Relevant bibliographies by topics / T-cell homeostasi

Academic literature on the topic 'T-cell homeostasi'

Author: Grafiati
Published: 9 March 2023

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Journal articles on the topic "T-cell homeostasi"

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Huang, Weishan, Junjie Luo, Lu Huang, Fei Huang, and Avery August. "ITK signals tune CD8+ T cell homeostatic proliferation and anti-tumor immunity (LYM4P.747)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 65.4. http://dx.doi.org/10.4049/jimmunol.192.supp.65.4.

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Abstract IL-2 inducible T cell kinase (ITK) is a Tec family non-receptor tyrosine kinase. Loss of ITK perturbs CD8+ T cell homeostasis and leads to spontaneous acquisition of innate memory/effector phenotype. However, Itk-/- naïve CD8+ T cells develop on an OTI Rag-/- background, and we use these cells to show here that ITK tunes lymphopenia-induced proliferation (LIP) and antigen sensitivity during CD8+ T cell homeostatic expansion. Experimental analysis and computational simulations revealed that in a lymphopenic environment, naïve Itk-/- CD8+ T cells exhibit massive and immediate homeostatic expansion, accompanied by significant death and followed by population collapse. The enhanced immediate expansion of Itk-/- cells is CD8+ T cell-intrinsic and is independent of recipient MHCI, but dependent on donor CD8+ T cell-T cell interaction. The lack of ITK resulted in enhanced antigen sensitivity and effector program in homeostatically expanded (HP) CD8+ T cells. These Itk-/- HP CD8+ T cells exhibit robust anti-tumor immunity in an antigen specific manner, independent of CD4+ T cell help. These data suggest that ITK intrinsically regulates TcR tuning of homeostatic cytokines during homeostasis of CD8+ T cells and that targeting ITK may have clinical benefit in cancer therapy by generating superior anti-tumor responses.
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Lucas, Philip J., Seong-Jin Kim, Spencer J. Melby, and Ronald E. Gress. "Disruption of T Cell Homeostasis in Mice Expressing a T Cell–Specific Dominant Negative Transforming Growth Factor β II Receptor." Journal of Experimental Medicine 191, no. 7 (April 3, 2000): 1187–96. http://dx.doi.org/10.1084/jem.191.7.1187.

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The immune system, despite its complexity, is maintained at a relative steady state. Mechanisms involved in maintaining lymphocyte homeostasis are poorly understood; however, recent availability of transgenic (Tg) and knockout mouse models with altered balance of lymphocyte cell populations suggest that cytokines play a major role in maintaining lymphocyte homeostasis. We show here that transforming growth factor (TGF)-β plays a critical role in maintaining CD8+ T cell homeostasis in a Tg mouse model that specifically overexpresses a dominant negative TGF-β II receptor (DNRII) on T cells. DNRII T cell Tg mice develop a CD8+ T cell lymphoproliferative disorder resulting in the massive expansion of the lymphoid organs. These CD8+ T cells are phenotypically “naive” except for the upregulation of the cell surface molecule CD44, a molecule usually associated with memory T cells. Despite their dominance in the peripheral lymphoid organs, CD8+ T cells appear to develop normally in the thymus, suggesting that TGF-β exerts its homeostatic control in the peripheral immune system.
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Jung, Yong Woo, Hyun Gyung Kim, Curtis J. Perry, and Susan M. Kaech. "CCR7 expression alters memory CD8 T-cell homeostasis by regulating occupancy in IL-7– and IL-15–dependent niches." Proceedings of the National Academy of Sciences 113, no. 29 (July 6, 2016): 8278–83. http://dx.doi.org/10.1073/pnas.1602899113.

