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Journal articles on the topic 'Immune response – Regulation'

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Published: 4 June 2021
Last updated: 6 September 2023

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1

Hurtley, S. M. "Immune Response Regulation." Science's STKE 2006, no. 358 (October 17, 2006): tw366. http://dx.doi.org/10.1126/stke.3582006tw366.

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2

Sekenova, A., and V. Ogay. "Role of mesenchymal stem cells in the regulation of immune response." BULLETIN of the L.N. Gumilyov Eurasian National University. BIOSCIENCE Series 123, no. 2 (2018): 69–83. http://dx.doi.org/10.32523/2616-7034-2018-123-2-69-83.

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3

Cooke, A. "Regulation of the Immune Response." Diabetic Medicine 6, no. 1 (January 2, 1989): 71–77. http://dx.doi.org/10.1111/j.1464-5491.1989.tb01143.x.

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4

Greene, Mark I., and Herman Waldmann. "Regulation of the immune response." Current Opinion in Immunology 22, no. 5 (October 2010): 549–51. http://dx.doi.org/10.1016/j.coi.2010.09.004.

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5

Kelsoe, Garnett. "Regulation of the immune response." Cellular Immunology 98, no. 1 (March 1986): 145–55. http://dx.doi.org/10.1016/0008-8749(86)90275-3.

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6

Gazzinelli-Guimaraes, Pedro H., and Thomas B. Nutman. "Helminth parasites and immune regulation." F1000Research 7 (October 23, 2018): 1685. http://dx.doi.org/10.12688/f1000research.15596.1.

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Helminth parasites are complex metazoans that belong to different taxonomic families but that collectively share the capacity to downregulate the host immune response directed toward themselves (parasite-specific immunoregulation). During long-standing chronic infection, these helminths appear able to suppress immune responses to bystander pathogens/antigens and atopic, autoimmune, and metabolic disorders. Helminth-induced immunoregulation occurs through the induction of regulatory T cells or Th2-type cells (or both). However, secreted or excreted parasite metabolites, proteins, or extracellular vesicles (or a combination of these) may also directly induce signaling pathways in host cells. Therefore, the focus of this review will be to highlight recent advances in understanding the immune responses to helminth infection, emphasizing the strategies/molecules and some of the mechanisms used by helminth parasites to modulate the immune response of their hosts.
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7

Bickett, Thomas E., and Sana D. Karam. "Tuberculosis–Cancer Parallels in Immune Response Regulation." International Journal of Molecular Sciences 21, no. 17 (August 26, 2020): 6136. http://dx.doi.org/10.3390/ijms21176136.

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Mycobacterium tuberculosis and cancer are two diseases with proclivity for the development of resistance to the host immune system. Mechanisms behind resistance can be host derived or disease mediated, but they usually depend on the balance of pro-inflammatory to anti-inflammatory immune signals. Immunotherapies have been the focus of efforts to shift that balance and drive the response required for diseases eradication. The immune response to tuberculosis has widely been thought to be T cell dependent, with the majority of research focused on T cell responses. However, the past decade has seen greater recognition of the importance of the innate immune response, highlighting factors such as trained innate immunity and macrophage polarization to mycobacterial clearance. At the same time, there has been a renaissance of immunotherapy treatments for cancer since the first checkpoint inhibitor passed clinical trials, in addition to work highlighting the importance of innate immune responses to cancer. However, there is still much to learn about host-derived responses and the development of resistance to new cancer therapies. This review examines the similarities between the immune responses to cancer and tuberculosis with the hope that their commonalities will facilitate research collaboration and discovery.
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8

Ernst, P. B., V. E. Reyes, S. E. Crowe, H. Haeberle, G. Ye, F. Song, K. B. Bamford, and G. R. Klimpel. "Regulation of the mucosal immune response." American Journal of Tropical Medicine and Hygiene 60, no. 4_suppl (April 1, 1999): 2–9. http://dx.doi.org/10.4269/ajtmh.1999.60.2.

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9

Lipniacki, Tomasz, Pawel Paszek, Allan R. Brasier, Bruce A. Luxon, and Marek Kimmel. "Stochastic Regulation in Early Immune Response." Biophysical Journal 90, no. 3 (February 2006): 725–42. http://dx.doi.org/10.1529/biophysj.104.056754.

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10

Siskind, Gregory W., and Eduardo Arreaza. "Network Regulation of the Immune Response." Allergy and Asthma Proceedings 10, no. 6 (November 1, 1989): 387–91. http://dx.doi.org/10.2500/108854189778935872.

