigen-specific tolerance as a potential therapy for MS." Multiple Sclerosis Journal 21, no. 10 (April 28, 2015): 1223–38. http://dx.doi.org/10.1177/1352458515581441.

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Ideal therapy for inflammatory disease in the nervous system would preserve normal immune function, while suppressing only the pathologic immune responses that damage tissue and allowing for repair. In principle, antigen-specific therapy would eradicate unwanted adaptive immune responses—antibody and T-cell mediated—while preserving the integrity of other adaptive responses to infectious agents and retaining the ability to fight malignancy. However, at this time, for multiple sclerosis (MS) we do not have compelling evidence that would support any particular dominant immune response to any specific antigen or even a limited group of antigens. In fact, there are adaptive immune responses to a wide swathe of proteins and lipids found on neurons and myelin in MS. Unless controlling a few of the known immune responses is sufficient, antigen-specific therapy in MS may not have enough of an impact to modulate clinical outcome. However, in other neuroinflammatory conditions, such as neuromyelitis optica, the adaptive immune response is highly focused. Trials of antigen-specific therapy for neuroinflammatory disease might first be tested in diseases with a more limited adaptive immune response like neuromyelitis optica. The likelihood of a significant success for this therapeutic strategy might then ensue.
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16

Nesslinger, Nancy J., Robert A. Sahota, Brad Stone, Kayli Johnson, Navraj Chima, Caitlin King, Devon Rasmussen, et al. "Standard Treatments Induce Antigen-Specific Immune Responses in Prostate Cancer." Clinical Cancer Research 13, no. 5 (March 1, 2007): 1493–502. http://dx.doi.org/10.1158/1078-0432.ccr-06-1772.

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17

Zhang, L., and S. S. Mohapatra. "Antigen- and isotype-specific immune responses to a recombinant antigen-allergen chimeric (RAAC) protein." Journal of Immunology 151, no. 2 (July 15, 1993): 791–99. http://dx.doi.org/10.4049/jimmunol.151.2.791.

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Abstract Ag-specific IgE and IgG antibody responses to a recombinant Ag-allergen chimeric (RAAC) protein were examined in B6D2F1 mice. The RAAC protein consisted of the truncated beta-galactosidase (beta-gal), linked at its C terminus to a polypeptide representing the conserved region of the recombinant Kentucky Bluegrass allergen encoded by the cDNA clone KBG8.3(rKBG8.3). Immunization of the mice with the RAAC protein in dextran sulfate as adjuvant led to the differential production of antibodies to the two constituents of RAAC protein with respect to their isotypic classes. Most of the antibody responses to both sets of determinants on the fusion protein were IgG1. In addition, the allergenic polypeptide of RAAC protein induced IgE antibodies, whereas the beta-gal elicited IgG2a antibodies. The same pattern of antibody isotypes was produced when the individual components, rKBG8.3 and beta-gal were separately used for immunization with dextran sulfate. On the other hand, immunization of mice with either RAAC or the beta-gal in CFA induced primarily a IgG response, and no IgE antibodies; however, under the same conditions of immunization rKBG8.3 induced IgG1 antibodies and also low levels of IgE antibodies. In contrast, the RAAC and the beta-gal induced IgG2a antibodies, whereas rKBG8.3 induced no detectable IgG2a antibodies. Furthermore, high titers of IgE antibodies were induced by the rKBG8.3 and not by the RAAC protein in dextran sulfate after the mice had been immunized twice with the same polypeptide in CFA. It is inferred from these results that the induction of isotype-specific immune responses in the animals with the same genetic background is dependent upon the Ag in question as well as the adjuvant; the latter, however, influences the magnitude but does not determine the isotype of the immune responses.
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18

Qiu, Zhijuan, and Kamal Khanna. "Visualize immune responses during murine cytomegalovirus infection (105.38)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 105.38. http://dx.doi.org/10.4049/jimmunol.186.supp.105.38.

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Abstract Cytomegalovirus (CMV) belongs to herpesviridae family, and can cause severe disease in immunocompromised individual. In the infected host CMV establishes a life-long latent infection even in the presence of concomitant anti-viral immunity. In humans and in mice, CMV infection leads to chronic clonal expansion of antigen specific CD8 and CD4 T cells, a phenomenon known as T cell inflation. The mechanisms that contribute to this phenomenon remain poorly defined. Furthermore, the source of antigen presentation to T cells during latency is not known. Here we used a combination of in-situ MHC class I tetramer staining and adoptive transfer studies to visualize the anatomy of the virus specific CD8 T cells in lymphoid and non-lymphoid organs of mice during primary and latent murine CMV (MCMV)-OVA infection. Our imaging studies revealed a complex spatial and temporal map of antigen presentation in the context of antigen specific CD8 T cell localization during acute and latent CMV infection. These data suggest that viral reactivation likely occurs intermittently and regionally within individual organs. Our studies provide important clues towards the mechanisms responsible for T cell inflation following CMV infection.
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19