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C-C receptor 7 (CCR7) is important to allow T cells and dendritic cells to migrate toward CCL19- and CCL21-producing cells in the T-cell zone of the spleen and lymph nodes. The role of this chemokine receptor in regulating the homeostasis of effector and memory T cells during acute viral infection is poorly defined, however. In this study, we show that CCR7 expression alters memory CD8 T-cell homeostasis following lymphocytic choriomeningitis virus infection. Greater numbers of CCR7-deficient memory T cells were formed and maintained compared with CCR7-sufficient memory T cells, especially in the lung and bone marrow. The CCR7-deficient memory T cells also displayed enhanced rates of homeostatic turnover, which may stem from increased exposure to IL-15 as a consequence of reduced exposure to IL-7, because removal of IL-15, but not of IL-7, normalized the numbers of CCR7-sufficient and CCR7-deficient memory CD8 T cells. This result suggests that IL-15 is the predominant cytokine supporting augmentation of the CCR7−/− memory CD8 T-cell pool. Taken together, these data suggest that CCR7 biases memory CD8 T cells toward IL-7–dependent niches over IL-15–dependent niches, which provides insight into the homeostatic regulation of different memory T-cell subsets.
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Ngoi, Soo M., Justine Lopez, and John T. Chang. "The microtubule-associated protein Lis1 regulates T lymphocyte homeostasis and differentiation." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 204.23. http://dx.doi.org/10.4049/jimmunol.196.supp.204.23.

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Abstract The microtubule-associated protein Lissencephaly 1 (Lis1) is a key regulator of cell division during stem cell renewal and differentiation. We examined the role of Lis1 in T lymphocyte homeostasis and fate diversification in response to microbial infection. T cell-specific deletion of Lis1 resulted in depletion of the peripheral CD4+ and CD8+ T lymphocyte pool, owing to a selective loss of homeostatic, cytokine-induced proliferation. By contrast, cognate antigen-triggered proliferation was relatively unaffected in CD8+ T cells, enabling Lis1-deficient T cells to differentiate into terminal effector cells in response to microbial infection. Strikingly, however, Lis1-deficient CD8+ T cells failed to develop into long-lived memory lymphocytes. Taken together, these findings suggest that Lis1 plays an important role in T cell homeostasis and the generation of memory T lymphocytes.
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Haegert, David G. "Multiple Sclerosis: A Disorder of Altered T-Cell Homeostasis." Multiple Sclerosis International 2011 (2011): 1–6. http://dx.doi.org/10.1155/2011/461304.

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Uncertainty exists as to whether similar or different mechanisms contribute to the pathogenesis of different subtypes of multiple sclerosis (MS). Detailed analysis of naive T cell homeostasis shows that patients with relapsing-remitting MS (RRMS) and with primary progressive MS (PPMS) have early-onset thymic involution that causes reduced thymic output. The reduced thymic output leads to secondary peripheral homeostatic alterations in naïve CD4 T-cells, which closely mimic T-cell alterations observed in an experimental animal model of diabetes mellitus. Homeostatic T-cell receptor (TCR) signalling and proliferation of naïve T cells are induced by self-peptides. Consequently, the findings of increased TCR signalling of naïve CD4 T-cells, without increased proliferation, in PPMS, and the increased homeostatic proliferation of naïve CD4 T-cells in RRMS favour the development of autoimmunity. Thus, it seems highly likely that peripheral T-cell alterations secondary to a thymic abnormality contribute to the pathogenesis of both MS subtypes.
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Davila, Micha L., Yaoyao Fu, Jie Yang, and Na Xiong. "Role of CCR10 and CCL27 in skin resident T cell development and homeostasis." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 137.7. http://dx.doi.org/10.4049/jimmunol.196.supp.137.7.