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11

Gostner, Johanna M., Kathrin Becker, Dietmar Fuchs, and Robert Sucher. "Redox regulation of the immune response." Redox Report 18, no. 3 (May 2013): 88–94. http://dx.doi.org/10.1179/1351000213y.0000000044.

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12

BRELOER, MINKA, and DAVID ABRAHAM. "Strongyloides infection in rodents: immune response and immune regulation." Parasitology 144, no. 3 (February 24, 2016): 295–315. http://dx.doi.org/10.1017/s0031182016000111.

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SUMMARYThe human pathogenic nematode Strongyloides stercoralis infects approximately 30–100 million people worldwide. Analysis of the adaptive immune response to S. stercoralis beyond descriptive studies is challenging, as no murine model for the complete infection cycle is available. However, the combined employment of different models each capable of modelling some features of S. stercoralis life cycle and pathology has advanced our understanding of the immunological mechanisms involved in host defence. Here we review: (i) studies using S. stercoralis third stage larvae implanted in diffusion chambers in the subcutaneous tissue of mice that allow analysis of the immune response to the human pathogenic Strongyloides species; (ii) studies using Strongyloides ratti and Strongyloides venezuelensis that infect mice and rats to extend the analysis to the parasites intestinal life stage and (iii) studies using S. stercoralis infected gerbils to analyse the hyperinfection syndrome, a severe complication of human strongyloidiasis that is not induced by rodent specific Strongyloides spp. We provide an overview of the information accumulated so far showing that Strongyloides spp. elicits a classical Th2 response that culminates in different, site specific, effector functions leading to either entrapment and killing of larvae in the tissues or expulsion of parasitic adults from the intestine.
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13

Disis, Mary L. "Immune Regulation of Cancer." Journal of Clinical Oncology 28, no. 29 (October 10, 2010): 4531–38. http://dx.doi.org/10.1200/jco.2009.27.2146.

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Innate and adaptive immune system cells play a major role in regulating the growth of cancer. Although it is commonly thought that an immune response localized to the tumor will inhibit cancer growth, it is clear that some types of inflammation induced in a tumor may also lead to cancer proliferation, invasion, and dissemination. Recent evidence suggests, however, that some patients with cancer can mount an antitumor immune response that has the potential to control or eliminate cancer. Indeed, a so-called “immune response” signature has been described in malignancy that is associated with improved outcomes in several tumor types. Moreover, the presence of specific subsets of T cells, which have the capability to penetrate tumor stroma and infiltrate deep into the parenchyma, identifies patients with an improved prognosis. Immune-based therapies have the potential to modulate the tumor microenvironment by eliciting immune system cells that will initiate acute inflammation that leads to tissue destruction.
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14

Mann, Mati. "A miRNA regulatory circuitry tightly tunes macrophage inflammatory response (INM1P.426)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 56.3. http://dx.doi.org/10.4049/jimmunol.194.supp.56.3.

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Abstract Regulation of the immune system is vital to preventing many pathogenic disorders, and mammals have developed a complex system of checks and balances for immune regulation in order to allow immune responses to foreign pathogens while avoiding chronic inflammatory responses. Recently, it has become evident that micro-RNAs (miRNAs) play an important role in regulating immune response. Among these, miR-155 and miR-146a were identified as inflammatory response miRNAs that are upregulated by NF-κB signaling. Here, we set to characterize the hierarchy and genetic interaction of miR-146a and miR-155 in regulating macrophage inflammatory response during acute and chronic conditions. We show a regulatory network where miR-155 expression amplify the inflammatory response by prolonged NF-κB activity through PI3K signanling, while miR-146a attenuates the inflammatory response by inhibiting NF-κB activity and miR-155 expression. This regulatory circuitry enables strong acute inflammatory response while avoiding the development of chronic inflammation.
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15

Crotts, Sydney B., David J. Friedman, Zheng Wang, Michael J. Shapiro, Matthew Rajcula, Shaylene McCue, Jie Sun, and Virginia Smith Shapiro. "Regulation of the immune response by ST8Sia6." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 228.18. http://dx.doi.org/10.4049/jimmunol.204.supp.228.18.