Li, Pan, Gaona Shi, Xiuyuan Zhang, Huijuan Song, Chuangnian Zhang, Weiwei Wang, Chen Li, Bing Song, Chun Wang, and Deling Kong. "Guanidinylated cationic nanoparticles as robust protein antigen delivery systems and adjuvants for promoting antigen-specific immune responses in vivo." Journal of Materials Chemistry B 4, no. 33 (2016): 5608–20. http://dx.doi.org/10.1039/c6tb01556e.

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20

Renshaw, B. R., W. C. Fanslow, R. J. Armitage, K. A. Campbell, D. Liggitt, B. Wright, B. L. Davison, and C. R. Maliszewski. "Humoral immune responses in CD40 ligand-deficient mice." Journal of Experimental Medicine 180, no. 5 (November 1, 1994): 1889–900. http://dx.doi.org/10.1084/jem.180.5.1889.

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Individuals with X-linked hyper-IgM syndrome fail to express functional CD40 ligand (CD40L) and, as a consequence, are incapable of mounting protective antibody responses to opportunistic bacterial infections. To address the role of CD40L in humoral immunity, we created, through homologous recombination, mice deficient in CD40L expression. These mice exhibited no gross developmental deficiencies or health abnormalities and contained normal percentages of B and T cell subpopulations. CD40L-deficient mice did display selective deficiencies in humoral immunity; basal serum isotype levels were significantly lower than observed in normal mice, and IgE was undetectable. Furthermore, the CD40L-deficient mice failed to mount secondary antigen-specific responses to immunization with a thymus-dependent antigen, trinitrophenol-conjugated keyhole limpet hemocyanin (TNP-KLH). By contrast, the CD40L-deficient mice produced antigen-specific antibody of all isotypes except IgE in response to the thymus-independent antigen, DNP-Ficoll. These results underscore the requirement of CD40L for T cell-dependent antibody responses. Moreover, Ig class switching to isotypes other than IgE can occur in vivo in the absence of CD40L, supporting the notion that alternative B cell signaling pathways regulate responses to thymus-independent antigens.
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21

Maldonado, Roberto A., Robert A. LaMothe, Joseph D. Ferrari, Ai-Hong Zhang, Robert J. Rossi, Pallavi N. Kolte, Aaron P. Griset, et al. "Polymeric synthetic nanoparticles for the induction of antigen-specific immunological tolerance." Proceedings of the National Academy of Sciences 112, no. 2 (December 29, 2014): E156—E165. http://dx.doi.org/10.1073/pnas.1408686111.

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Current treatments to control pathological or unwanted immune responses often use broadly immunosuppressive drugs. New approaches to induce antigen-specific immunological tolerance that control both cellular and humoral immune responses are desirable. Here we describe the use of synthetic, biodegradable nanoparticles carrying either protein or peptide antigens and a tolerogenic immunomodulator, rapamycin, to induce durable and antigen-specific immune tolerance, even in the presence of potent Toll-like receptor agonists. Treatment with tolerogenic nanoparticles results in the inhibition of CD4+ and CD8+ T-cell activation, an increase in regulatory cells, durable B-cell tolerance resistant to multiple immunogenic challenges, and the inhibition of antigen-specific hypersensitivity reactions, relapsing experimental autoimmune encephalomyelitis, and antibody responses against coagulation factor VIII in hemophilia A mice, even in animals previously sensitized to antigen. Only encapsulated rapamycin, not the free form, could induce immunological tolerance. Tolerogenic nanoparticle therapy represents a potential novel approach for the treatment of allergies, autoimmune diseases, and prevention of antidrug antibodies against biologic therapies.
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22

Matsuzaka, Yasunari, and Ryu Yashiro. "Regulation of Extracellular Vesicle-Mediated Immune Responses against Antigen-Specific Presentation." Vaccines 10, no. 10 (October 10, 2022): 1691. http://dx.doi.org/10.3390/vaccines10101691.