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Abstract The skin hosts numerous immune cell subsets which generate synergistic responses to a variety of stimuli including foreign antigens, pathogens and commensal bacteria. Each stimulus is unique and calls for a specific and balanced response; any disruption of this homeostasis can lead to complications such as inflammatory diseases. T cells in the skin are a key player in the response to infection, maintenance of commensal bacterial, and tissue homeostasis. Thus, elucidating the mechanisms regulating T cell migration, establishment, and maintenance within the skin is a high priority. CCR10, a receptor expressed on the majority of skin resident T cells, has a complex role in the development of skin-resident T cells through interaction with its skin-specific receptor CCL27. Preliminary data from our analysis of T-cell specific phenotypes in CCL27a knockout mice demonstrates a preferential reduction of Treg cells in the skin, highlighting the importance of CCL27a in the establishment of skin resident Treg cells under homeostatic conditions. Furthermore, we found CCR10+ resident CD8+ T cells contribute to the homeostatic maintenance of Treg and CD4+ effector T cells in the skin. Defective establishment of CCR10-knockout CD8+ T cells in the skin was shown to correlate with a reduction of skin-resident Treg cells. Skin-resident CD8+ T cells express high amounts of B7.2, a ligand for CTLA-4 which is highly expressed on Treg cells in the skin. In vitro co-culture of purified skin CD8+ and Treg cells suggests B7-2/receptor interaction is important for CD8+ cell-mediated survival of Treg cells. These findings will greatly aid in further understanding the development and homeostasis of skin resident T cells.
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Lucas, Philip J., Seong-Jin Kim, Crystal L. Mackall, William G. Telford, Yu-Waye Chu, Frances T. Hakim, and Ronald E. Gress. "Dysregulation of IL-15-mediated T-cell homeostasis in TGF-β dominant-negative receptor transgenic mice." Blood 108, no. 8 (October 15, 2006): 2789–95. http://dx.doi.org/10.1182/blood-2006-05-025676.

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AbstractT-cell subpopulations, defined by their expression of CD4, CD8, naive, and memory cell-surface markers, occupy distinct homeostatic compartments that are regulated primarily by cytokines. CD8+ memory T cells, as defined by CD44hi surface expression, are dependent on IL-15 as a positive regulator of their homeostatic maintenance. Manipulation of IL-15 signaling through gene aberration, overexpression, or receptor alterations has been shown to dramatically affect T-cell homeostasis, with overexpression leading to fatal leukemia. Here we show that TGF-β is the critical negative regulator of murine CD8+ memory T-cell homeostasis with direct opposition to the positive effects of IL-15. This negative regulation is mediated, at least in part, by the ability of TGF-β to modulate expression of the β-chain of the IL-15 receptor, thus establishing a central axis between these 2 cytokines for homeostatic control of CD8+ memory T-cell populations. These data establish TGF-β as a critical and dominant tumor-suppressor pathway opposing IL-15-mediated CD8+ T-cell expansion and potential malignant transformation.
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Ikegawa, Shuntaro, Yusuke Meguri, Takumi Kondo, Hiroyuki Sugiura, Yasuhisa Sando, Makoto Nakamura, Miki Iwamoto, Yoshinobu Maeda, and Ken-ichi Matsuoka. "PTCy ameliorates GVHD by restoring regulatory and effector T-cell homeostasis in recipients with PD-1 blockade." Blood Advances 3, no. 23 (December 10, 2019): 4081–94. http://dx.doi.org/10.1182/bloodadvances.2019000134.

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Key Points PD-1 blockade exacerbated GVHD by altering the homeostasis of Tregs and effector T cells after HSCT. PTCy ameliorated GVHD after PD-1 blockade by restoring the homeostatic balance of T-cell subsets.
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Gustafson, Claire Ellen, Simon Lambert, Cornelia M. Weyand, and Jorg J. Goronzy. "Homeostatic maintenance of human T cells in bioengineered secondary lymphoid organoids – a model for studying age-related immune decline." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 154.2. http://dx.doi.org/10.4049/jimmunol.204.supp.154.2.