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Abstract Sialic acids are the terminal modification on glycoproteins and glycolipids. The sialic acid transferase ST8Sia6 generates a2,8-linked disialic acids on O-linked glycoproteins, which bind to the inhibitory receptor Siglec-E on innate immune cells and suppress immune activation. Recently, our lab has shown that ST8Sia6 expression on tumor cells inhibits the immune response through Siglec-E, leading to increased tumor growth and decreased survival. Therefore, the products of ST8Sia6 can modulate the immune response to tumors. Our lab has generated ST8Sia6 knockout (KO) mice, and we seek to understand the role of ST8Sia6 in regulating the immune response to pathogens. We find that ST8Sia6 KO mice, when challenged with influenza virus, clear the infection significantly faster than wildtype controls, suggesting that absence of ST8Sia6 reduces inhibition of the innate compartment, thereby increasing immune recruitment to infection. This data suggests an important role for interactions between Siglec-E and ST8Sia6-generated disialic acids in immune regulation and recruitment to infection sites.
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16

Landis-Piwowar, Kristin R. "Overview of the Immune Response and Regulation." American Society for Clinical Laboratory Science 28, no. 1 (January 2015): 35–37. http://dx.doi.org/10.29074/ascls.28.1.35.

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17

Chen, Lanfen, and Celia F. Brosnan. "Regulation of Immune Response by P2X7 Receptor." Critical Reviews™ in Immunology 26, no. 6 (2006): 499–513. http://dx.doi.org/10.1615/critrevimmunol.v26.i6.30.

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18

VERCELLI, D. "Molecular regulation of the IgE immune response." Clinical Experimental Allergy 25, s2 (November 1995): 43–45. http://dx.doi.org/10.1111/j.1365-2222.1995.tb00420.x.

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19

Santarém, Nuno, Ricardo Silvestre, Joana Tavares, Marta Silva, Sofia Cabral, Joana Maciel, and Anabela Cordeiro-da-Silva. "Immune Response Regulation byLeishmaniaSecreted and Nonsecreted Antigens." Journal of Biomedicine and Biotechnology 2007 (2007): 1–10. http://dx.doi.org/10.1155/2007/85154.

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Leishmaniainfection consists in two sequential events, the host cell colonization followed by the proliferation/dissemination of the parasite. In this review, we discuss the importance of two distinct sets of molecules, the secreted and/or surface and the nonsecreted antigens. The importance of the immune response against secreted and surface antigens is noted in the establishment of the infection and we dissect the contribution of the nonsecreted antigens in the immunopathology associated with leishmaniasis, showing the importance of these panantigens during the course of the infection. As a further example of proteins belonging to these two different groups, we include several laboratorial observations onLeishmaniaSir2 andLicTXNPx as excreted/secreted proteins andLmS3arp andLimTXNPx as nonsecreted/panantigens. The role of these two groups of antigens in the immune response observed during the infection is discussed.
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20

Chakraborty, Juhi, Subhadeep Roy, and Sourabh Ghosh. "Regulation of decellularized matrix mediated immune response." Biomaterials Science 8, no. 5 (2020): 1194–215. http://dx.doi.org/10.1039/c9bm01780a.

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21

Murray, J. J., M. D. Mullins, H. R. Knapp, S. L. Keller, W. E. Serafin, L. J. Roberts, B. J. Struthers, and J. A. Oates. "REGULATION OF THE IMMUNE RESPONSE BY EICOSANOIDS." American Journal of Therapeutics 2, no. 10 (October 1995): 739–48. http://dx.doi.org/10.1097/00045391-199510000-00002.

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22

Poulsen, L. K., L. Baron, J. H. Heinig, P. Stahl Skov, and K. Bendtzen. "Biomolecular regulation of the IgE immune response." Allergy 47, no. 5 (October 1992): 560–67. http://dx.doi.org/10.1111/j.1398-9995.1992.tb00682.x.

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23

Ryan, John J., Johanna K. Morales, Yves T. Falanga, Josephine F. A. Fernando, and Matthew R. Macey. "Mast Cell Regulation of the Immune Response." World Allergy Organization Journal 2, no. 10 (2009): 224–32. http://dx.doi.org/10.1097/wox.0b013e3181c2a95e.

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24

Antel, Jack P., and Voon Wee Yong. "Human glial cell regulation of immune response." Journal of Neuroimmunology 40, no. 1 (September 1992): 122. http://dx.doi.org/10.1016/0165-5728(92)90221-6.

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25

Wahn, U. "Infection and regulation of the immune response." Immunology Letters 122, no. 2 (February 2009): 138–40. http://dx.doi.org/10.1016/j.imlet.2008.12.007.