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Extracellular vesicles (EVs) produced by various immune cells, including B and T cells, macrophages, dendritic cells (DCs), natural killer (NK) cells, and mast cells, mediate intercellular communication and have attracted much attention owing to the novel delivery system of molecules in vivo. DCs are among the most active exosome-secreting cells of the immune system. EVs produced by cancer cells contain cancer antigens; therefore, the development of vaccine therapy that does not require the identification of cancer antigens using cancer-cell-derived EVs may have significant clinical implications. In this review, we summarise the molecular mechanisms underlying EV-based immune responses and their therapeutic effects on tumour vaccination.
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23

Kervevan, Jérôme, Aurélie Bouteau, Juliane S. Lanza, Adele Hammoudi, Sandra Zurawski, Mathieu Surenaud, Lydie Dieudonné, et al. "Targeting human langerin promotes HIV-1 specific humoral immune responses." PLOS Pathogens 17, no. 7 (July 29, 2021): e1009749. http://dx.doi.org/10.1371/journal.ppat.1009749.

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The main avenue for the development of an HIV-1 vaccine remains the induction of protective antibodies. A rationale approach is to target antigen to specific receptors on dendritic cells (DC) via fused monoclonal antibodies (mAb). In mouse and non-human primate models, targeting of skin Langerhans cells (LC) with anti-Langerin mAbs fused with HIV-1 Gag antigen drives antigen-specific humoral responses. The development of these immunization strategies in humans requires a better understanding of early immune events driven by human LC. We therefore produced anti-Langerin mAbs fused with the HIV-1 gp140z Envelope (αLC.Env). First, we show that primary skin human LC and in vitro differentiated LC induce differentiation and expansion of naïve CD4+ T cells into T follicular helper (Tfh) cells. Second, when human LC are pre-treated with αLC.Env, differentiated Tfh cells significantly promote the production of specific IgG by B cells. Strikingly, HIV-Env-specific Ig are secreted by HIV-specific memory B cells. Consistently, we found that receptors and cytokines involved in Tfh differentiation and B cell functions are upregulated by LC during their maturation and after targeting Langerin. Finally, we show that subcutaneous immunization of mice by αLC.Env induces germinal center (GC) reaction in draining lymph nodes with higher numbers of Tfh cells, Env-specific B cells, as well as specific IgG serum levels compared to mice immunized with the non-targeting Env antigen. Altogether, we provide evidence that human LC properly targeted may be licensed to efficiently induce Tfh cell and B cell responses in GC.
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24

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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25

Bos, Rinke, Suzanne van Duikeren, Thorbald van Hall, Marjolein M. Lauwen, Mark Parrington, Neil L. Berinstein, Bryan McNeil, et al. "Characterization of Antigen-Specific Immune Responses Induced by Canarypox Virus Vaccines." Journal of Immunology 179, no. 9 (October 18, 2007): 6115–22. http://dx.doi.org/10.4049/jimmunol.179.9.6115.

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26

Mazia, C. G. "Antigen-Specific Adaptive Immune Responses in Fingolimod-Treated Multiple Sclerosis Patients." Yearbook of Neurology and Neurosurgery 2011 (January 2011): 121–22. http://dx.doi.org/10.1016/j.yneu.2011.05.033.

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27

Müller, Kerstin E., Aad Hoek, Victor P. M. G. Rutten, Wilbert E. Bernadina, and G. Henk Wentink. "Antigen-specific immune responses in cattle with inherited β2-integrin deficiency." Veterinary Immunology and Immunopathology 58, no. 1 (August 1997): 39–53. http://dx.doi.org/10.1016/s0165-2427(96)05753-4.

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28

Khatri, Bhagwati, Adam Whelan, Derek Clifford, Agnese Petrera, Peter Sander, and H. Martin Vordermeier. "BCG Δzmp1 vaccine induces enhanced antigen specific immune responses in cattle." Vaccine 32, no. 7 (February 2014): 779–84. http://dx.doi.org/10.1016/j.vaccine.2013.12.055.

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29

Rufer, Nathalie. "Molecular tracking of antigen-specific T-cell clones during immune responses." Current Opinion in Immunology 17, no. 4 (August 2005): 441–47. http://dx.doi.org/10.1016/j.coi.2005.06.003.

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Sastry, K. Jagannadha, Pramod N. Nehete, and Cherylyn A. Savary. "Impairment of antigen-specific cellular immune responses under simulated microgravity conditions." In Vitro Cellular & Developmental Biology - Animal 37, no. 4 (April 2001): 203–8. http://dx.doi.org/10.1007/bf02577530.

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Yoshikawa, Tomoaki, Susumu Imazu, Jian-Qing Gao, Kazuyuki Hayashi, Yasuhiro Tsuda, Mariko Shimokawa, Toshiki Sugita, et al. "Augmentation of antigen-specific immune responses using DNA-fusogenic liposome vaccine." Biochemical and Biophysical Research Communications 325, no. 2 (December 2004): 500–505. http://dx.doi.org/10.1016/j.bbrc.2004.10.056.