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Abstract During aging, homeostatic maintenance of naïve T cells in secondary lymphoid tissues (SLT) is lost, leading to reduced cell numbers, a loss of stem-like properties and partial differentiation. The underlying mechanisms that drive these changes are unclear. Moreover, mechanistic studies in humans are currently limited by poor T cell homeostasis in standard in vitro culture and in humanized mice. Thus, we sought to develop a robust culture system mimicking SLT that maintains human T cell survival and homeostasis. In our system, we encapsulate human T cells into a bioengineered matrix containing primary fibroblastic reticular cells (FRC), which are stromal cells that support T cell homeostasis within SLT in vivo. Within these SLT-like organoids, resting naïve T cells from young donors exhibited significantly higher viability and dramatically longer survival times (> 3 weeks) compared with two-dimensional (2D) T cell-FRC cultures. Survival was not driven by T cell receptor activation or proliferation. Moreover, naïve T cells maintained a quiescent-like phenotype (CD45RAhighCD27high), which is a phenotype preferentially lost by naïve T cells in 2D culture as well as during aging. Using small molecule screening, we found that inhibition of adenosine receptor signaling caused naïve T cells to break quiescence and acquire a partially differentiated phenotype (CD45RAlow) similar to that of naïve T cells from older individuals. As old naïve T cells expressed similar levels of adenosine receptors as young, these data suggest that the loss of adenosine within SLT may contribute to immune aging. Thus, we have developed a new, malleable model system that allows for mechanistic investigation into human T cell homeostasis and the effects of aging.
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Afzal, Samia, Zhenyue Hao, Momoe Itsumi, Yasser Abouelkheer, Dirk Brenner, Yunfei Gao, Andrew Wakeham, et al. "Autophagy-independent functions of UVRAG are essential for peripheral naive T-cell homeostasis." Proceedings of the National Academy of Sciences 112, no. 4 (January 12, 2015): 1119–24. http://dx.doi.org/10.1073/pnas.1423588112.

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UV radiation resistance-associated gene (UVRAG) encodes a tumor suppressor with putative roles in autophagy, endocytic trafficking, and DNA damage repair but its in vivo role in T cells is unknown. Because conditional homozygous deletion of Uvrag in mice results in early embryonic lethality, we generated T-cell–specific UVRAG-deficient mice that lacked UVRAG expression specifically in T cells. This loss of UVRAG led to defects in peripheral homeostasis that could not be explained by the increased sensitivity to cell death and impaired proliferation observed for other autophagy-related gene knockout mice. Instead, UVRAG-deficient T-cells exhibited normal mitochondrial clearance and activation-induced autophagy, suggesting that UVRAG has an autophagy-independent role that is critical for peripheral naive T-cell homeostatic proliferation. In vivo, T-cell–specific loss of UVRAG dampened CD8+ T-cell responses to LCMV infection in mice, delayed viral clearance, and impaired memory T-cell generation. Our data provide novel insights into the control of autophagy in T cells and identify UVRAG as a new regulator of naïve peripheral T-cell homeostasis.
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Dissertations / Theses on the topic "T-cell homeostasi"

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Basilissi, M. "T-CELL HOMEOSTASIS, MODIFICATIONS OF MUCOSAL IMMUNITY POPULATIONS AND ASSOCIATION WITH HIV-MEDIATE MICROBIAL TRANSLOCATION AND DYSBYOSIS: EXTENSIVE IMMUNE PHENOTYPING DURING 1 YEAR OF SUCCESSFUL COMBINATION ANTIRETROVIRAL THERAPY (CART)." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/489804.

