Immune Function Primer
Vocab
Antigens: Stimulate immune response
Antibodies: Proteins secreted by Plasma Cells (activated B cells) which bind to Antigens with high specificity and affinity
Cytokines and Chemokines: Signaling molecules for immune response
Leukocytes: Hematology > Buffy coat (1%)
Complement system: Protein cascade helping kill and clear pathogens (non-cellular)
Humoral: Soluble immune components (antibodies + complements)
Functions
Innate immunity
For more on innate immunity, see here: Innate Immunity and the Complement System
Non-specific. Does not change with age. It is fast and immediate to activate. Skin barriers are part of this immune system as are general defenses like macrophages.
Microbe Associated Molecular Patterns (MAMPs) and DAMPs are non-specific molecule targets on pathogens identified by sentinel cells (epithelial, dendritic, macrophages) using Pattern Recognition Receptors (PRRs).
Phagocytosis | Antigen presentation | Mediator releasing (degranulation) | |
---|---|---|---|
Macrophage | X | X | |
Dendritic Cell | X | X | |
Neutrophil | X | ||
Eosinophil | X | X | |
Basophil | X | ||
Mast cell | X |
Macrophages
Phagocytose. Release chemokines/cytokines causing local inflammation, increased vascular permeability, cell recruitment
Dendritic cells
Connect to the adaptive immune system by phagocytosing bacteria and presenting the antigens to T-cells in lymph nodes. These are the ONLY cells which can activate naive T-cells.
Neutrophils
Phagocytose or degranulate (vomit pathotoxic materials). It'll then self-destruct.
Eosinophils
Hypersensitivity and allergy. Will also bully large parasites and worms.
Mast cells
Hypersensitivity and allergy. Will also bully large parasites and worms.
Natural Killer (NK) T-cell
Not myeloid
Adaptive immunity
Specific to antigens. Is slow, taking days to weeks to respond to an initial exposure, although subsequent exposures will be faster. Primarily B and T lymphocytes.
Clonal expansion: Activated cells massively proliferate each time they encounter a pathogen → stronger, faster response
Clonal deletion: Cells die off after the immune response, with the exception of memory cells
B-cell
Produced/matures in the bone marrow and secretes antibodies when activated. Does not require Major Histocompatibility Complex (MHC) presentation of the antigen in order bind it, will sniff it out right on the pathogen.
T-cell
Produced in bone marrow, matures in the thymus. Activated by antigens on Major Histocompatibility Complex (MHC).
MHC-I presents endogenous antigens (found on all cells)
MHC-II presents exogenous antigens (found on antigen presenting cells)
CD4 (Helper) T Cells secrete cytokines to coordinate immune
response and activate B/CD8 T cells. Can only see antigens presented on MHC II molecules.
CD8 (Cytotoxic) T cells kill target cells can only see antigens presented on MHC I molecule.
All T-cells are have CD3.
Clonality: B/T cells express a single antigen receptor. Innate cells will not be clonal.
Steps to Immune Response
1. Macrophage engulfs pathogen and release cytokines
Cytokines recruit other cells and result in fever and swelling/redness.
2. Recruitment of innate defenders
Neutrophils, macrophages.
3. Dendritic cells eat a pathogen and activate Helper T-Cells
Dendritic cells travel to lymph nodes and activate CD4 Helper T-Cells using MHC-II.
4. CD8 T-Cells and B Cells are activated
By Helper T-Cells. Cytotoxic Killer T-Cells immediately go to assist with the infection.
Some B cells are converted to plasma cells, which passively secrete low-moderate affinity antibodies, while others become memory cells which remain dormant until a secondary immune response is required and secrete high affinity antibodies.
These memory cells will mount a defense much faster than the initial infection.