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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
There are various types of T cells. CTLs are responsible for killing infected cells and tumour cells. TH cells perform a range of functions mediated through the action of secreted cytokines. Regulatory T cells (Treg) play a role in inhibiting immune responses and inadequate Treg function may be a factor in autoimmune diseases. T-cell specificity is determined by the TCR (Figure 2.12), which like antibodies, uses combinatorial gene rearrangement to achieve the necessary diversity of receptors. T-cell receptors recognize short peptide fragments presented on the surface of target cells by major histocompatibility complex (MHC) proteins, which are also referred to as human leukocyte antigens (HLAs).
COVID-19
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Immunity involves a partnership of memory B- and T-cells. B-cells are responsible for humoral immunity which produces specific antibodies to the virus. However, T-cells are an important component to the immune system. T-cells respond directly to the virus in a form of cell-mediated immunity.31 CD4+ and CD8+ T-cells show a response to COVID-19 in 100% and 70% of convalescent COVID patients, respectively. T-cell responses target the spike, M, N, and other ORFs.31 T-cell reactivity to SARS-CoV-2 epitopes is also detected in approximately 50% of non-exposed individuals.31 Tests to measure T-cell reactivity are not routinely available. However, both the B-cell and T-cell arms of the immune system contain memory cells which activate within minutes of exposure to the virus, even after detectable levels are not evident. Mild COVID-19 may elicit strong T-cell responses in the absence of detectable virus-specific antibodies. Scientists see signs of lasting immunity to COVID-19, even after mild infections. Approximately 50% of patients who have had colds (coronavirus) have T-cells active against COVID-19.31 100% of patients who recover have T-cells active against COVID-19.31 The T-cell arm of the immune system contributes to herd immunity (Figure 15.3).
Biomarkers for the Immune Checkpoint Inhibitors
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Weijie Ma, Sixi Wei, Eddie C. Tian, Tianhong Li
Figure 14.1 illustrates the interaction between tumor and immune cells with an emphasis in the immune checkpoint regulation. The first clinically targeted immune checkpoint was CTLA-4 protein. CTLA-4 is a protein receptor expressed on the surface of T cells. CTLA-4 counteracts the activity of T-cell co-stimulatory protein CD28 by binding CD80/CD86 in APCs with a greater affinity and inhibits T-cell activation. CTLA-4 is also expressed on activated effect CD8+ T cells, in which it suppresses the activity of helper T cells and enhances the activity of regulatory T (Treg) cells. PD-1 is a surface receptor that has variable expression on resting T cells, whose expression can be induced or increased by T cell activation. High PD-1 expression is a marker for T cell exhaustion. PD-1 ligands PD-L1 and PD-L2, normally expressed on APCs and endothelia, can be expressed and upregulated by various tumor cells. Engagement of PD-1 with its ligands leads to inhibition of T cell receptor signaling and lowers the T cell apoptotic threshold. Although CTLA-4 and PD-1 are the pharmacological targets of immune checkpoint antibodies, their expression has not been consistently proven as predictive immune biomarkers in clinical evaluation of different ICIs [12, 16]. Figure 14.2 illustrates the currently available immune monitoring assays and their targets for patients receiving ICIs.
The CD8+ T cell exhaustion mechanisms in chronic hepatitis B infection and immunotherapeutic strategies: a systematic review
Published in Expert Review of Clinical Immunology, 2023
Esmaeil Allahmoradi, Ramtin Mohammadi, Peyman Kheirandish Zarandi, Seyed Moayed Alavian, Mohammad Heiat
T cell exhaustion is a dysfunctional condition caused by prolonged antigen stimulation during chronic viral infections or tumor development [14]. Several viruses, such as lymphocytic choriomeningitis virus (LCMV), human immunodeficiency virus (HIV), hepatitis C virus (HCV), and HBV, have a well-established association with T cell exhaustion [14–17]. CD8+ T cell exhaustion is a condition of T cell malfunction and reduction that plays a crucial role in the progression of CHB infection [18]. Exhausted CD8+ T cells subsets as known with varying degrees of phenotypic and functional changes [19,20]. Exhaustion indicators or inhibitory receptors (IRs) are slowly expressed in T cells [14]. Co-expression of various IRs, such as programmed cell death protein-1 (PD-1), T cell immunoglobulin and mucin domain-3 (TIM-3), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), lymphocyte-activation gene 3 (LAG-3), T cell immunoreceptor with Ig and ITIM domains (TIGIT), CD244 (2B4), and CD160, is a crucial hallmark of human CD8+ and CD4+ T cell exhaustion [14,21–23] (Figure 1). Multiple studies consistently indicate that IRs expression is elevated on HBV-specific CD8+ T cells [24,25]. A new study has shown that during CHB infection, CD8+ T cells express high levels of PD-1, TIM3, and CTLA4 [18]. In addition, other inhibitory pathways, such as immunoregulatory cells, immunosuppressive cytokines, and inhibitory mediators, also play an important role in the occurrence of T cell exhaustion, which have been less studied.
Extremely low frequency electromagnetic fields exposure during the prenatal and postnatal periods alters pro-inflammatory cytokines levels by gender
Published in Electromagnetic Biology and Medicine, 2022
Hilal Ozturk, Devrim Saribal, Yusuf Metin Gelmez, Gunnur Deniz, Abdullah Yilmaz, Asli Kirectepe, Alev Meltem Ercan
The spleen represents one of the primary organs of the immune system, which regulates T cell numbers and can influence the functions of lymphocytes (Luo et al. 2016). Lymphocytes include natural killer cells, T cells and subsets, and B cells. T cells are a type of white blood cell (WBC) that plays a major role in protecting the body. These cells are defined by the expression of alpha and beta chains, which are T cell antigen receptors, an important component of adaptive immunity. Then cytotoxic T (Tc) cells or helper T (Th) cells are classifed by the expression of cluster of differentiation (CD) CD8+ or CD4+, respectively (Overgaard et al. 2015). Intracellular pathogens are destroyed by Tc cells (CD8+ T cells), while Th cells (CD4+ T cells) play an important role in adaptive immunity and have a major impact on innate immune responses (Leung et al. 2013; Steidley et al. 1992). After birth, T and B lymphocytes show a great expansion which is probably after a large antigenic stimulation from the postnatal environment (Comans-Bitter et al. 1997; Hannet et al. 1992; Juretic’ et al. 2000). Immune cells are prone to respond to all internal stress factors such as microorganisms or cancer cells as well as external stressors, including electromagnetic fields (EMFs) (Rosado et al. 2018).
Approaches in broadening the neutralizing antibody response of the influenza vaccine
Published in Expert Review of Vaccines, 2021
Ruiqi Zhang, Ivan Fan-Ngai Hung
Influenza virus infection triggers immune response in host and activates B lymphocytes and T lymphocytes [5]. T cells are crucial parts of immune response. CD8 + T cells with cytotoxic activity can eliminate virus by recognizing and killing virus-infected cells [6–8], whereas CD4 + T cells are associated with the proliferation, activation, and antibody class switching of B cells [9–11]. As a key component of humoral immunity, B cells are activated by antigen and secrete antigen-specific antibodies after influenza infection [12,13]. Antibodies can protect the host from virus infection through (1) neutralizing virus to inhibit infection or (2) binding to viral proteins on infected cell membrane and inducing lysis of infected cells [14–16]. The major part of the neutralizing antibodies against influenza virus is the anti-hemagglutinin (HA) antibody [17]. The anti-HA neutralizing antibody can bind the globular head region of HA to block the interaction between HA and receptor (sialic acid) or inhibit conformational change and membrane fusion by binding the HA stem domain [16–18].