Acquired Immunity
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
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.
The immune and lymphatic systems, infection and sepsis
Peate Ian, Dutton Helen in Acute Nursing Care, 2020
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.
ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
During their development in the thymus or bone marrow, lymphocytes are effectively tested for reactivity to body components: clearly one does not want immune cells capable of destroying the host body. (When this does happen it is known as an AUTOIMMUNE DISEASE). Cells with the capacity for autoimmune damage are dealt with by APOPTOSIS, preserving the 'self tolerance' of the body. All the cells in the body are marked by cell surface markers—self-antigens. These are GLYCOPROTEINS (in humans they are called HUMAN LEUKOCYTE ANTIGENS—HLA) and they are coded by a GENE complex known as the MAJOR HISTOCOMPATIBILITY COMPLEX (MHC). There are two classes of these: class I MHC are present on all cells that have nuclei (that is, virtually all cells in the body); class II MHC are found on specialized cells such as macrophages, B cells, activated T cells and cells in the thymus gland. The function of these MHCs is to present antigens to T cells: an infected cell will use the class I MHC to deliver antigen to a cytotoxic T cell (TC); class II MHC molecules are involved in presenting antigens collected by macrophages to helper T cells (TH). The function of the cytotoxic T cell is to destroy invading cells. The helper T cells on the other hand have a signalling role: they release various types of CYTOKINE (such as INTERLEUKIN) which stimualte cytotoxic T cells and B cells. A third type of T cell—suppressor T cells (TS)—appear to be involved in terminating immune response, but their mechanism of action is as yet unclear.
Recent progress in antibody-based therapeutics for triple-negative breast cancer
Published in Expert Opinion on Drug Delivery, 2022
Wen-Jing Ning, Xue Liu, Hong-Ye Zeng, Zhi-Qiang an, Wen-Xin Luo, Ning-Shao Xia
The PD1/PD-L1 axis is the quintessential immune checkpoint pathway. PD1 is a type I transmembrane protein preferentially expressed in immune cells such as T cells, B cells, natural killer (NK) cells and activated monocytes and belongs to the CD28 superfamily [49]. The ligand PD-L1 is a member of the B7 family of antigen presentation costimulatory/coinhibitory molecules and is expressed in most tumour cells and some host cells. In the normal immune system, cytotoxic T cells can recognize mutated cancer cells and initiate their programmed cell death. To prevent excessive activation of normal cells by accident, PD1 inhibits the function of T lymphocytes by binding to the ligand PD-L1/PD-L2, thereby inhibiting the autoimmune response and maintaining the immune balance of the entire body [50]. However, tumour cells can confuse cytotoxic T lymphocytes (CTLs) by overexpressing PD-L1 themselves, sending an inhibitory signal to the CTLs [51]. Studies have confirmed that PD1-positive tumour-infiltrating lymphocytes (TILs) are associated with poor prognosis and OS of breast cancer, suggesting that researchers can modulate the immunosuppressive tumour microenvironment by blocking the PD-1/PD-L1 signalling pathway and thereby enhancing the antitumour immune effect [52].
Pathogenesis guided therapeutic management of COVID-19: an immunological perspective
Published in International Reviews of Immunology, 2021
Ashutosh Kumar, Pranav Prasoon, Prakash S. Sekhawat, Vikas Pareek, Muneeb A. Faiq, Chiman Kumari, Ravi K. Narayan, Maheswari Kulandhasamy, Kamla Kant
In case of the infection by a new viral strain, following the first line of defence presented by innate immune cells, cell mediated immunity by T cells have an exclusive role [12]. Dendritic cells bring captured pathogen antigen to the T cells residing at lymph nodes where they are identified by the cytotoxic T cells (CD4+ and CD8+) in major histocompatibility complex (MHC) restricted manner [12]. Cells containing the pathogen uniquely flag MHC markers on their surface [12]. Once, cytotoxic T cells identify the pathogen, they attack and destroy the cells containing that pathogen and clear source of further infection. Helper T cells create memory of the pathogen and also direct differentiation of the B lymphocytes at germinal centers of the lymph nodes and other lymphoid tissue to secrete pathogen specific antibodies (which are mediators of humoral immunity) [12].
RNA-electroporated T cells for cancer immunotherapy
Published in OncoImmunology, 2020
Fernanda Pohl-Guimarães, Lan B. Hoang-Minh, Duane A. Mitchell
Effective T cell-based therapies require a directed and synchronized process in order to generate an adaptive cell-mediated immune response. In order to mount an effective immune response, T cells are initially primed by tumor peptides presented by major histocompatibility complexes (MHCs) on antigen-presenting cells (APCs) in the lymph nodes. T cells recognize tumor-associated antigens or tumor-specific antigens through the TCR, a transmembrane complex composed of two subunits (α and β chains).57 This recognition leads to the activation and migration of T cells to the tumor, consequently eliciting cytotoxic T cell functions.57 However, most tumors are poorly immunogenic,58–61 and the peripheral T cell repertoire typically anergic,62 devoid of high-avidity tumor-reactive T cells63 and favoring the differentiation of regulatory over cytotoxic T cell responses.64 Therefore, preclinical research has focused on developing methods to reprogram T cells ex vivo so they can express a diverse repertoire of tumor-specific antigen recognition receptors such as TCRs or CARs. While tumor-specific αβ TCRs typically recognize processed antigens that are presented by tumor cells’ MHC Class I, CARs have been designed to overcome this MHC-restricted recognition through targeting antigenic peptides expressed at the cell surface.46
Related Knowledge Centers
- Cancer Cell
- Cd8
- Mhc Class I
- White Blood Cell
- Glycoprotein
- Cancer
- T Cell
- Antigen
- T-Cell Receptor
- Immune Response