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SASTRY, K. JAGANNADHA, PRAMOD N. NEHETE, and CHERYLYN A. SAVARY. "IMPAIRMENT OF ANTIGEN-SPECIFIC CELLULAR IMMUNE RESPONSES UNDER SIMULATED MICROGRAVITY CONDITIONS." In Vitro Cellular & Developmental Biology - Animal 37, no. 4 (2001): 203. http://dx.doi.org/10.1290/1071-2690(2001)037<0203:ioasci>2.0.co;2.

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Zhu, Yong-de, Kevin Koo, Jeffrey D. Bradshaw, William F. Sutton, LaRene Kuller, Richard Bucala, David Anderson, Sally P. Mossman, François Villinger, and Nancy L. Haigwood. "Macaque blood-derived antigen-presenting cells elicit SIV-specific immune responses." Journal of Medical Primatology 29, no. 3-4 (November 27, 2003): 182–92. http://dx.doi.org/10.1034/j.1600-0684.2000.290312.x.

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Xie, Jianhui, Liang Guo, Yuanyuan Ruan, Haiyan Zhu, Lan Wang, Lei Zhou, Xiaojing Yun, and Jianxin Gu. "Laminarin-mediated targeting to Dectin-1 enhances antigen-specific immune responses." Biochemical and Biophysical Research Communications 391, no. 1 (January 2010): 958–62. http://dx.doi.org/10.1016/j.bbrc.2009.11.173.

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Mehling, Matthias, Patricia Hilbert, Stefanie Fritz, Bojana Durovic, Dominik Eichin, Olivier Gasser, Jens Kuhle, et al. "Antigen-specific adaptive immune responses in fingolimod-treated multiple sclerosis patients." Annals of Neurology 69, no. 2 (February 2011): 408–13. http://dx.doi.org/10.1002/ana.22352.

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Cutler, Antony J., Marina Botto, Dominic van Essen, Roberta Rivi, Kevin A. Davies, David Gray, and Mark J. Walport. "T Cell–dependent Immune Response in C1q-deficient Mice: Defective Interferon γ Production by Antigen-specific T Cells." Journal of Experimental Medicine 187, no. 11 (June 1, 1998): 1789–97. http://dx.doi.org/10.1084/jem.187.11.1789.

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The role of the classical complement pathway in humoral immune responses was investigated in gene-targeted C1q-deficient mice (C1qA−/−). Production of antigen-specific immunoglobulin (Ig)G2a and IgG3 in primary and secondary responses to T cell–dependent antigen was significantly reduced, whereas IgM, IgG1, and IgG2b responses were similar in control and C1qA−/− mice. Despite abnormal humoral responses, B cells from C1qA−/− mice proliferated normally to a number of stimuli in vitro. Immune complex localization to follicular dendritic cells within splenic follicles was lacking in C1qA−/− mice. The precursor frequency of antigen-specific T cells was similar in C1qA−/− and wild-type mice. However, analysis of cytokine production by primed T cells in response to keyhole limpet hemocyanin revealed a significant reduction in interferon-γ production in C1qA−/− mice compared with control mice, whereas interleukin 4 secretion was equivalent. These data suggest that the classical pathway of complement may influence the cytokine profile of antigen-specific T lymphocytes and the subsequent immune response.
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Stabel, J. R., and S. Robbe-Austerman. "Early Immune Markers Associated withMycobacterium aviumsubsp.paratuberculosisInfection in a Neonatal Calf Model." Clinical and Vaccine Immunology 18, no. 3 (January 12, 2011): 393–405. http://dx.doi.org/10.1128/cvi.00359-10.

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ABSTRACTThe objective of this study was to observe early markers of cell-mediated immunity in naïve calves infected withMycobacterium aviumsubsp.paratuberculosisand how expression of these markers evolved over the 12-month period of infection. Groups for experimental infection included control (noninfected), oral (infected orally withM. aviumsubsp.paratuberculosisstrain K-10), oral/DXM (pretreatment with dexamethasone before oral inoculation), intraperitoneal (i.p.) inoculation, and oral/M (oral inoculation with mucosal scrapings from a cow with clinical disease) groups. One of the earliest markers to emerge was antigen-specific gamma interferon (IFN-γ). Only i.p. inoculated calves had detectable antigen-specific IFN-γ responses at 7 days, with responses of the other infection groups becoming detectable at 90 and 120 days. All infection groups maintained robust IFN-γ responses for the remainder of the study. At 1 month, calves in the oral and oral/M groups had higher antigen-stimulated interleukin-10 (IL-10) levels than calves in the other treatment groups, but IL-10 secretion declined by 12 months for all calves. T-cell activation markers such as CD25, CD26, CD45RO, and CD5 were significantly upregulated in infected calves compared to noninfected controls. Oral inoculation of calves resulted in significantly increased antigen-specific lymphocyte proliferation at 9 and 12 months, as well as inducible nitric oxide synthase (iNOS) secretion at 6 and 12 months. These results demonstrate that infection of naïve calves withM. aviumsubsp.paratuberculosisinvoked early immunologic responses characterized by robust antigen-specific IFN-γ responses and induction of CD25 and CD45RO expression on T-cell subsets. These were followed by antigen-specific lymphocyte proliferation, iNOS secretion, and expression of CD26 and CD5brightmarkers in the latter part of the 12-month study.
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Dhabhar, F. S., and B. S. McEwen. "Stress-induced enhancement of antigen-specific cell-mediated immunity." Journal of Immunology 156, no. 7 (April 1, 1996): 2608–15. http://dx.doi.org/10.4049/jimmunol.156.7.2608.