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In the era of combination antiretroviral therapy (cART), a reduction of HIV and AIDS-comorbidities and death has been described. Nonetheless, immune defects persist during treatment and may be linked to increased morbidity and mortality of HIV-infected subjects compared to the general population. Microbial translocation and dysbiosis as well as impaired mucosal immunity likely represent underlying pathogenic mechanisms of the peripheral immune flaws observed during therapy. However, a systematic investigation of these parameters in a longitudinal cohort of HIV-infected individuals starting cART is currently lacking. In this context, the overall objective of our research is to understand the extent by which enduring gut abnormalities represent a cause of impaired T-cell homeostasis during cART. In particular, we aim to study the modifications of T-cell homeostasis, microbial translocation, gastrointestinal function and faecal microbiota composition in a cohort of HIV-infected, antiretroviral-naïve subjects prior to and following 12 months of cART (aim 1). A further goal is to investigate the contribution of Th17/Th22, “gut-homing” and Tscm cells in sustaining peripheral immune defects in HIV-infected, antiretroviral-naïve subjects prior to and following 12 months of cART (aim 2, immunological substudy). In Aim 1 we consecutively enrolled 160 HIV-infected, antiretroviral-naïve subjects introducing cART (T0), and presenting virological suppression (<40 cp/mL) and active follow-up after 12 months of treatment (T12). We performed: i) flow cytometry surface staining (naïve, memory, activated CD4/CD8 T-cells); ii) microbial translocation parameters analysis (LPS, sCD14, EndocAb); iii) gastrointestinal functional marker assessment (LAC/MAN fractional ration, I-FABP); iv) faecal calprotectin quantification and microbial population analysis. In Aim 2 we selected a subgroup of 28 HIV-infected, antiretroviral-naïve subjects introducing cART (T0) with available cryopreserved biological samples from the cohort of patients enrolled in Aim 1. 18 HIV-uninfected age- and sex-matched individuals were selected as controls. After lymphocyte separation, we performed flow Cytometry surface staining to assess CD4+ and CD8+ activation (HLA-DR+CD38+), maturation (naïve: CCR7+CD45RA+; central memory: CCR7+CD45RA-; effector memory: CCR7-CD45RA-; terminally differentiated: CCR7-CD45RA+) exhaustion (PD-1+), the frequency of stem cell-like memory T cells (Tscm; CCR7+CD45RA+CD27+CD95+) and that of CD4+ T-cells with a “gut homing” (CCR9+α4β7+) and a “Th17/Th22” phenotype (CCR6+CD161+). Our Aim 1 results showed a significant increase in central memory (p<0.0001;) and naïve CD4+ T-cells (p<0.0001) which paralleled the reduction of activated (p=<0.0001) and memory activated T-cells (p<0.0001). No differences were observed in terms of naive and central memory CD8+ T-cells. No changes were observed in microbial translocation parameters and intestinal permeability at T12, while we registered an increase in I-FABP (p=0.0002) and a decay in faecal calprotectin levels (p=0.0099) after introducing cART. Qualitative analysis of the faecal microbiome revealed an outgrowth of Lactobacillus (p<0.0001) and Bacteroides spp. (p=0.0006) as well as Proteobacteria (p=0.027) following cART. Regarding Aim 2, we registered a significant reduction of activated CD4+ (p=0.02) and CD8+ lymphocytes (p=0.0003) following cART introduction, reaching levels comparable to those observed in uninfected controls. Analysis of T-cell maturation showed a significant reduction in CD4+ effector memory subsets in the course of cART (p=0.01), leading to persistent impairment of this subset compared to controls. Measure of PD-1 displayed a hierarchy in PD-1 expression, with the highest levels in cART-naïve subjects, followed by those measured in treated individuals and uninfected controls. Study of Tscm revealed significant reduction of the CD4+ Tscm subset in HIV-infected subjects during the first 12 months of cART (p=0.002) and no variations of the CD8+ Tscm pool. Overall, HIV infection accounted for lower CD4+ and CD8+ Tscm frequencies compared to uninfected controls. Interestingly, Tscm correlated negatively with naïve cells (CD4+: r=-0.7; p=0.004; CD8+: r=-0.7; p=0.006) and positively with effector memory cells in healthy controls. (CD4+: r=0.6; p=0.01; CD8+; r=0.6; p=0.01). In HIV disease, these correlations were lost in the course untreated infection and only the relationship between CD4+ naïve and Tscm cells was restored in the course of cART. Analysis of Th17/Th22 frequency showed enrichment in the course of cART (p=0.03;), but significantly lower frequencies compared to HIV-uninfected controls (p=0.04). Interestingly, this subset correlated positively with CD4+ Tscm prior to cART (r=0.6; p=0.002). Finally, a progressive contraction of CD4+ T-cells with a “gut-homing phenotype was reported (p=0.02), which maintained significantly lower frequencies compared to HIV-uninfected controls (p=0.04). A positive correlation was found between T cells with a “gut-homing” phenotype and plasma HIV RNA prior to cART introduction (r=0.5; p=0.003). In line with this finding, this phenotype also correlated with activated CD4+ T-cells (r=0.5, p=0.003) at the same time-point; this association was nonetheless lost in the course suppressive treatment. In conclusion our study demonstrated that 1 year of virally-successful cART results in an amelioration of peripheral T-cell homeostasis with reduction of T-cell activation and exhaustion parameters despite persistent microbial translocation and intestinal damage/permeability, possibly linked to the impairment of Th17/Th22 and cells with a “gut-homing” immunephenotype. Further research is necessary to investigate the effects of longer cART on circulating T-cell subpopulations and markers of gut homeostasis and function.
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Aloufi, Nawaf. "The role of sCD127 in IL-7-Mediated T Cell Homeostasis in Vivo." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41089.

