Immune Pt.2 Flashcards
How do bacteria create illness?
- toxins in membranes (endotoxins)
- toxins released (exotoxin)
How do viruses create illness?
Invade “self” cells and take over and multiply
How do cancer cells create illness?
They genetically alter “self” cells, and overgrow into normal tissue
How do immune distinguish “self” from foreign Antigens?
MCH (major histocompatibility complex) surface makers on “self” cells
Where are MHC class 1 surface markers found?
On ALL nucleated body cells
Where are MHC class 2 cells found?
On macrophages, B cells and dendritic cells
( antigen presenting cells)
What are the two ways to remove lymphocytes that attack “self cells”
Clonal deletion and Clonal inactivation
Clonal deletion occurs where
In bone marrow (b cells)
- thymus (T cells)
Clonal deletion
Lymphocytes that attack “self” antigens that are destroyed by apoptosis (programmed cell death=suicide)
Clonal inactivation occurs where
In the spleen, lymph nodes and in the tonsils, appendix
Clonal inactivation
If lymphocytes create antigen receptors to “self” ; they’re inactivated
What are the specific immune system effector cells?
B and T lymphocytes
What are the “hallmark” features of specific immune response?
- specificity = lymphocyte clones recognize antigens unique pathogens
- diversity = potential to recognize all foreign antigens
- distinguish self vs non-self = t/b lymphocytes must differentiate
- memory = after infection, immunity to that antigen remains
The 3 processes of specific immune system
- Recognize pathogens
- Activate immune mechanisms
- Respond to the pathogens
What are the two branches of the specific immune system process?
(Hint: one by B cells and one by T)
- Humoral mediated immunity (b cells)
- Cell mediated immunity (T cytotoxic cells)
How do T &B cells recognize foreign antigens?
Antigen specific surface receptors
Antibody receptor
Recognizes bacteria & free virus
- on B cells
T cell receptor
Recognize cancer cells and virally infected cells ( abnormal “self” cells)
- T cells
Humoral medicated
Into the blood ( fluids)
Humoral mediated immunity mechanism
- activated B lymphocytes become plasma cells ➡️ secretes antibodies into blood ➡️ Antibodies bind to antigens on bacteria/free virus : marking them for destruction (optimize)
- Memory B lymphocytes remain (allow for faster response next time)
Clonal selection
5 unique B lymphocyte clones
1 is activated by antigen from pathogen
Where Do small clones of B lymphocytes live in?
Lymph nodes, spleen, tonsils
Antibody
Protein with quaternary surface
What are the 2 regions on an antibody
Variable region & constant region
Variable region
Part of fab region, where unique top for each B cell clone
Constant region
Part of Fc region that stays the same depending on an class
What are the 6 ways that antibodies facilitate pathogen destruction?
- Neutralize
- Agglutinate
- Precipitate
- Enhance phagocytosis
- Activate complement
- Stimulate nk cells
Does binding of antibody to antigen destroy the cell?
No! It needs to be inactivated and destroyed or inactivated and phagocytosis
Neutralization
Covers/ masks dangerous parts of bacteria, viruses so no damage can occur
Agglutination
Cell bonds or clumps together
Precipitation
Breaks down into soluble antigens
Complement
Create membrane attack complexes that form pores that lysis to kill cell
Nk (natural killer) cell
Antibody- antigen complex beings nk cell close to pathogen/cancer
NK cells secrete what 2 things
- Perforin ( creates pores)
- Granzyme ( kills cancer cell)
IgG
Main form in circulation (blood), increasing after immunization ; secrete in Secondary Response
IgM
Function as Ag receptor on B lymphocytes, secreted in Primary Response
Class switch from IgM ➡️IgG
1st infection = primary response (IgM) ➡️ memory B cell ➡️ 2nd infection = secondary response (IgG) ➡️ bigger memory B cell
How do B cells get turned on?
( require dual activation)
- Immune cell ids pathogen antigen ( chooses correct clone/ create memory cell)
- Cytokines from helper T cells
( enhances B lymphocyte response)
What are the 2 types of T lymphocytes
- Cystotoxic T lymphocytes
- Helper T lymphocytes
Cytotoxic T lymphocytes
- secretes perforin (pores) & granzyme ( kills invader)
- perforates and lyses virally infected cells & cancer cells
Helper T lymphocytes
Secretes cytokines
- helps activate cytotoxic T cell responses (& b lymphocytes)
How do cytotoxic T cells get turned on?
(Require dual activation)
- Immune cell ids pathogen antigen
(Choose correct clone) - Cytokines from helper T cells
( enhance cytotoxic T lymphocyte response)
How can T & B cells recognize antigens?
Receptors
How can T & B cells recognize different antigens?
Genetic recombination
How can B & T cells differentiate (destroy)
Clonal deletion & clonal inactivation
How can B & T cells respond faster a second time?
Memory lymphocytes
Antibiotic
Drug designed to kill/inhibit bacterial growth
Antibodies
Receptor & effector molecule of B cells
- facilitates antigen destruction
Significance of primary and secondary immune response
- 1st response = w/out or with minimal Illness
-2nd response = less or no illness
Acquisition of immunity can be?
( mechanisms of immunization)
Natural acquired & artificial acquired
If acquisition of immunity is Passive, then it is
Borrowed from someone (short lasting)
If acquisition of immunity is Active, then it is created by
Created by exposure to antigens (long lasting)
-Provides immunity through memory cells