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26

Zinkernagel, R., and Ph Lagrange. "Regulation of Immune Response to Infectious Agents." International Archives of Allergy and Immunology 83, no. 1 (1987): 1–13. http://dx.doi.org/10.1159/000234385.

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27

Sun, Shao-Cong. "Deubiquitylation and regulation of the immune response." Nature Reviews Immunology 8, no. 7 (July 2008): 501–11. http://dx.doi.org/10.1038/nri2337.

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28

Ming-Lum, A. "SHIP AGONIST REGULATION OF THE IMMUNE RESPONSE." Transplantation Journal 90 (July 2010): 397. http://dx.doi.org/10.1097/00007890-201007272-00733.

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29

Poulsen, L. K., C. M. Reimert, C. Bindslev-Jensen, M. B. Hansen, and K. Bendtzen. "Biomolecular Regulation of the IgE Immune Response." International Archives of Allergy and Immunology 106, no. 1 (1995): 55–61. http://dx.doi.org/10.1159/000236890.

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30

Hjelm, F., F. Carlsson, A. Getahun, and B. Heyman. "Antibody-Mediated Regulation of the Immune Response." Scandinavian Journal of Immunology 64, no. 3 (September 2006): 177–84. http://dx.doi.org/10.1111/j.1365-3083.2006.01818.x.

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31

Zinkernagel, R. M. "Regulation of the Immune Response by Antigen." Science 293, no. 5528 (July 13, 2001): 251–53. http://dx.doi.org/10.1126/science.1063005.

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32

Charley, Bernard. "Regulation and modulation of the immune response." Veterinary Immunology and Immunopathology 35 (February 1993): 19–23. http://dx.doi.org/10.1016/0165-2427(93)90129-r.

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33

Boothby, Mark, and Robert C. Rickert. "Metabolic Regulation of the Immune Humoral Response." Immunity 46, no. 5 (May 2017): 743–55. http://dx.doi.org/10.1016/j.immuni.2017.04.009.

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34

March, Michael E., and Kodi Ravichandran. "Regulation of the immune response by SHIP." Seminars in Immunology 14, no. 1 (February 2002): 37–47. http://dx.doi.org/10.1006/smim.2001.0340.

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35

Bröker, Barbara M., Silva Holtfreter, and Isabelle Bekeredjian-Ding. "Immune control of Staphylococcus aureus – Regulation and counter-regulation of the adaptive immune response." International Journal of Medical Microbiology 304, no. 2 (March 2014): 204–14. http://dx.doi.org/10.1016/j.ijmm.2013.11.008.

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36

Hashemi, Seyed Mahmoud. "Immune Regulation by Regulatory Cells." Immunoregulation 5, no. 1 (July 1, 2022): 1–2. http://dx.doi.org/10.32598/immunoregulation.5.1.8.

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Inflammation is a protective response that occurs in response to tissue injury and microbial infections. A significant advancement has been made in our understanding of inflammation, which is one of the most fundamental concepts in medicine. Immunoregulation of immune-mediated inflammatory diseases depends on Th17/Treg balance. Costimulatory receptors, cytokines, metabolic pathways, and the intestinal microbiome all affect this balance in inflammatory conditions. Maintaining a functional equilibrium between these two subsets is very important to design an appropriate and effective treatment strategy.
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37

Lunin, Sergey M., Elena G. Novoselova, Olga V. Glushkova, Svetlana B. Parfenyuk, Tatyana V. Novoselova, and Maxim O. Khrenov. "Cell Senescence and Central Regulators of Immune Response." International Journal of Molecular Sciences 23, no. 8 (April 7, 2022): 4109. http://dx.doi.org/10.3390/ijms23084109.

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Pathways regulating cell senescence and cell cycle underlie many processes associated with ageing and age-related pathologies, and they also mediate cellular responses to exposure to stressors. Meanwhile, there are central mechanisms of the regulation of stress responses that induce/enhance or weaken the response of the whole organism, such as hormones of the hypothalamic–pituitary–adrenal (HPA) axis, sympathetic and parasympathetic systems, thymic hormones, and the pineal hormone melatonin. Although there are many analyses considering relationships between the HPA axis and organism ageing, we found no systematic analyses of relationships between the neuroendocrine regulators of stress and inflammation and intracellular mechanisms controlling cell cycle, senescence, and apoptosis. Here, we provide a review of the effects of neuroendocrine regulators on these mechanisms. Our analysis allowed us to postulate a multilevel system of central regulators involving neurotransmitters, glucocorticoids, melatonin, and the thymic hormones. This system finely regulates the cell cycle and metabolic/catabolic processes depending on the level of systemic stress, stage of stress response, and energy capabilities of the body, shifting the balance between cell cycle progression, cell cycle stopping, senescence, and apoptosis. These processes and levels of regulation should be considered when studying the mechanisms of ageing and the proliferation on the level of the whole organism.
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38

