Ch8 Immune System
Copyright © 2025 Mark Song
Immune system is a distributed set of cells in blood, lymph fluid, tissues, and organs
It can distinguish self and non-self
protect against infections
isolate and remove foreign substances
remove cancer cells
Leukocytes, AKA WBC
Cell-cell interactions and communications
Innate response
defend without distinguish identities
Self vs non-self
via Pattern Recognition Receptors (PRR) recognize if it is a pathogen
Own cell express protein that inactivate complement system (against C3b by ComplementReceptor1 etc.)
NK cells use a combination of activating (self protein) and inhibitory receptors (non-self or stress protein) which the two protein will occur in a specific balance
- Physical Barriers
e.g., skins, hair, mucus, stomach acid, antimicrobial chemicals
- Phagocytes
Cells that engulf pathogens and cellular debris (phagocytosis) and merge with lysosomes
Including Neutrophils (chemotaxis) and Macrophages (PRRs and complement system)
- Natural Killer cells
Recognition and destruction of cancer cells/virally infected cells
- Complement system
Circulating protein in the plasma that assist destruction of pathogens
- Inflammation
A local response to infection and injury that destroy potential pathogens
Example: response to a splinter
- cells, including epithelial and leukocytes senses tissue damages and releases signal molecules, that increase capillary permeability and dilate local arterioles causing edema (swelling)
- Neutrophils (and other phagocytes) moves out of blood to the inflamed area, which is a multistage movement and is a “chemotaxis” (directed migration of a cell in response to a chemical signal)
- Killings of pathogens via engulfment by phagocytes and complement system
Complement system effects:
C3b interacts with pathogen membrane and marks it for destruction via phagocytosis or activation of MAC
Adaptive immunity
depends on recognizing specific pathogens
Lymphocytes, cells in adaptive immune response system, from bone marrow and found in the lymphatic system and blood
B Cells (plasma cells, memory B cells)
Helper T Cells
Cytotoxic T Cells
Antigens
any kind of markers that the immune system can recognize
Proteins or sugars on the outside of viruses
Immune system read antigens with specificity
exist on viruses, bacteria, allergens, parasites, proteins, tumor cells, normal cells
B Cells
each express one antigen receptors
the receptor is immunoglobulin, which contains multisubunit protein
When antigen binds, B cell undergoes division (clonal expansion) which give rise to antibody-secreting plasma cells and memory B cells
The stem (Fc) portion of antibody interacts with receptors on phagocytes and stimulating phagocytosis and can also activate complement system
Helper T cells
Binds to antigen complexed with MHC Class II molecules made by some cells (including Macrophages and B cells)
It also require co-stimuli to fully activates
Secret signals that further activate themself and paracrine effects to B cells, Cytotoxic T cells, and NK cells
Cytotoxic T cells
Activated with MHC Class I (expressed by all cells), requires signal from helper T cells for activation
Cytotoxic T cells are activated by antigen complexed with MHC Class I (except red blood cell, present virus to the outside) that target cancer and virally infected cells, and required activation by helper T cell. This will lead to cells apoptosis
After an infection
Most activated lymphocytes undergo apoptosis
Antibodies can last for days-months
Memory B cells remains
Some helper T and cytotoxic T remains as memory cells
The first antigen exposure would have small amount of specific antibody (7-10 days after infection), but the second would have significantly more specific antibody (2-5 days after infection)
Roles of adaptive immunity
Encounter and antigen recognition
Lymphocytes activation
Coordinate attack
Memory
Active vs Passive Immunity of Adaptive immunity
Active: resistance due to exposure to pathogens of vaccinations
Passive: transfer of antibodies from gestation, breast feeding, therapy
Central tolerance, during early development, B and T cells with high affinity to self antigen go through apoptosis, which is in a process called Clonal Deletion
Peripheral tolerance, regulatory T cells, modulate immune response which prevent attacking self
Regulatory T cells, recognizes MHC class II and then signal to autoreactive B-cell, which would cause apoptosis (for example)
Autoimmune disease
Immunity attack cell, e.g., Multiple sclerosis (myelin in CNS), type 1 diabetes mellitus (beta islet cells in the pancreas)
Causes
- Failure to clonal deletion of lymphocytes
- Problem with regulatory T cells
- Exposure to pathogens that contains antigens similar to out own protein can lead to cross-reactivity
Innate immune responses
Rapid, no specificity, no memory
Adaptive immune responses
Slower, specificity, with immunological memory
Interaction between Innate and Adaptive immune responses
Antibodies can recruit complement (C1b) system and phagocytes
Inflammation recruits lymphocytes
Macrophage present MHC class II to helper T cells
Helper T cells increase activity of natural killer cells