Ch. 12 Flashcards
adaptive immunity
remembers invaders. slower response compared to innate. SPECIFIC to a particular antigen or foreign invader
immunological memory
secondary exposure to the same antigen is rapid and effective and frequently will not experience disease symptoms or it can be mild
what do adaptive responses have?
MEMORY! when you’re exposed to an infectious agent you’ve previously fought, ur adaptive response responds so rapidly u may not even develop symptoms
adaptive immunity includes two facets:
- humoral immunity: antibodies made by activated B cells
- cellular immunity: T cell mediated
mature T and B reside where?
lymphoid tissues
where do T cells mature?
Thymus
where do B cells mature?
Bone marrow
epitopes
particular sites on antigen that B and T cells recognize
T cell activation
effector cells
B cell activation
effector cells are called plasma cells and they make abys
T cytotoxic cells
DIRECTLY DESTROY infected, foreign, cancer cells
T helper cells
do not directly seek and destroy, they stimulate other WBCs, call for help using cytokines. Releasing cytokines activate other WBCs and call them to the area. main organizers of cellular and humoral immunity. most abundant
B cells
stimulated by T helper cells. Activated B cells (plasma cells) will secrete antibodies
immunogenicity
ability to stimulate immune response
haptens
incomplete antigens; they themselves are not able to stimulate immune responses but if they are linked to something like a protein, then they can
self-tolerance
property of immune cells by which they will not attack normal self-cells; the ability to differentiate self from foreign and only attack foreign substances.
antigen
any substance that causes your immune system to produce antibodies against it
T helper 1 cells
mainly activate T cytotoxic cells, macrophages, and natural killer cells to destroy pathogens inside of host cells.
T helper 2 cells
primarily stimulate B cells to make antibodies and are therefore key stimulators of humoral immune responses.
T regulatory cells
control functions of other WBCs, including dendritic cells, mast cells, B cells, and other T cells to ensure that immune responses taper off once a threat subsides; this reduces risk for auto-inflammatory disorders and collateral host tissue damage from sustained inflammation.
T cells are screened for self-tolerance
T cells are screened in the thymus = recognizes MHCs = no is apoptosis/yes is asking if it’s potentially self reactive = yes is apoptosis/no is passes self-tolerance screening and migrates to lymphoid tissues
B cells are screened for self-tolerance
B cells are screened in bone marrow = Could make abys to self antigens? = yes is apoptosis/no is passes self tolerance screening and migrates to lymphoid tissues
What MHC proteins are present on T and B cell surfaces?
T cell: MHC 1
B cell: MHC 1 & 2
T cell receptors
Antigen recognition receptors on T cells.
B cell receptors
Antigen recognition receptors on B cells. bind to epitopes
Stage 1 of adaptive immunity
Stage 1 – Antigen Presentation
- Dendritic cells and certain other white blood cells act as antigen-presenting cells (APCs)
- APCs show antigen to T cells
- B cells do not require APCs to show them antigens; they can directly interact with an antigen
Stage 2 of adaptive immunity
Stage 2 – Lymphocyte Activation
- After antigen presentation, lymphocytes activated by a collection of released signaling molecules called cytokines
- Activated T cells influence B cell activation
Stage 3 of adaptive immunity
Stage 3 – Lymphocyte Proliferation and Differentiation
- Activated B and T cells undergo multiple rounds of cell division to proliferate (clonal expansion)
- Effector cells: relatively short-lived activated cells that defend the body in an immune response
- Memory cells: long-lived immune cells capable of recognizing foreign particles they were previously exposed to
Stage 4 of adaptive immunity
Stage 4 – Antigen Elimination and Memory
- Cellular and humoral responses collaborate to eliminate the antigen against which they were activated
- threat passes- effector cells die off
***Memory cells endure for years in lymphatic tissues
MHC I
location: on all body cells except RBCs; serves as the body’s uniform
interacts w/: CD8 on T cytotoxic cells
antigens presented: intracellular antigens
MHC II
location: only on antigen-presenting cells (APCs); main APCs are dendritic cells
interacts w/: CD4 on T helper cells
Antigens presented: extracellular antigens
superantigens
inappropriately activate T cells against self- factors
T-independent antigens
antigens directly bind to B cells to activate them w/o T cell assistance
T-dependent antigens
require activated T helper cells to fully activate B cells
immunoglobins
IgG, IgA, IgM, IgE, IgD
IgG
most abundant - 85%
found in all bodily fluids
we’re exposed to it
IgA
15% of all abys
prevalent in mucous membranes and found in secretions (saliva, sweat, etc.)
protects nursing infants; can survive stomach acid and can reach intestines
IgM
10% of all abys
are made early in infxn upon a primary antigen exposure; indicates recent exposure to antigen
found in the blood
IgE
present in low concentrations; found mostly in the lungs, skin, and mucous membranes; fights off parasitic infxns and helps mediate allergic responses; causes mast cells and basophils to release allergy mediators like histamine
IgD
least abundant. found on surface of B cells
antibody titer
total aby present in the body
primary antigen exposure
generates IgM abys first and the IgG
IgM spike around day 7 and drop off around day 15
IgG spike around day 14 and persists until about day 28
not produced right away
secondary antigen exposure
could be from vaccines, exposed to it, etc. and produced right away
IgG will spike right away and peak around day 14/15
IgM produced right away but doesn’t rlly spike
requires coordinated activity of memory B and memory T cells
naturally acquired active immunity
immunity from a previous infxn. long term protection. immune system made memory cells so body can make abys against antigens
naturally acquired passive immunity
abys pass across the placenta. not long term
artificially acquired active immunity
vaccination triggers immune response. long term
artificially acquired passive immunity
given abys thru medical means. antivenom neutralizes toxins. not long term
serological testing
looking for aby titer in the body
good for diagnosing a particular antigen
can be used on Sars-CoV-2, Zikka virus, HIV
convalescent plasma
can be used in infectious diseases for which there are no approved therapies.
used to treat emerging diseases
take blood plasma from infectious person and inject the noninfectious person
monoclonal abys
abys that are highly specific for a single epitope
can treat patients in dire need
can be used on cancer patients
A given B cell can undergo ______ BUT can’t change _______
isotope switching
what epitope it recognizes in variable region