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Interleukin-7 is an essential cytokine that plays a major role in the development and homeostatic maintenance of T-cells. The presence of soluble forms of various cytokine receptors have been proposed to be involved in the endogenous regulation of cytokine activity. Due to the natural ability of soluble CD127 (sCD127) to bind to IL-7, there is an interest in its potential application as an immunotherapeutic agent in diseases, where IL-7 has been found to be relevant, including HIV infection. In this study, I hypothesize that by administering sCD127 to healthy mice, IL-7 activity should be enhanced, thus enhancing T cell proliferation in vivo. The work presented here focuses on three main objectives: 1) evaluating the effect of IL-7 with or without sCD127 on T cell proliferation in healthy mice; 2) validating a mouse model of T cell depletion using anti-CD4 and CD8 antibodies; and 3) determining the effect of sCD127 treatment with or without IL-7 on T cell reconstitution and proliferation in the T cell depletion model. To assess the effect of administering exogenous sCD127, IL-7 or the combination on T cell proliferation, peripheral blood mononuclear cells and spleen were isolated, and stained to characterize T cell number, proliferation, and surface CD127 expression by flow cytometry. For the T cell depletion model, wild type C57BL/6 mice were injected intra-peritoneally with 150 μg single dose of anti-CD4 and anti-CD8 depleting antibodies. Consequently, mice were bled weekly to demonstrate the kinetics of T cell reconstitution following depletion (from d7 to d63). Our results demonstrated that in healthy mice daily treatment with murine IL-7 significantly stimulated T cell proliferation and consequently increased cell number. This observation was further boosted by pre-complexing IL-7 with sCD127. For T cell depletion experiments, the kinetics of T-cell reconstitution was different between the CD4+ and CD8+ T cells. CD4+ T cell reconstitution was almost complete 6 weeks following T cell depletion, while CD8+ T cells were only partially reconstituted at this time point. Treatment with IL-7 or combined therapy had a transient and significant effect on T cell proliferation and reconstitution, and this influence was abrogated after treatment discontinuation. Interestingly, CD8+ T cells exert greater responses to our treatments in that a more pronounced proliferation and significant increase in cell number was observed relative to the effect seen on CD4+ T cells in both healthy and depleted mice. In conclusion, antibody-mediated T cell depletion is a potentially valuable tool to investigate lymphopenia-induced proliferation and potential therapies thereof. This study suggests that combining sCD127 and IL-7 therapies enhances IL-7-mediated T cell proliferation, and provides important information for the potential therapeutic use of sCD127 and its impact on IL-7 function.
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Almeida, Afonso Rocha Martins de. "CD4+ T cell homeostasis : the thymus, the cells and the environment." Doctoral thesis, Porto : Edição do Autor, 2002. http://hdl.handle.net/10216/64644.

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Almeida, Afonso Rocha Martins de. "CD4+ T cell homeostasis : the thymus, the cells and the environment." Tese, Porto : Edição do Autor, 2002. http://catalogo.up.pt/F?func=find-b&local_base=UPB01&find_code=SYS&request=000090183.

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Goldrath, Ananda W. "T cell homeostasis : a role for specific peptide/MHC ligands in homeostasis driven proliferation of naive CD8⁺ T cells /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8332.

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Bains, I. K. "Mathematical modelling of T cell homeostasis." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/20159/.

