Unit 4 - Immune System K-M Flashcards
Adaptive Immunity creates…
antigen-specific responses
- adaptive immune responses are ANTIGEN-SPECIFIC EVENTS in which the body recognizes a particular foreign substance & selectively reacts to it
Adaptive Immunity
Basic Steps of PRIMARY Response/Exposure:
- Naïve T and B LYMPHOCYTES exposed to antigen for first time (first exposure)
- Clonal expansion occurs (mitosis of B-cells and T-cells that have BCRs/TCRs specific for the antigen)
- Differentiate into effector cells and memory cells.
Effector B-cells = Plasma cells.
Effector T-cells = Helper T cells and Cytotoxic T-Cells - Plasma B cells produce antibodies, Memory B cells remain in circulation (humoral immunity).
Naïve T and B lymphocytes
at birth, each clone of lymphocytes is represented by only a few cells, called native lymphocytes
Clonal expansion
b/c the small # of cells in each naive clone isn’t enough to fight off foreign invaders, the 1st exposure to an antigen activates the appro. clone & stimulates it to cells in the clone
- this process (clonal expansion), creates add. cells in the clone
- naive cells continue to be generated throughout an individual’s lifetime
Effector cells
carry out the immediate response & then die within a few days
Memory cells
long-lived & continue reproducing themselves
Effector B-cells =
Plasma cells
Effector T-cells =
Helper T cells and Cytotoxic T-Cells
Plasma B cells
produce antibodies
- to create humoral immunity, the soluble antibodies of the plasma
Memory B cells
remain in circulation (humoral immunity)
- stay alive, waiting for the next exposure to the same antigen
Antibody production is _____ & ______ in magnitude in the primary immune response b/c _______
SLOWER
LOWER
the body has not encountered the antigen before
Adaptive Immunity
Basic Steps of SECONDARY Response/Exposure: (Immune Memory)
is _____ & ______ b/c _______
QUICKER
LARGER
of the memory B cells that remained behind after the 1st exposure
Adaptive Immunity
Basic Steps of SECONDARY Response/Exposure: (Immune Memory)
- Many MEMORY T and B LYMPHOCYTES in circulation are exposed to same antigen that initiated their formation.
- Clonal expansion occurs more quickly (there is a larger population of memory T and B cells for the specific antigen than there was for Naïve T and B cells during the first exposure).
- Increased number of effector T and B cells and memory T and B cells are formed.
- More plasma cells, results in increased antibody production compared to primary response. More cytotoxic cells allows for faster more effective destruction of infected host cells.
- Overall more cells = more response to 2nd exposure
Adaptive Immunity – Cell Mediated Immunity
Effective against virus infected cells and cancerous cells
Adaptive Immunity – Cell Mediated Immunity
Steps for secondary response:
- Pathogen invades tissues
- Phagocytosis by resident macrophage or dendritic cell.
- Antigen presentation to TYPE 1 Helper T-cells (CD4+) by binding of TCR to antigen-MHC-II.
- Activated Type 1 Helper T cells secrete IL-2 (cytokine) which activates Cytotoxic T-Lymphocytes (CD8+)
- Cytotoxic T-Lymphocyte TCRs bind to antigen-MHC-I complexes on infected host cells.
- Cytotoxic T-Lymphocytes release perforin onto infected host cell membrane, creating a pore.
- Cytotoxic T-Lymphocytes release granzymes into infected host cell which will digest the cell.
- Infected host cell undergoes apoptosis (lysis).
Steps for primary response would be similar (to secondary response for CELL MEDIATED IMMUNITY), but would involve…
antigen presentation to Naïve T cells followed by clonal expansion in between step 2 and 3
Adaptive Immunity – Humoral Immunity
Antibody mediated immunity.
Adaptive Immunity – Humoral Immunity
Steps for secondary response:
- Pathogen invades tissues
- Pathogen recognized by TLRs (Toll like-receptors) or opsonized by complement or antibodies.
- Phagocytosis of pathogen by resident macrophage or dendritic cell.
- Antigen presentation to TYPE 2 Helper T-cells (CD4+) by binding of TCR to antigen-MHC-II.
- Activated TYPE 2 Helper T cells secrete IL-4, IL-5, IL-6 (cytokines) which activate B-cells to proliferate (clonal expansion) and Plasma cells to produce antibodies.
- Antibodies facilitate:
a. phagocytosis (e.g. act as opsonins)
b. cell lysis (apoptosis) via activation of classical complement pathway or
activating degranulation of NKCs and/or eosinophils
c. Facilitate production of more antibodies (though action on B cells)
Adaptive Immunity – Humoral Immunity
- Antibodies facilitate:
a. phagocytosis (e.g. act as opsonins)
b. cell lysis (apoptosis) via activation of classical complement pathway or activating degranulation of NKCs and/or eosinophils
c. Facilitate production of more antibodies (though action on B cells)
Steps for primary response would be similar (to secondary response for HUMORAL IMMUNITY), but would involve…
antigen presentation to Naïve B cells followed by clonal expansion in between steps 3 and 4
Adaptive Immunity – Humoral Immunity
Two categories of humoral immunity:
- Active Immunity
a. Natural
b. Artificial - Passive Immunity
a. Natural
b. Artificial
Adaptive Immunity – Humoral Immunity
- Active Immunity
body is exposed to the pathogen and produces its own antibodies via humoral immune response
Adaptive Immunity – Humoral Immunity
- Active Immunity
a. Natural
pathogen infects body through natural means (crosses barriers, evades innate immune system and triggers a normal humoral immune response that leads to the production of antibodies. Person becomes ill and then recovers.
Adaptive Immunity – Humoral Immunity
- Active Immunity
b. Artificial
Vaccination:
i. Vaccines mimic the pathogen. Can be composed of:
- Attenuated or killed pathogen
- Purified macromolecules
- DNA
All cause slow primary responses, which makes them harmless (mild symptoms at worst)
ii. Fake pathogen triggers creation of antibodies and memory cells (long-term immunity)
iii. Subsequent exposure to real pathogen (the memory cells) produces fast and more effective secondary response.
i. e. vaxxed person is later infected by the pathogen