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Libros sobre el tema "Th1 and Th17 cells"

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Publicado: 11 de marzo de 2023

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1

TH17 cells in health and disease. New York: Springer, 2011.

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2

Jiang, Shuiping, ed. TH17 Cells in Health and Disease. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9371-7.

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3

The Th1-Th2 paradigm in disease. Austin, Tex: R.G. Landes Company, 1997.

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4

Romagnani, S. The Th1/Th2 paradigm in disease. New York: Springer, 1997.

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5

L, Adorini, ed. Immunointervention in autoimmunity by Th1/Th2 regulation. New York: Springer, 1997.

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6

Waisman, Ari y Burkhard Becher. T-helper cells: Methods and protocols. New York: Humana Press, 2014.

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7

Espéli, Marion y Michelle Linterman. T follicular helper cells: Methods and protocols. New York, NY: Humana Press, 2015.

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8

Velikova, Tsvetelina. Th17 Cells in Health and Disease. Nova Science Publishers, Incorporated, 2020.

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9

Velikova, Tsvetelina. Th17 Cells in Health and Disease. Nova Science Publishers, Incorporated, 2020.

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10

Jiang, Shuiping. TH17 Cells in Health and Disease. Springer, 2014.

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11

Coffman, Robert L. y Sergio Romagnani. Redirection of Th1 and Th2 Responses. Springer London, Limited, 2013.

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12

Coffman, Robert L. y Sergio Romagnani. Redirection of Th1 and Th2 Responses. Springer Berlin / Heidelberg, 2013.

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13

Eljaafari, Assia y Pierre Miossec. Cellular side of acquired immunity (T cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0049.

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The adaptive T-cell response represents the most sophisticated component of the immune response. Foreign invaders are recognized first by cells of the innate immune system. This leads to a rapid and non-specific inflammatory response, followed by induction of the adaptive and specific immune response. Different adaptive responses can be promoted, depending on the predominant effector cells that are involved, which themselves depend on the microbial/antigen stimuli. As examples, Th1 cells contribute to cell-mediated immunity against intracellular pathogens, Th2 cells protect against parasites, and Th17 cells act against extracellular bacteria and fungi that are not cleared by Th1 and Th2 cells. Among the new subsets, Th22 cells protect against disruption of epithelial layers secondary to invading pathogens. Finally these effector subsets are regulated by regulatory T cells. These T helper subsets counteract each other to maintain the homeostasis of the immune system, but this balance can be easily disrupted, leading to chronic inflammation or autoimmune diseases. The challenge is to detect early changes in this balance, prior to its clinical expression. New molecular tools such as microarrays could be used to determine the predominant profile of the immune effector cells involved in a disease process. Such understanding should provide better therapeutic tools to counteract deregulated effector cells.
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14

Cvetanovich, Gregory. Molecular regulatory circuitry of human regulatory T cells and Th17 cells. 2012.

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15

L, Adorini, ed. Immunointervention in autoimmunity by Th1/Th2 regulation. Austin, Tex: Landes Bioscience, 1997.

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16

(Editor), Robert L. Coffman y S. Romagnani (Editor), eds. Redirection of Th1 and Th2 Responses (Current Topics in Microbiology and Immunology). Springer, 1999.

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17

Romagnani, S., ed. Th1 and Th2 Cells in Health and Disease. S. Karger AG, 1996. http://dx.doi.org/10.1159/isbn.978-3-318-01912-4.

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18

Piccio, Laura y Anne H. Cross. Immunology of Multiple Sclerosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199341016.003.0004.

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Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system that targets myelin but affects both white matter and gray matter. Multiple sclerosis is thought to be mediated by cells of the adaptive and innate immune systems. CD4+ T lymphocytes of the Th1 and Th17 subtypes are believed to be critical for the initiation of multiple sclerosis. Treatment with monoclonal antibodies that deplete B lymphocytes has proven that B cells are critical to relapse development in multiple sclerosis. While immunopathophysiology is clearly important in MS, whether multiple sclerosis is truly an autoimmune disorder and the target or targets of the autoimmunity remain unknown.
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19

Th1 and Th2 Cells in Health and Disease (Chemical Immunology). S. Karger Publishers (USA), 1996.

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20

Waisman, Ari y Burkhard Becher. T-Helper Cells: Methods and Protocols. Springer New York, 2016.

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21

Adorini. Immunointervention in Autoimmunity. Springer, 1998.

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22

Espéli, Marion y Michelle Linterman. T Follicular Helper Cells: Methods and Protocols. Springer New York, 2016.

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23

Barsoum, Rashad S. Schistosomiasis. Editado por Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.
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24

Mease, Philip. Biologic treatments for psoriatic arthritis apart from TNF inhibition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0030.

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Psoriatic arthritis (PsA) is an immunologically mediated inflammatory disease characterized by arthritis, enthesitis, dactylitis, spondylitis, and psoriasis. Prior to the introduction of targeted biologic medications, such as TNF inhibitors, the ability to control disease activity was limited, with only modest effects noted with traditional oral medications such as methotrexate and sulfasalazine. The introduction of TNF inhibitors substantially changed the outlook of PsA patients, yielding significant response in all relevant clinical domains and demonstrating the ability to inhibit progressive structural damage of joints. However, not all patients responded to these agents and many patients displayed initial response which waned over time, partly due to immunogenicity (development of antibodies which blocked full therapeutic effect of the biologic protein), or because of tolerability and side effect issues. Thus, it has been important to develop new medicines which target other key cytokines and immunologic pathways. Several medicines with a different mechanism of action have been approved or are in development for the treatment of PsA. Ustekinumab inhibits both IL12 and IL23 and thus is felt to work in both the TH1 and TH7 pathways of inflammation. The oral medicine apremilast inhibits phosphodiesterase 4, thus modulating the cyclic AMP pathway in immunologic cells, yielding an anti-inflammatory effect. Both of these medicines have been approved for the treatment of PsA as well as psoriasis. An emerging group of therapies, the IL17 inhibitors, has demonstrated significant effectiveness in psoriasis and PsA and one of these, Secukinumab, has been approved for psoriasis, PsA, and AS. Other medicines in development include the co-stimulatory blockade agent, abatacept, oral Janus Kinase (JAK) inhibitors, and an emerging group of therapies which inhibit IL23. As modulators of immune cell function, these agents have the potential to increase risk for infection, as well as other side effects. These must be discussed with the patient and considered when determining overall risk benefit analysis regarding their use. The emergence of medicines with a different mechanism of action than TNF inhibition has broadened and strengthened our ability to effectively treat PsA.
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25

Jankovic, Dragana y Carl G. Feng, eds. CD4+ T cell differentiation in infection: amendments to the Th1/Th2 axiom. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-565-7.

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26

Elewaut, Dirk, Heleen Cypers, Matthew L. Stoll y Charles O. Elson. Extra-articular manifestations: inflammatory bowel disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0017.

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A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.
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