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T cell homeostasis describes the process through which the immune system regulates cell survival, proliferation, differentiation and death to maintain T cell numbers and diversity in a range of different conditions. The aim of this thesis is to better understand how this process leads to the development of the naive CD4+ T cell compartment during childhood. Mathematical modelling is used in combination with experimental observations to estimate naive T cell kinetics over the lifetime of an individual. The analysis described here shows that post-thymic proliferation contributes more than double the number of cells entering the pool each day from the thymus. This ratio is preserved from birth to age 20 years; as the thymus involutes, the average time between naive T-cell divisions in the periphery lengthens with age and the naive population is maintained by improved naive cell survival. Thymic output is quantified from birth to age 60 years by combining models to interpret naive T cell TRECs and Ki67 expression data. Three distinct phases of thymic T cell output are identified: (i) increasing production from birth to age 1 year; (ii) steep decline to age 8 years; (iii) slow decline from age 8 years onwards. Finally, the role of inter-cellular variation in T cell residency times is explored. It is able to explain the persistence of PTK7+ naive CD4+ T cells in thymectomised individuals. Importantly, the model predicts the accumulation of veteran PTK7+ T cells in older individuals and suggests that the residual population in thymectomised individuals will also consist predominantly of veteran PTK7+ T cells. The model has implications for the use of PTK7 as a marker of recent thymic emigration and also naturally explains improved T cell survival in older individuals.
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Raynor, Jana L. "Regulatory T Cell Homeostasis in Aging." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1416570329.

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Sather, Blythe Duke. "CD4+ Foxp3+ regulatory T cell homing & homeostasis /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8343.

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Aksoylar, Halil I. "A Critical Role for Gimap5 in CD4+ T Cell Homeostasis and Maintenance of Peripheral Immune Tolerance." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367937122.

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Boucher, Louis-martin. "T-cell receptor associated signals that modulate lymphocyte homeostasis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0028/NQ49933.pdf.

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Books on the topic "T-cell homeostasi"

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Panea, Casandra M. The role of intestinal mononuclear phagocytes in control of mucosal T cell homeostasis. [New York, N.Y.?]: [publisher not identified], 2016.

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Chen, Jun Kui. Roles of transcription factor T-bet in memory CD4+ T cell generation, function, homeostasis and tissue targeting. [New York, N.Y.?]: [publisher not identified], 2017.

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Dörner, Thomas, and Peter E. Lipsky. Cellular side of acquired immunity (B cells). Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0050.

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B cells have gained interest in rheumatoid arthritis (RA) beyond being the precursors of antibody-producing plasma cells since they are also a broader component of the adaptive immune system. They are capable of functioning as antigen-presenting cells for T-cell activation and can produce an array of cytokines. Disturbances of peripheral B-cell homeostasis together with the formation of ectopic lymphoid neogenesis within the inflamed synovium appears to be a characteristic of patients with RA. Enhanced generation of memory B cells and autoreactive plasma cells producing IgM-RF and ACPA-IgG antibodies together with formation of immune complexes contribute to the maintenance of RA, whereas treatment with B-cell-directed anti-CD20 therapy provides clinical benefit.
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Boucher, Louis-martin. T-cell receptor associated signals that modulate lymphocyte homeostasis. 1999.

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Eljaafari, Assia, and 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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Petterson, Frida Ekholm. T-Cell Differentiation & Immunological Homeostasis in Lymphopenic and Kappa Light Chain Deficient Mice. Uppsala Universitet, 2002.

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Book chapters on the topic "T-cell homeostasi"

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Drylewicz, Julia, Kiki Tesselaar, and José A. M. Borghans. "T-Cell Homeostasis." In Encyclopedia of AIDS, 1–8. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9610-6_207-1.

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Drylewicz, Julia, Kiki Tesselaar, and José A. M. Borghans. "T-Cell Homeostasis." In Encyclopedia of AIDS, 1985–91. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_207.

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Flomerfelt, Francis A., and Ronald E. Gress. "Analysis of Cell Proliferation and Homeostasis Using EdU Labeling." In T-Cell Development, 211–20. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2809-5_18.

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Henson, Sian M., and Arne N. Akbar. "Memory T-Cell Homeostasis and Senescence during Aging." In Memory T Cells, 189–97. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6451-9_15.

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Bourgeois, Christine, and Delphine Sauce. "Age-Specific T Cell Homeostasis." In Handbook of Immunosenescence, 273–301. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99375-1_81.

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Bourgeois, Christine, and Delphine Sauce. "Age-Specific T Cell Homeostasis." In Handbook of Immunosenescence, 1–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-64597-1_81-1.

