Lymphocytes activations and functions

Biyq...ZPA1
26 Jan 2024
53

A lymphocyte is a type of white blood cell found in the immune system of most vertebrates. Lymphocytes include natural killer cells, T cells, and B cells. [1]

T cells and B cells
T cells (thymus cells) and B cells (bone marrow) are the main cellular components of the adaptive immune response. T cells are involved in cell-mediated immunity, while B cells are mainly responsible for humoral immunity. The function of T cells and B cells is to recognize specific "non-self" antigens during a process known as antigen presentation. After detecting an invader, cells produce specific responses tailored to eliminate certain pathogens. B cells then respond to pathogens by producing antibodies to neutralize foreign objects such as bacteria and viruses. Some T cells, called helper T cells, produce cytokines that drive the immune response, while other T cells, called cytotoxic T cells, produce toxic granules containing powerful enzymes that cause the death of pathogen-infected cells. After activation, B cells and T cells leave a permanent legacy of the antigens they encounter in the form of memory cells. Throughout an animal's life, these memory cells will "remember" each specific pathogen encountered and, if the same pathogen is detected again, will be able to mount a strong and rapid response; this is known as acquired immunity. [1,2]

natural killer cell
NK cells are part of the innate immune system and protect the host from tumors and virally infected cells. It modulates the functions of other cells, including NK cells, macrophages, and T cells, and distinguishes infected cells and tumors from normal and uninfected cells by recognizing changes in a surface molecule called MHC (major histocompatibility complex) class I. NK cells are activated in response to a family of cytokines called interferons. Activated NK cells release cytotoxic (cell-killing) granules. which destroys the modified cells. [2]
Lymphocyte activation
Lymphocyte activation occurs when lymphocytes (B cells or T cells) are triggered through antigen-specific receptors on their cell surface. This causes the cells to proliferate and differentiate into specialized effector lymphocytes. For example, activated B cells can give rise to antibody-producing cells and some activated T cells become cytotoxic T cells. [3]
T cell activation
T cells can be activated as a result of antigen presentation by APCs such as dendritic cells (DCs) or macrophages. Antigenic molecules are displayed on the surface of APCs by major histocompatibility proteins (MHC) and activate T cell receptors (TCRs) on lymphocytes (Figure). Lymphocyte activation after TCR stimulation can result in T cell differentiation, cytokine production or cytotoxic activity. Antigens are presented by APCs to the ligand-binding portion (αβ subunits) of TCRs (Figure). TCR activation, known as signal 1, is transmitted via the γ, Δ, ε and ζ chains of the CD3 portion of the TCR. After stimulation, TCR signaling is initiated by lymphocyte-specific protein tyrosine kinase phosphorylation of tyrosines on immunoreceptor tyrosine-based activation motifs located in the tails of CD3 components. These phosphorylated residues provide docking sites for the SH2 domains of zeta chain-associated protein kinase-70, which inserts and phosphorylates tyrosines to the binder of activated T cells. In the case of a small subset of lymphocytes known as invariant natural killer T cells, lipid antigens replace peptide antigens on APCs and MHC is replaced by CD1 antigen presenting molecules. [4]Figure 1 Cyclic AMP (cAMP) signaling inhibits TCR and CD28 signaling in lymphocytes.

Activation of B cells
Igs present on the B-cell surface behaves as specific receptors for antigens. When an antigen enters our body, it reacts with the B-cells of appropriate specificity. This interaction stimulates B-cells to undergo blastoid transformation, converting them into plasmablasts (clone formation) and finally into plasma cells. [3]
Each B-cell possesses genetic instructions to produce an antibody of unique antigen specificity as a membrane receptor. Once the signal is received, B-cells are differentiated into plasma cells, which produce and secrete antibodies. [3]
T cell-dependent activation
Once a BCR binds a TD antigen, the antigen is taken up into the B cell through receptor-mediated endocytosis, degraded, and presented to T cells as peptide pieces in complex with MHC-II molecules on the cell membrane. T helper (TH) cells, typically follicular T helper (TFH) cells recognize and bind these MHC-II-peptide complexes through their T cell receptor (TCR). Following TCR-MHC-II-peptide binding, T cells express the surface protein CD40L as well as cytokines such as IL-4 and IL-21. CD40L serves as a necessary co-stimulatory factor for B cell activation by binding the B cell surface receptor CD40, which promotes B cell proliferation, immunoglobulin class switching, and somatic hypermutation as well as sustains T cell growth and differentiation. T cell-derived cytokines bound by B cell cytokine receptors also promote B cell proliferation, immunoglobulin class switching, and somatic hypermutation as well as guide differentiation. After B cells receive these signals, they are considered activated. [5]
T cell-independent activation
As with TD antigens, B cells activated by TI antigens need additional signals to complete activation, but instead of receiving them from T cells, they are provided either by recognition and binding of a common microbial constituent to toll-like receptors (TLRs) or by extensive crosslinking of BCRs to repeated epitopes on a bacterial cell. B cells activated by TI antigens go on to proliferate outside lymphoid follicles but still in SLOs (GCs do not form), possibly undergo immunoglobulin class switching, and differentiate into short-lived plasmablasts that produce early, weak antibodies mostly of class IgM, but also some populations of long-lived plasma cells. [5]
Memory B cell activation
Memory B cell activation begins with the detection and binding of their target antigen, which is shared by their parent B cell. Some memory B cells can be activated without T cell help, such as certain virus-specific memory B cells, but others need T cell help. Upon antigen binding, the memory B cell takes up the antigen through receptor-mediated endocytosis, degrades it, and presents it to T cells as peptide pieces in complex with MHC-II molecules on the cell membrane. Memory T helper (TH) cells, typically memory follicular T helper (TFH) cells, that were derived from T cells activated with the same antigen recognize and bind these MHC-II-peptide complexes through their TCR. Following TCR-MHC-II-peptide binding and the relay of other signals from the memory TFH cell, the memory B cell is activated. 5]

REFERENCE
https://en.wikipedia.org/wiki/Lymphocyte
https://www.nature.com/subjects/lymphocyte-activation#:~:text=Lymphocyte%20activation%20occurs%20when%20lymphocytes,differentiate%20into%20specialized%20effector%20lymphocytes.
https://www.lecturio.com/magazine/lymphocyte-activation/
https://www.ahajournals.org/doi/10.1161/ATVBAHA.111.226837#d3e553
https://en.wikipedia.org/wiki/B_cell

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