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Abstract The studies described here demonstrate that the activation of the physiologic stress response systems of the body can enhance immune function in vivo. This enhancement is observed as a large and long lasting increase in allergic contact sensitivity or delayed-type hypersensitivity, an immune reaction which involves an Ag-specific, cell-mediated immune response. In contrast, acute stress has no effect on the course of irritant contact sensitivity, an immune reaction that does not involve an Ag-specific memory response. A comparison of infiltrating leukocyte numbers in sections of inflamed skin from unstressed and stressed animals shows that stress induces a significant and persistent increase in numbers of leukocytes at the site of the delayed-type hypersensitivity reaction. These results demonstrate that a relatively mild behavioral manipulation can enhance an important class of immune responses that mediate harmful (allergic dermatitis) as well as beneficial (resistance to certain viruses, bacteria, and tumors) aspects of immune function. The implications that these studies have for clinical, diagnostic, and experimental manipulations involving cell-mediated immune function are discussed.
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Moss, Ronald B., Mark R. Wallace, Paola Lanza, Wieslawa Giermakowska, Fred C. Jensen, Georgia Theofan, Carolyn Chamberlin, Steven P. Richieri, and Dennis J. Carlo. "In Vitro p24 Antigen-Stimulated Lymphocyte Proliferation and β-Chemokine Production in Human Immunodeficiency Virus Type 1 (HIV-1)-Seropositive Subjects after Immunization with an Inactivated gp120-Depleted HIV-1 Immunogen (Remune)." Clinical Diagnostic Laboratory Immunology 5, no. 3 (May 1, 1998): 308–12. http://dx.doi.org/10.1128/cdli.5.3.308-312.1998.

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ABSTRACT We examined the effect of immune stimulation by a human immunodeficiency virus type 1 (HIV-1) immunogen (Remune) compared to a non-HIV vaccine (influenza) on HIV-1-specific immune responses in HIV-1-seropositive subjects. HIV-1 p24 antigen-stimulated lymphocyte proliferation was not augmented after immunization with the influenza vaccine. In contrast, subjects increased their lymphocyte proliferative responses to p24 antigen after one immunization with HIV-1 immunogen (Remune) (gp120-depleted inactivated HIV-1 in incomplete Freund’s adjuvant). Furthermore, p24 antigen-stimulated β-chemokine production (RANTES, MIP-1α, MIP-1β) was also augmented after immunization with the HIV-1 immunogen but not influenza vaccine. Taken together, these results suggest that in this cohort, HIV-specific immune responses to p24 antigen can be augmented after immunization with an HIV-1 immunogen. The ability to upregulate immune responses to the more conserved core proteins may have important implications in the development of immunotherapeutic interventions for HIV-1 infection.
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Strutt, Tara M., K. Kai McKinstry, Richard W. Dutton, and Susan L. Swain. "Influenza-specific memory CD4 T cells regulate acute inflammation independent of innate immune recognition (130.10)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 130.10. http://dx.doi.org/10.4049/jimmunol.182.supp.130.10.

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Abstract It is generally accepted that the flow of immunologically relevant information during the early stages of responses against pathogens is one-way, - that inflammation induced upon pattern recognition by highly conserved receptors of the innate immune dramatically impacts subsequent antigen-specific T and B cell responses. We asked if the reverse occurs, and if cells of the adaptive immune system can influence the character and magnitude of innate inflammatory responses. We show here that resting, antigen-specific memory CD4 T cells can dramatically alter innate inflammatory responses within 36 hours of viral infection in a manner independent of other T cells and TLR signaling. Virus-specific memory CD4 T cells transferred to naïve mice that are then challenged with influenza induce greater expression of multiple inflammatory mediators both at the site of infection and systemically upon cognate recognition of antigen in an IFN-gamma independent fashion. Our results show that the adaptive immune system can profoundly influence the character of inflammation following pathogen challenge, demonstrating a new role for memory CD4 T cells in controlling virus titers during protective immune responses.
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Oberhardt, Valerie, Maike Hofmann, Robert Thimme, and Christoph Neumann-Haefelin. "Adaptive Immune Responses, Immune Escape and Immune-Mediated Pathogenesis during HDV Infection." Viruses 14, no. 2 (January 20, 2022): 198. http://dx.doi.org/10.3390/v14020198.

