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The Inducible Defense System: The Induction and Development of the Inducible Defence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Michael A. Hickey, Diane Wallace Taylor
Cytotoxic T cells are able to recognize and directly kill cancerous and virus-infected cells. Since cytotoxic T cells have the ability to kill, their function must be highly regulated so that they kill only “the bad” cells and not normal, healthy neighboring cells. Cytotoxic T cells do not Interact directly with viruses, rather they only kill cells that are infected with virus. Since viruses live in the cytoplasm of the ceil, viruses cannot be detected by cytotoxic T cells unless some of the viral proteins are transported to the cell surface. Likewise, tumor cells often produce abnormal self-proteins, and these too must be presented on the cell surface to be recognized. Host cells have the ability to process intracellular proteins, including tumor and viral antigens, into peptides that are then presented on the cell surface in association with Class I molecules (Figure 8.12). As a result, Intracellular viruses “blow their cover,” and infected cells can be killed by cytotoxic T cells.
The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
differentiation into one of the following, depending on the nature of the antigen: T helper cells respond by secretion of interleukins or messenger proteins, promoting the proliferation of B lymphocytes, other T lymphocytes and natural killer cells to phagocytose.T helper cells also promote the maturation of B cells and T lymphocytes, once interleukins have been released.Cytotoxic T cells recognise and destroy cells infected by viruses and cells altered by cancer.Memory cells continue to exist after an infection has resolved. They remember antigens and quickly expand if the infection is encountered again.T suppressor or regulatory cells downregulate the immune response when the objective has been achieved.
Acquired Immunity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
T- and B-cell immunity extends the ability to fight infection and cancers. In contrast to phagocytes which only recognize extracellular organisms (mostly bacteria), T cells can combat intracellular infections such as viruses as well as organisms that parasitize macrophages such as fungi, and some bacteria (e.g. mycobacteria, legionella, listeria, brucella and salmonella). Such intracellular infections are controlled by cytotoxic and helper T lymphocytes. Cytotoxic T cells recognize tiny fragments of virus or cancer antigen that are expressed on the surface of affected cells and destroy the cell and pathogen within it. Helper T cells produce cytokines that activate macrophages to kill organisms within them and further activate cytotoxic cells because they are unable to destroy cells or pathogens directly. Helper T cells also activate NK cells to kill virally infected and tumour cells. Antibody has potent neutralizing actions on viruses and toxins and participates in antigen presentation. It also enhances innate immunity by opsonizing foreign particles.
Generation of a novel fully human non-superagonistic anti-CD28 antibody with efficient and safe T-cell co-stimulation properties
Published in mAbs, 2023
Abdullah Elsayed, Christian Pellegrino, Louis Plüss, Frederik Peissert, Ramon Benz, Franziska Ulrich, Gudrun Thorhallsdottir, Sheila Dakhel Plaza, Alessandra Villa, Jacqueline Mock, Emanuele Puca, Roberto De Luca, Markus G. Manz, Cornelia Halin, Dario Neri
Cytotoxic T cells are key mediators of the adaptive immune system to fight cancer. The discovery of the T-cell receptor (TCR) revealed the mechanism of how T cells become activated upon antigen recognition.1–3 TCR engagement is initiated by recognizing antigenic peptides, such as tumor antigens, presented by the major histocompatibility complex (MHC) on antigen-presenting cells (APCs) and tumor cells.4,5 TCRs lack an intracellular signaling domain. Therefore, their association with CD3 and other co-receptors (e.g., CD4, CD8) is necessary to trigger an activation signal cascade, referred to as “signal 1.”6–9 However, signal 1 alone is typically insufficient for the full activation of T cells. The absence of an additional signal induces T-cell anergy and impairs T-cell activity.10,11 The CD28 receptor provides a crucial costimulatory signal that enhances T-cell proliferation, survival, and production of key cytokines (e.g., IL-2); this costimulatory effect is referred to as “signal 2.”12–15 CD28 is a homo-dimeric glycoprotein that is constitutively expressed on the surface membrane of most T cells (around 95% of CD4+ and 50% of CD8+ T cells).16 In the immune synapse, CD28 binds to its counter receptors, CD80 and CD86, primarily expressed on APCs.17–21
The molecular basis of immuno-radiotherapy
Published in International Journal of Radiation Biology, 2023
Ioannis M. Koukourakis, Dina Tiniakos, Vassilis Kouloulias, Anna Zygogianni
A specific subset of T-cells plays an essential role in the adaptive anti-tumor immunity, the so-called regulatory or suppressor T-cells (CD4+ T-cells expressing FOXP3+ and CD25+) (Chen 2011). These emerge from the differentiation of naïve CD4+/CD25-T-cells. Exposure to TGFβ and IL-10, produced by macrophages or CCs and cancer stroma fibroblasts, is involved in this transformation. TGFβ is an essential immunosuppressive molecule, and its secretion characterizes activated CD4+ Tregs (Tauriello et al. 2018). These cells suppress cytotoxic T-cell activity to sustain tolerance to self-antigens and prevent auto-immunity. TGFβ binds to specific receptors (TGFRs) on T-cells and NK-cells, blocking their cytolytic and anti-tumor activity. Tregs and tumor-associated macrophages (TAMs) also express chemokine receptors (CCRs) that mediate their chemotaxis into the tumor environment, following stimulation by chemokine ligands (CCLs) produced by both CCs and tumor stroma fibroblasts (Chow et al. 2015). IL-6 and IL-8 production by CCs and tumor stroma are also potent chemotactic molecules for Tregs (Eikawa et al. 2010). Other important cell-surface molecules expressed on Tregs are CD73, CD38, and CD39 (ecto-apyrase) ectonucleotidases converting ATP released by stressed or dying cells into adenosine, an important immune-suppressive molecule that binds on specific P1-receptors and blocks T-cell proliferation and activation (Sek et al. 2018). Of interest, such ectoenzymes are expressed by CCs, and adenosine production occurs within the tumor microenvironment (Giatromanolaki et al. 2020).
Ritonavir nanosuspensions prepared by microfluidization with enhanced solubility and desirable immunological properties
Published in Pharmaceutical Development and Technology, 2022
Alptug Karakucuk, Hande Canpinar, Nevin Celebi
For the evaluation of RTV coarse powder, Norvir®, and HPMC stabilized RTV NS formulations on the immune system, the percent distribution of CD3+ T Pan T cells, and its subgroups CD4+ helper T cells and CD8+ suppressive T cells, and CD4+/CD8+ ratio was determined for control and study groups. CD3+ T cells are called pan T cells and are divided into subgroups as CD4+ helper T cells and CD8+ cytotoxic T cells. CD4+ helper T cells are essential in the adaptive immune system (Ivanova and Orekhov 2015). CD4+ T cells play a crucial role in ensuring immunity regulation and eliminating intracellular pathogens. It also acts on differentiating B cells into antibody-expressing cells. CD8+ cytotoxic T cells are also essential for regulating various immunological mechanisms and protecting against viral infections. The distribution of CD3+ T cell subgroups in the peripheral system reflects immunological functions. Decreased numbers of CD3+ and CD4+ T cells indicate a poor immunity. The CD8+ cytotoxic T cells suppress the immune response. They play a negative role in the immune response, primarily inhibiting CD4+ helper T cells and B cell functions.