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Helper T-Lymphocytes in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Vinay Kumar, Sahil Gupta, Rachel Rosenzweig, Shyam S. Bansal
Diminished blood flow, increased pre- or afterload, or damage to the vascular endothelium initiate a cascade of immune responses characterized by the activation and infiltration of innate and adaptive immune cells, as well as heightened inflammatory mediators such as cytokines and chemokines3. Such immune responses are physiologically necessary to initiate healing processes and/or promote fibrotic scar formation. Early immune responses are associated predominantly with the activation of innate immune cells, as they do not require specific antigen-mediated activation mechanisms4. Once at the site of injury, they process neo-antigens consisting of altered or unaltered cytosolic or nuclear proteins that are released from the injured tissues, and they act as damage-associated molecular patterns (DAMPs) to interact with Toll-like receptors (TLRs) expressed on the surface of innate immune cells5. However, as the injury progresses (as in chronic disease) and inflammation is sustained, these antigens are further processed by the antigen-presenting cells (APCs) and, in conjunction with MHC-I or MHC-II, are presented to the adaptive immune cells such as cytotoxic CD8+ or helper CD4+ T-cells, respectively. Similar to nonsterile injury, recent evidence also suggests that sterile immune activation can also induce memory against self-antigens, as accumulation of memory T-cells has also been described in some CVDs6–8, leading to autoimmune-like responses.
Role of Epigenetics in Immunity and Immune Response to Vaccination
Published in Mesut Karahan, Synthetic Peptide Vaccine Models, 2021
The second type of adaptive immunity is cell-mediated immunity. Cell-mediated immunity functions via T cells which are released into circulation following their maturation in the thymus. T cells are categorized as CD4+ cells and CD8+ cells according to the type of T cell receptor (TCR) they express. The helper T cells express CD4 receptors while cytotoxic T cells express CD8 TCR (Margolick, Markham, and Scott 2006). There are two types of helper T cells, Th1 and Th2. Th1 cells are involved in cell-mediated immunity and Th2 cells are involved in antibody-mediated immunity (O’Garra and Arai 2000). In contrast to B cells, T cells require antigen processing by antigen-presenting cells for antigen recognition. Following activation and clonal expansion, memory T cells are produced to induce a rapid immune response for subsequent infections (Pennock et al. 2013). Following their formation, memory T cells can provide immunity for approximately ten years (Hammarlund et al. 2003).
Pathogenesis of Tuberculosis
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Divya B. Reddy, Jerrold J. Ellner
Infection with MTB results in the differentiation of naïve T cells into effector T cells that expand to great numbers in the host. CD4T cells differentiate into Th1 and Th2 cells, whereas CD8T cells differentiate into cytotoxic T cells. Together, the effector CD4 and CD8T cell compartments of the adaptive immune response put forth a coordinated effort to clear the infection. As infection clears, the effector T cells (TE) undergo extensive apoptosis and T cell numbers return to homeostasis in the host. Importantly, during this time period, a small number of Ag-specific T cells survives either as short-lived T effector memory (TEM) or as long-lived central memory T cells (TCM).141
Phenylboronic ester-modified polymeric nanoparticles for promoting TRP2 peptide antigen delivery in cancer immunotherapy
Published in Drug Delivery, 2022
Qiyan Wang, Zhipeng Dong, Fangning Lou, Yunxue Yin, Jiahao Zhang, Hanning Wen, Tao Lu, Yue Wang
As we all known, memory T-Cell play a vital role in developing a long-term protection to fight against the second attack of pathogen infection. So, we tested the induction of memory T cells in restimulated splenocyte from vaccinated mice. Memory T cells are classified to central memory T cell (TCM) and effector memory T cells (TEM). TCM, highly expressing molecule CD62L, showed higher antitumor activities than TEM. After restimulating, these cells were stained by CD44-APC, CD62L-PE to analyze percentage of TCM. As shown in, PEG-b-PAsp-g-PBE/TRP2 group showed significant increase (10%) in the CD8+ TCM population (CD8+CD44+ CD62L+), compared with untreated mice. In contrast, treatment with TRP and PEG-b-PAsp/TRP2 induced the generation of slightly more (2.4%, 3.9%) TCM than vaccination with PBS group. Similarly, in CD4+ TCM analysis, PEG-b-PAsp-g-PBE/TRP2 group elicited significantly higher central memory T cells than other groups (Figure 9). Taken together, typical flow cytometry results of PEG-b-PAsp-g-PBE/TRP2 adjuvant-free nanovaccine can induce the strong memory T-cell immune response for long-term prevention against tumors.
Superior antitumor immunotherapy efficacy of kynureninase modified CAR-T cells through targeting kynurenine metabolism
Published in OncoImmunology, 2022
Quanjun Yang, Juan Hao, Mengyi Chi, Yaxian Wang, Bo Xin, Jinglu Huang, Jin Lu, Jie Li, Xipeng Sun, Chunyan Li, Yan Huo, Jianping Zhang, Yonglong Han, Cheng Guo
The cytotoxicity of CD8 + T cells was characterized by both lytic granule contents (particularly granzymes) and enhanced cytokine production (particularly interferon-γ). Based on a preliminary experiment, when CD8 + T cells were treated with 120 μM Kyn for 24 hours, intracellular interferon-γ- and granzyme B-positive cells were significantly decreased (Figure 1(f)). This indicated that a high concentration of Kyn would impair CD8 + T cell cytotoxicity. Previous studies showed that Kyn treatment resulted in exhaustion of CD4 + T cells after exposure to antigen.32 For CD8 + T cells, Kyn treatment at 120 μM did not significantly change the expression of the exhaustion marker PD-1 (Figure 1(g)). Moreover, the subsets of memory T cells were not significantly altered based on the expression of CCR7 and CD62L.
Prolongation of allograft survival by artemisinin treatment is associated with blockade of OX40-OX40L
Published in Immunopharmacology and Immunotoxicology, 2021
Lihua Liu, Juanzhi Zhao, An Li, Xuan Yang, Ben Sprangers, Shengqiao Li
In general, the expression of CD44 is low on naıve T cells and high on activated T cells. The markers CD44 and CD62L are co-expressed on memory T cells. To further investigate whether ART affects memory T cells, the expression of CD44 and CD62L on CD4+ cells was evaluated in T cells. As shown in Figures 2(B) and 3(A), in in vivo experiments there was a trend toward a lower proportion of CD44hiCD62Lhi cells in CD4+ cells in ART-treated mice compared to control mice (10.3 ± 1.6% in control; 9.3 ± 1.5% in ART, p = .17, n = 5). Treatment with CsA resulted in a reduction of CD44hiCD62Lhi cells (7.9 ± 2.3% in CsA and 6.6 ± 2.1% in CsA combining with ART, p < .05 compared to control animals, respectively, n = 5). Again, in vitro experiments showed a significant decrease in CD44hiCD62Lhicells in CD4+ cells only at high ART concentrations (25.3 ± 0.7% in control; 25.3 ± 2.3% in ART at 10 µmol/L, p > .05 compared to control; 23.1 ± 0.9% in ART at 50 µmol/L, p < .05 compared to control, respectively, n = 3) (Figure 3(B)). Taken together, these data suggest that ART in high doses significantly suppress CD4+CD44hiCD62Lhi T memory cells.