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The hepatitis delta virus (HDV) is the smallest known human virus, yet it causes great harm to patients co-infected with hepatitis B virus (HBV). As a satellite virus of HBV, HDV requires the surface antigen of HBV (HBsAg) for sufficient viral packaging and spread. The special circumstance of co-infection, albeit only one partner depends on the other, raises many virological, immunological, and pathophysiological questions. In the last years, breakthroughs were made in understanding the adaptive immune response, in particular, virus-specific CD4+ and CD8+ T cells, in self-limited versus persistent HBV/HDV co-infection. Indeed, the mechanisms of CD8+ T cell failure in persistent HBV/HDV co-infection include viral escape and T cell exhaustion, and mimic those in other persistent human viral infections, such as hepatitis C virus (HCV), human immunodeficiency virus (HIV), and HBV mono-infection. However, compared to these larger viruses, the small HDV has perfectly adapted to evade recognition by CD8+ T cells restricted by common human leukocyte antigen (HLA) class I alleles. Furthermore, accelerated progression towards liver cirrhosis in persistent HBV/HDV co-infection was attributed to an increased immune-mediated pathology, either caused by innate pathways initiated by the interferon (IFN) system or triggered by misguided and dysfunctional T cells. These new insights into HDV-specific adaptive immunity will be discussed in this review and put into context with known well-described aspects in HBV, HCV, and HIV infections.
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Vujadinovic, Marija, and Jort Vellinga. "Progress in Adenoviral Capsid-Display Vaccines." Biomedicines 6, no. 3 (July 26, 2018): 81. http://dx.doi.org/10.3390/biomedicines6030081.

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Adenoviral vectored vaccines against infectious diseases are currently in clinical trials due to their capacity to induce potent antigen-specific B- and T-cell immune responses. Heterologous prime-boost vaccination with adenoviral vector and, for example, adjuvanted protein-based vaccines can further enhance antigen-specific immune responses. Although leading to potent immune responses, these heterologous prime-boost regimens may be complex and impact manufacturing costs limiting efficient implementation. Typically, adenoviral vectors are engineered to genetically encode a transgene in the E1 region and utilize the host cell machinery to express the encoded antigen and thereby induce immune responses. Similarly, adenoviral vectors can be engineered to display foreign immunogenic peptides on the capsid-surface by insertion of antigens in capsid proteins hexon, fiber and protein IX. The ability to use adenoviral vectors as antigen-display particles, with or without using the genetic vaccine function, greatly increases the versatility of the adenoviral vector for vaccine development. This review describes the application of adenoviral capsid antigen-display vaccine vectors by focusing on their distinct advantages and possible limitations in vaccine development.
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43

Hossain, Mohammad S., John D. Roback, Brian P. Pollack, David L. Jaye, Amelia Langston, and Edmund K. Waller. "Chronic GvHD decreases antiviral immune responses in allogeneic BMT." Blood 109, no. 10 (February 8, 2007): 4548–56. http://dx.doi.org/10.1182/blood-2006-04-017442.

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Abstract Chronic graft-versus-host disease (cGvHD) is associated with functional immunodeficiency and an increased risk of opportunistic infections in allogeneic bone marrow transplantation (BMT). We used a parent to F1 model of allogeneic BMT to test the hypothesis that cGvHD leads to impaired antigen-specific antiviral immunity and compared BM transplant recipients with cGvHD to control groups of allogeneic BM transplant recipients without GvHD. Mice with and without cGvHD received a nonlethal dose of murine cytomegalovirus (MCMV) +100 days after transplantation. Recipients with cGvHD had more weight loss and higher viral loads in the spleen and liver. MCMV infection led to greater than 25-fold expansion of donor spleen–derived MCMV peptide–specific tetramer-positive CD8+ T cells in blood of transplant recipients with and without cGvHD, but mice with cGvHD had far fewer antigen-specific T cells in peripheral tissues and secondary lymphoid organs. The immunosuppression associated with cGvHD was confirmed by vaccinating transplant recipients with and without cGvHD using a recombinant Listeria expressing MCMV early protein (Lm-MCMV). Secondary adoptive transfer of lymphocytes from donor mice with or without cGvHD into lymphopenic congenic recipients showed that cGvHD impaired tissue-specific homing of antigen-specific T cells. These results indicate that cGvHD causes an intrinsic immunosuppression and explain, in part, the functional immunodeficiency in allogeneic transplant recipients.
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Apostolopoulos, Vasso, Theresia Thalhammer, Andreas G. Tzakos, and Lily Stojanovska. "Targeting Antigens to Dendritic Cell Receptors for Vaccine Development." Journal of Drug Delivery 2013 (October 8, 2013): 1–22. http://dx.doi.org/10.1155/2013/869718.