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Seddon, Benedict, Sanket Rane, and Andrew J. Yates. "Modelling Naive T Cell Homeostasis." In Mathematical, Computational and Experimental T Cell Immunology, 45–64. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57204-4_3.

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Gustafson, Claire E., David L. Lamar, Cornelia M. Weyand, and Jörg J. Goronzy. "Age, T Cell Homeostasis, and T Cell Diversity in Humans." In Handbook of Immunosenescence, 303–22. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-99375-1_9.

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Gustafson, Claire E., David L. Lamar, Cornelia M. Weyand, and Jörg J. Goronzy. "Age, T Cell Homeostasis, and T Cell Diversity in Humans." In Handbook of Immunosenescence, 1–20. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64597-1_9-1.

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Surh, Charles D., Joyce Tan, William C. Kieper, and Bettina Ernst. "Factors Regulating Naïve T Cell Homeostasis." In Advances in Experimental Medicine and Biology, 73–80. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0757-4_10.

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Conference papers on the topic "T-cell homeostasi"

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Baba, Junko, Satoshi Watanabe, Kosuke Ichikawa, Jun Koshio, Takao Miyabayashi, Junta Tanaka, Hiroshi Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, and Ichiei Narita. "Abstract 1920: Chemo-resistant regulatory T cells inhibit the augmentation of antitumor immunity during homeostatic T cell proliferation." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1920.

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Xu, Mo, and Dan R. Littman. "Abstract A098: Helicobacter-specific T cell responses in gut homeostasis and disease." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a098.

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Prigge, A., R. Ma, B. Coates, and K. M. Ridge. "Deletion of Vimentin in Regulatory T Cells Augments Suppression Without Altering Homeostasis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5565.

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Robertson-Tessi, Mark, Derek Park, Kimberly Luddy, Adam Mailloux, Pearlie K. Burnette, and Alexander Anderson. "Abstract A86: Harnessing T-cell homeostasis to diagnose and treat solid and liquid tumors." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a86.

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Ludwig, Lindsey M., Lauren E. Roach, Samuel G. Katz, Jill K. Fisher, Melissa Burns, Matthew R. Schnorenberg, Riyue Bao, et al. "Abstract 294: BCL-2 family compensation regulates T cell homeostasis and reveals a BIM:BCL-W axis in T-ALL." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-294.

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Chopra, Martin R., Marlene Biehl, Carina A. Bäuerlein, Christian Brede, Ana-Laura Jordan Garotte, Sabrina Kraus, Simone S. Riedel, et al. "Abstract 1438: TNF-TNFR interactions influence tumor growth and metastasis by manipulating regulatory T cell homeostasis." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1438.

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Mendoza, Alejandra. "Abstract A203: Role of nonimmune functions of regulatory T-cells in inflammation and tissue homeostasis." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a203.

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Nelson, Nadine, Shengyan Xiang, Xiaohong Zhang, Karoly Szekeres, and Ghansah Tomar. "Abstract A83: The role of Ikaros in effector and regulatory T cell homeostasis in a murine pancreatic cancer model." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-a83.

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Nelson, Nadine, Shengyan Xiang, Xiaohong Zhang, Shari Pilon-Thomas, Nasreen Vohra, and Tomar Ghansah. "Abstract LB-270: The role of Ikaros in T cell homeostasis and function in a murine pancreatic cancer model." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-270.

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Arita, Masashi, Satoshi Watanabe, Takahashi Miho, Miyuki Sato, Aya Ohtsubo, Kosuke Ichikawa, Rie Kondo, et al. "Abstract 5654: Lymphodepletion induces T cell homeostatic proliferation and augments antitumor effects of PD-1/PD-L1 blockade therapy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5654.

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Reports on the topic "T-cell homeostasi"

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Baccala, Roberto. Homeostatic T Cell Expansion to Induce Anti-Tumor Autoimmunity in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada456894.

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Kwon, Eugene D. Lowering T Cell Activation Thresholds and Deregulating Homeostasis to Facilitate Immunotherapeutic Responses to Treat Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada460762.

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Kwon, Eugene D. Lowering T Cell Activation Thresholds and Deregulating Homeostasis to Facilitate Immunotherapeutic Responses to Treat Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada460766.

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