Wen, Jie, Yiru Wu, Jianwei Han, Yufei Tian, and Chaolai Man. "Stress-induced immunosuppression affecting immune response to Newcastle disease virus vaccine through “miR-155-CTLA-4” pathway in chickens." PeerJ 11 (February 27, 2023): e14529. http://dx.doi.org/10.7717/peerj.14529.

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MiR-155 and CTLA-4 are important factors involved in the regulation of immune function. However, there is no report about their involvement in function regulation of stress-induced immunosuppression affecting immune response. In this study, the chicken model of stress-induced immunosuppression affecting immune response (simulation with dexamethasone and immunization with Newcastle disease virus (NDV) attenuated vaccine) was established, then the expression characteristics of miR-155 and CTLA-4 gene were analyzed at several key time points during the processes of stress-induced immunosuppression affecting NDV vaccine immune response at serum and tissue levels. The results showed that miR-155 and CTLA-4 were the key factors involved in stress-induced immunosuppression and NDV immune response, whose functions involved in the regulation of immune function were different in different tissues and time points, and 2 day post immunization (dpi), 5dpi and 21dpi were the possible key regulatory time points. CTLA-4, the target gene of miR-155, had significant game regulation relationships between them in various tissues, such as bursa of Fabricius, thymus and liver, indicating that miR-155-CTLA-4 pathway was one of the main mechanisms of their involvement in the regulations of stress-induced immunosuppression affecting NDV immune response. This study can lay the foundation for in-depth exploration of miR-155-CTLA-4 pathway involved in the regulation of immune function.
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39

Phillips, S. M., J. J. Lin, D. J. Walker, G. P. Linette, N. G. Fathelbab, and P. J. Perrin. "The regulation of resistance to Schistosoma mansoni by auto-anti-idiotypic immunity. II. Global qualitative and quantitative regulation." Journal of Immunology 144, no. 10 (May 15, 1990): 4005–10. http://dx.doi.org/10.4049/jimmunol.144.10.4005.

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Abstract These studies explore the suppression of resistance to schistosomiasis mansoni through interactions of autologous immune functions derived from an induced anti-idiotypic response. This anti-clonotypic response is induced by immunization with syngeneic L3T4+ receptor-bearing lymphoblasts and for the sake of description is termed "auto-anti-idiotypic". It is antigenically restricted and cannot be induced by allogeneic cells. Anti-idiotypic immunization profoundly suppressed the development of protective immunity after exposure to irradiated cercariae and altered a wide variety of functional humoral and cellular immune responses to the parasite. In addition to quantitative suppressive effects, the anti-idiotypic network also regulated qualitative aspects of the immune response by increasing the heterogeneity and reducing the functional binding avidity of antibody for Ag. These effects also were reflected in analogous alterations in cellular reactivity, using the criteria of the Ag mediated blast transformation and delayed type hypersensitivity. Thus idiotypic regulation can mold the specificity and sensitivity of the immune response to Schistosoma mansoni by affecting quantitative and qualitative responses. Manipulation of idiotypic recognition provides an approach to optimize the expression of protective resistance to schistosomiasis.
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40

Tzeng, Hong-Tai, I.-Tsu Chyuan, and Wei-Yu Chen. "Shaping of Innate Immune Response by Fatty Acid Metabolite Palmitate." Cells 8, no. 12 (December 13, 2019): 1633. http://dx.doi.org/10.3390/cells8121633.

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Innate immune cells monitor invading pathogens and pose the first-line inflammatory response to coordinate with adaptive immunity for infection removal. Innate immunity also plays pivotal roles in injury-induced tissue remodeling and the maintenance of tissue homeostasis in physiological and pathological conditions. Lipid metabolites are emerging as the key players in the regulation of innate immune responses, and recent work has highlighted the importance of the lipid metabolite palmitate as an essential component in this regulation. Palmitate modulates innate immunity not only by regulating the activation of pattern recognition receptors in local innate immune cells, but also via coordinating immunological activity in inflammatory tissues. Moreover, protein palmitoylation controls various cellular physiological processes. Herein, we review the updated evidence that palmitate catabolism contributes to innate immune cell-mediated inflammatory processes that result in immunometabolic disorders.
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41

Kim, Min Young, Ji Eun Lee, Lark Kyun Kim, and TaeSoo Kim. "Epigenetic memory in gene regulation and immune response." BMB Reports 52, no. 2 (February 28, 2019): 127–32. http://dx.doi.org/10.5483/bmbrep.2019.52.2.257.