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Dendritic cells (DCs) are highly specialized antigen presenting cells of the immune system which play a key role in regulating immune responses. Depending on the method of antigen delivery, DCs stimulate immune responses or induce tolerance. As a consequence of the dual function of DCs, DCs are studied in the context of immunotherapy for both cancer and autoimmune diseases. In vaccine development, a major aim is to induce strong, specific T-cell responses. This is achieved by targeting antigen to cell surface molecules on DCs that efficiently channel the antigen into endocytic compartments for loading onto MHC molecules and stimulation of T-cell responses. The most attractive cell surface receptors, expressed on DCs used as targets for antigen delivery for cancer and other diseases, are discussed.
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Honda, Tetsuya, Gyohei Egawa, and Kenji Kabashima. "Antigen presentation and adaptive immune responses in skin." International Immunology 31, no. 7 (February 15, 2019): 423–29. http://dx.doi.org/10.1093/intimm/dxz005.

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Abstract For the induction of adequate cutaneous immune responses, the antigen presentation and recognition that occur in both the skin and skin-draining lymph nodes are essential. In each process of cutaneous immune responses, several distinct subsets of immune cells, including dendritic cells and T cells, are involved, and they elicit their respective functions in a harmonious manner. For example, in the elicitation phase of cutaneous acquired immunity, immune cells form a specific lymphoid structure named inducible skin-associated lymphoid tissue (iSALT) to facilitate efficient antigen presentation in situ. In this short review, we will overview the mechanisms of how antigens are presented and how cutaneous adaptive immune responses are conducted in the skin, especially focusing on contact hypersensitivity, a prototypic adaptive immune response in the skin.
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Tremain, Andrew C., D. Scott Wilson, and Jeffrey Hubbell. "Antigen-specific suppression of previously activated T cell responses via polymeric GalNAc antigen conjugation." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 238.13. http://dx.doi.org/10.4049/jimmunol.204.supp.238.13.

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Abstract Current treatments for autoimmunity, allergy, and drug hypersensitivity require continuous global immune suppression. Here we demonstrate in vivo therapeutic efficacy of antigen-specific T cell tolerance induction following prior immunization in various models of murine immunity. Our lab has engineered an N-acetylgalactosamine polymer (pGal) that can be conjugated to protein antigen and delivered intravenously to immunosuppressive hepatic antigen presenting cells, thereby inducing lasting immune regulation without off target effects. In this work, we show treatment with pGal-ovalbumin (OVA) conjugates can suppress previously activated T cells in an antigen-specific fashion. We describe the suppressive effects and underlying signatures of tolerogenic T cell reprogramming by comparing treatment with native OVA to pGal-OVA. Therapeutic treatment with pGal-OVA results in reduced T cell expansion and activation after secondary challenge, higher expression levels of suppressive/exhausted markers such as PD1 and TOX, and markedly lower production of cytokines including IFNg, TNFa, and IL-17 following in vitro restimulation with antigen. Further investigation of antigen-specific tolerance induction utilizing pGal-conjugates can lead to potentially curative approaches for controlling aberrant immunity to self or innocuous foreign protein.
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Kim, Jong J., Joo-Sung Yang, Thomas C. VanCott, Daniel J. Lee, Kelledy H. Manson, Michael S. Wyand, Jean D. Boyer, Kenneth E. Ugen, and David B. Weiner. "Modulation of Antigen-Specific Humoral Responses in Rhesus Macaques by Using Cytokine cDNAs as DNA Vaccine Adjuvants." Journal of Virology 74, no. 7 (April 1, 2000): 3427–29. http://dx.doi.org/10.1128/jvi.74.7.3427-3429.2000.

