Where do T cell gain their immune competence
In thymus, where they mature
Cytotoxic T cell activation
By helper T cell and antigen recognition, specifically recognition of the endogenous antigen
Exogenous vs endogenous antigens
Exo: recognized by helper T cells, foreign material from outside teh body, produced elsewhere
Endo: recognized by cytotoxic T cells, antigens produced by infected body cells themselves, materials produced by possessed cell (like virus proteins) would be exposed on MHC1 receptor (modification)
How do cytotoxic T cells do their thing
When fully activated, they produce their own memory cells and kill cells presenting endogenous antigens on their surfaces
Does so by recognizing and releasing perforin and granzyme
Shut off mechanism of cytotoxic T cells
Like a shut off mechanism
To activate teh cytotoxic T cells it needs its CD28 and T cell receptor to recognize the antigen and B7
To de-activate, you have to upregulate CTLA4, a receptor in the T cell with a higher affinity to B7 than CD28, so it’ll break that bond
Note: cytotoxic T cells activation here required helper T cell cytokines as well as its TCR binding to the modified MHC1 complex and its CD28 to the B7 of invador cell
Checkpoint inhibition of cytotoxic T cells
Think of the shut off mechanism, uses CTLA4s higher affinity to B7 to disconnect it from CD28
Inhibition of this shut off would involve blocking the CTLA4 with an antibody so that it wont deactivate
Factors that affect your bodies ability to resist infection
Protein-calorie malnutrition: think of it as supply low of materials needed to keep up with production
Pre-existing diseases
Stress/state of mind
Sleep deprivation: associated to decreased immune efficiency
Moderate exercise: apparently has good effects
Immunodeficiency diseases (2)
SCIDs: severe combined immunodeficiency disease, deficiency in cytokine resulting in being unable to produce B and T cells, in some cases NK cells too
AIDS: acquired immunodeficiency syndrome: specifically targets the helper T cells
Side note of AIDS: if cytotoxic T cells aren’t activated, they cant patrol for cancer cells and take care of them, thus why lots of aids patients get cancer
Why do we reject transplants (brief)
Due to how unique our MHC1 receptors are, the donated tissue will be covered in MHC1 of someone else, which our body will perceive as foreign and it will therefore attack it
Avoiding organ rejection
Immunosuppressants required
Target lymphocytes, goal is to decrease lymphocyte population
Ex: cyclosporine: blocks cytokine production in helper T cell, preventing it from activating the other lymphocytes (basically decreasing your ability to detect and react to foreign cells)
Why do we perceive RBCs as foreign
Not due to MHC1, they dont have any since they have no nucleus
But they do have membrane proteins and carbohydrates ( A antigen, B antigen)
If you’re type A, what antigens and antibodies do you have
Type A antigen (carb) and anti-B antibodies (will attack B)
Rh factor and pregnancy
Only a problem when mom and baby dont have the same Rh factor, but even that is usually not an issue since she wont come into contact with baby’s blood (if all goes well)
May happen at birth tho, and if it does she will develop antigens to the Rh, which could cause catastrophic problems in her next pregnancy
What is an allergy
Reaction to something that most others tolerate
Types of allergic reactions
Immediate hypersensitivity: immediate reaction
Delayed hypersensitivity: appearing 12-72 hours after exposure
In either case reaction typically localized to site of exposure
Mast cells
Release histamines granules when they are called to sites where antigens were detected
Histamines are vasodilators, effective in inflammatory response
Consequence of too much histamine
Systemic/ too much release of histamines can cause anaphylaxis
Systemic meaning into blood stream where all are affected
Vasodilation everywhere will cause a drop in BP and bronchiolar constriction, circulatory and respiratory failure
Autoimmune disease
When theres an inappropriate immune response triggered by self cells
Antibodies be recognizing us, self reactive T cells
Ex: type 1 diabetes, multiple sclerosis, rheumatoid arthritis, etc