-ˋˏ ༻ Chapter One ༺ ˎˊ-
Stage Two
The path of a Killer T cell
First stage:
also known as cytotoxic T cells, are immune cells that destroy infected or abnormal cells by releasing toxic substances
Recognition, Attack, Signaling, Memory
Antigens: Molecules that trigger an immune response and can be produced by viruses, bacteria, cancer cells, or intracellular signals
T-cell receptors (TCRs): Receptors on the surface of killer T cells that bind to specific antigens
Major histocompatibility complex (MHC) Class I molecules: Molecules on the surface of cells that present antigens to T cells
CD8 receptors: Receptors on the surface of killer T cells that interact with MHC Class I molecules
killer T cells release perforin and granzymes to kill the infected cell
Killer T cells use cytokines to send chemical instructions to the rest of the immune system to increase its response
The signal for a killer T cell response is the binding of the T cell receptor (TCR) and CD8 on the killer T cell to the MHC/Epitope on the surface of a virus-infected cell. This binding triggers a series of events that result in the infected cell's destruction
The granules in the killer T cell release perforins, granzymes, and chemokines.
The perforins polymerize to create pores in the infected cell's membrane
The granzymes activate caspases, which destroy the cell's cytoskeleton, nucleoprotein, and DNA
When the body is first exposed to a pathogen, rare T cells that are specific to that antigen expand rapidly. However, most of these cells are eliminated, leaving a small number that survive to become memory T cells.
When the body encounters the same pathogen again, the memory T cells quickly expand into large numbers of effector T cells. This rapid response, along with antibody responses, can quickly eliminate the pathogen
There are different subtypes of memory T cells, including central memory T cells (Tcm cells) and effector memory T cells (Tem cells and Temra cells)
Second stage:
Macrophages
Macrophages eat other cells and are able to pull apart their proteins in order to present them to T cells.
Phagocytosis
The seven steps of phagocytosis are:
Detection: Phagocytic cells use receptors to detect the target particle
Binding: The receptors bind to foreign substances, such as antibodies that have marked a pathogen
Engulfment: The cytoplasm engulfs the bound pathogen through endocytosis
Phagosome formation: The engulfed particle is enclosed in a bubble-like structure called a phagosome
Phagosome-lysosome fusion: The phagosome fuses with a lysosome to become a phagolysosome
Digestion: Enzymes in the lysosomes digest the food particle
Exocytosis: Remnants are propelled out through exocytosis
The cell membrane extends projections called pseudopodia around the particle.
The pseudopodia fuse to form a vesicle called a phagosome
The phagosome matures by fusing with endosomes and lysosomes, becoming a phagolysosome
The phagolysosome's hydrolytic enzymes break down the particle
Stage Three
The path of a B-Lymphocyte
B lymphocytes originate from hematopoietic stem cells
Hematopoietic stem cells give rise to different types of blood cells, in lines called myeloid and lymphoid. Myeloid and lymphoid lineages both are involved in dendritic cell formation
Types of myeloid cells include Granulocytes a type of white blood cell that includes neutrophils, eosinophils, and basophils
Enzymes in neutrophil granules include:
Neutrophil serine proteases (NSPs):
NSPs kill bacteria directly, and are involved in the non-oxidative mechanism of bacterial killing
These enzymes include cathepsin G (CG)
Cleaves and inactivates chemoattractants
Cathepsin G breaks down components of the extracellular matrix
Cathepsin G activates matrix metalloproteinases, which degrade the extracellular matrix
neutrophil elastase (NE)
NE can promote tumor growth by remodeling the tumor microenvironment and promoting metastasis
and proteinase 3 (PR3)
breaks down proteins
myeloid cells are involved in bacterial defense and regulating inflammation
Eosinophils help maintain homeostasis in the body
homeostasis is the ability to maintain a relatively stable internal state that persists despite changes in the world outside
Basophils release histamine
Basophils release heparin to prevent blood clots from forming in areas where there is damage
Basophils are a major source of IL-4, a cytokine that links innate and adaptive immunity
The B lymphocytes that respond to an infection mature into plasma cells. These plasma cells make and release immunoglobulins, also called antibodies
B cells use their B cell receptors (BCRs) to identify a specific protein, or antigen, on a pathogen
Protein antigens are broken down into peptide epitopes
Peptide epitopes bind to MHC II molecules
B cell activation: The BCR, MHC II complex, and TCR interact, activating helper T cells and releasing cytokines
Activated B cells differentiate and produce antibodies
Activated B cells create memory cells
Lucy’s Nature
Lucy’s Experience
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Harlow’s Nature
Harlow’s Experience
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Dalton’s Nature
Asparagine: A polar amino acid that's involved in protein synthesis, nucleotide biosynthesis, and regulating the uptake of other amino acids
Dalton’s Experience
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