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ABSTRACT An important limitation of DNA immunization in nonhuman primates is the difficulty in generating high levels of antigen-specific antibody responses; strategies to enhance the level of immune responses to DNA immunization may be important in the further development of this vaccine strategy for humans. We approached this issue by testing the ability of molecular adjuvants to enhance the levels of immune responses generated by multicomponent DNA vaccines in rhesus macaques. Rhesus macaques were coimmunized intramuscularly with expression plasmids bearing genes encoding Th1 (interleukin 2 [IL-2] and gamma interferon)- or Th2 (IL-4)-type cytokines and DNA vaccine constructs encoding human immunodeficiency virus Env and Rev and simian immunodeficiency virus Gag and Pol proteins. We observed that the cytokine gene adjuvants (especially IL-2 and IL-4) significantly enhanced antigen-specific humoral immune responses in the rhesus macaque model. These results support the assumption that antigen-specific responses can be engineered to a higher and presumably more desirable level in rhesus macaques by genetic adjuvants.
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Zheng, Mingquan, Rekha R. Rapaka, Amy C. Yu, Judd E. Shellito, and Jay K. Kolls. "Role of Interleukin-23-Dependent Antifungal Immune Responses in Dendritic Cell-Vaccinated Mice." Infection and Immunity 79, no. 9 (July 11, 2011): 3778–83. http://dx.doi.org/10.1128/iai.05163-11.

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ABSTRACTCD40 ligand (CD40L) transduction of antigen-pulsed dendritic cells (DCs) can result in antigen-specific humoral immune responses even in CD4+T-cell-depleted settings. Here, we show that CD40L transduction of DCs results in the induction of interleukin-12p40 (IL-12p40), IL-12p70, and IL-23. Using DCs that were deficient in IL-12p40, IL-12p35, or IL-23p19, we show that these molecules are dispensable for primary IgG1 responses toPneumocystis, but IgG2c was dependent on IL-12p40 and IL-23p19 but not IL-12p35. Antigen-specific recall responses in CD4-deficient mice were critically dependent on IL-12p40 and IL-23p19 expression in DCs and were not affected by the lack of IL-12p35. To confirm that this defect in recall was due to IL-23, transduction of IL-12p40−/−DCs with a recombinant adenovirus expressing functional IL-23 restored recall responses in DC-vaccinated CD4-deficient mice. These data show that DC-produced IL-23 is critical for vaccine-induced antigen-specific IgG2c and recall antibody responses in the setting of CD4+T-cell depletion.
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Han, Yanyan, Jiangting Long, and Xiangjun Zhou. "To clone tumor specific T cell receptor in cancer patients after immunotherapy with patient-specific antigens." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 215.1. http://dx.doi.org/10.4049/jimmunol.196.supp.215.1.

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Abstract Background Adoptive T cell transfer was recently often used to treat cancer patients who have failed in standard therapies. An immunotherapy named MASCT (Multiple Antigen Stimulating Cellular Therapy) was applied to cancer patients, which is composed of patient-specific antigen pulsed dendritic cells (DCs) and autologous tumor specific T lymphocytes. Methods Patients were treated by the autologous T cells stimulated with mature DCs pulsed with multiple tumor antigens. The tumor antigen specific immune responses were examined during the treatment, and the antigens were selected accordingly. The tumor specific T cell receptor (TCR) would be further cloned from these patients who have demonstrated both immunological and clinical responses. Results A human papilloma virus (HPV) positive cervical cancer patient with bone metastasis on the right sacroiliac joint have repeatedly received treatment of MASCT. Specific responses against tumor antigens were detected by IFNγ ELISPOT assay, such as telomerase, CEA, and HPV18/58. Based on patient’s specific immune response, we adjusted her antigen peptide pool by saving the antigens, which had induced specific responses and removed the peptides that did not. The adjusted antigen pool clearly further boosted the specific responses. Moreover, this patient was evaluated as partial remission after MASCT treatment with patient-specific antigens. Therefore, we are now trying to clone the CEA and telomerase specific TCRs from this patient. Conclusion Our study provides a promising method to clone tumor specific TCRs from cancer patients, who have shown enhanced immunological responses as well as clinical benefits after immunotherapy with patient-specific antigens.
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Tesch, H., W. Müller, and K. Rajewsky. "Lymphokines regulate immunoglobulin isotype expression in an antigen-specific immune response." Journal of Immunology 136, no. 8 (April 15, 1986): 2892–95. http://dx.doi.org/10.4049/jimmunol.136.8.2892.

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Abstract The control of immunoglobulin class switching appears to involve T cell-derived lymphokines. Such lymphokines have been shown to affect isotype expression in polyclonally activated B cells. We show in this paper that the same lymphokines similarly control isotype expression in an antigen-specific response acting in concert with a "T cell independent" antigen. In this situation, B cell growth factor II (BCGF II) enhances the production of antigen-specific IgM antibodies, whereas the production of antigen-specific IgG1 antibodies is only observed in the presence of B cell differentiation factor gamma (BCDF gamma). These results suggest that these lymphokines (and perhaps additional ones) are involved in the control of isotype expression in antigen-specific responses.
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