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42

Gutierrez, Fredy RS, Renata Sesti-Costa, Grace Kelly Silva, Martha L. Trujillo, Paulo MM Guedes, and João S. Silva. "Regulation of the immune response during infectious myocarditis." Expert Review of Cardiovascular Therapy 12, no. 2 (January 22, 2014): 187–200. http://dx.doi.org/10.1586/14779072.2014.879824.

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43

Kadagidze, Z. G., A. I. Chertkova, T. N. Zabotina, O. V. Korotkova, E. G. Slavina, and A. A. Borunova. "New capabilities of regulation of antitumor immune response." Malignant tumours, no. 1 (May 20, 2015): 26. http://dx.doi.org/10.18027/2224-5057-2015-1-24-30.

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44

Lobanova, E. G. "ROLE OF ENDOCANNABINOID RECEPTORS IN IMMUNE RESPONSE REGULATION." Medical Immunology (Russia) 14, no. 3 (July 20, 2014): 189. http://dx.doi.org/10.15789/1563-0625-2012-3-189-194.

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45

Wu, Qi, Xin Yu, Juanjuan Li, Shengrong Sun, and Yi Tu. "Metabolic regulation in the immune response to cancer." Cancer Communications 41, no. 8 (June 18, 2021): 661–94. http://dx.doi.org/10.1002/cac2.12182.

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46

Crouch, Elizabeth E., Zhiyu Li, Makiko Takizawa, Stefan Fichtner-Feigl, Polyxeni Gourzi, Carolina Montaño, Lionel Feigenbaum, et al. "Regulation of AID expression in the immune response." Journal of Experimental Medicine 204, no. 5 (April 23, 2007): 1145–56. http://dx.doi.org/10.1084/jem.20061952.

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The B cell–specific enzyme activation-induced cytidine deaminase (AID) has been shown to be essential for isotype switching and affinity maturation of antibody genes during the immune response. Conversely, AID activity has also been linked to autoimmunity and tumorigenesis. Determining how AID expression is regulated in vivo is therefore central to understanding its role in health and disease. Here we use phylogenetic footprinting and high-resolution histone acetylation mapping to accurately demarcate AID gene regulatory boundaries. Based on this strategy, we identify a novel, positive regulatory element required for AID transcription. Furthermore, we generate two AID indicator mouse strains using bacterial artificial chromosomes that faithfully recapitulate endogenous AID expression. The first strain uses a green fluorescent protein reporter to identify B cells that actively express AID during the immune response. In the second strain, AID transcription affects the permanent expression of a yellow fluorescent protein reporter in post–germinal center and terminally differentiated lymphocytes. We demonstrate the usefulness of these novel strains by resolving recent contradictory observations on AID expression during B cell ontogeny.
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47

SAUER, A., C. CREUZOT-GARCHER, C. CHIQUET, JP BERROD, M. SALEH, D. GAUCHER, E. CANDOLFI, G. PREVOST, and T. BOURCIER. "Regulation of immune response in post-operative endophthalmitis." Acta Ophthalmologica 90 (August 6, 2012): 0. http://dx.doi.org/10.1111/j.1755-3768.2012.f085.x.

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48

LONG, KURT Z., and JOSE IGNACIO SANTOS. "Vitamins and the regulation of the immune response." Pediatric Infectious Disease Journal 18, no. 3 (March 1999): 283–90. http://dx.doi.org/10.1097/00006454-199903000-00018.

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49

Ryan, John J., Johanna K. Morales, Yves T. Falanga, Josephine F. A. Fernando, and Matthew R. Macey. "Mast Cell Regulation of the Immune Response: Erratum." World Allergy Organization Journal 3, no. 1 (2010): 14. http://dx.doi.org/10.1097/wox.0b013e3181d1d60f.

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50

HOYNE, GERARD F., and JONATHAN R. LAMB. "Peptide-mediated regulation of the allergic immune response." Immunology and Cell Biology 74, no. 2 (April 1996): 180–86. http://dx.doi.org/10.1038/icb.1996.25.

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