Everything You Need To Know About The Immune System

Front 1

What recognizes MHC1? What does it say?

Back 1

Cytotoxic T cells and NK cells

"I am a cell that belongs in your body and we are unique"

Front 2

Where are MHC 1s found?

Back 2

All cells except RBC

Front 3

What do MHC1s bind with?

Back 3

Virus infected cells, non self cells or abnormal self cells

Front 4

What do MHC2 cells do?

Back 4

Antigen presenting and activate adaptive immunity

Found on Antigen Presenting Cells: macrophages, dendritic cells and B cells

Front 5

What recognizes the MHC2 cells? What do they bind with?

Back 5

T helper cells

Front 6

What does the helper T cell do?

Back 6

Detects the antigen on the MHC2 and activates either the B or T cell response

Front 7

What happens when a helper T cell initiates a B cell response?

Back 7

Has to find the B cell with the complementary B cell with the right receptor, triggering to make many copies of itself. One set is banked as a memory cell in the lymphatic system. Others are effectors, undergoing final differentiation to create plasma cells. Terminal differentiation to secrete fighting antibodies.

Front 8

What happens when a helper T cell initiates a T cell response?

Back 8

Helper finds the complementary CD8 cell to make many copies of itself. One set banked, another set is the effector set.

Front 9

Generation of clonal diversity

Back 9

process of developing "library" of B and T cells that can respond to any antigen that we encounter. Mainly occurs in childhood, but a bit later in life too.

We produce all of the B and T cells before we ever encounter the pathogen.

Front 10

What happens to the Pre T in the Thymus

Back 10

Gets CD4 or CD8 surface marker and T cell receptor, which indicates cell specificity -- what antigen the T cell can fight.

Front 11

How is clonal diversity for T cells made? What is the problem with this?

Back 11

V J and C genes are randomly mixed up. Because it is random, it can sometimes make combinations that target our own auto reactive cells. And thus there is clonal deletion.

Don't need to know more than that

Front 12

Where does clonal deletion happen?

Back 12

In epithelia just outside thymus. Represents all self antigens in the body. This way, if a new T happens to bind to the self antigen on its way out, it is a signal for the thymus to destroy that T cell

Front 13

Central tolerance

Back 13

We tolerate ourselves. We do not makes cells that target ourselves. Central = happens in central lymph nodes and thymus gland.

Almost identical with B cells

Front 14

What part of the brain helps trigger inflammation? What else in the body?

Back 14

Hypothalamus, liver and bone marrow are targets for systemic inflammation

Front 15

What are the cytokines names? What is their ultimate goal?

Back 15

IL1 IL6 and TNF Alpha

To make sure an immune response is triggered via systemic inflammation

Front 16

What do cytokines act on? What does it do?

Back 16

Liver: increase production of acute phase response proteins (CRP and NBL) to increase complement activation

Brain: hypothalamus to make general malaise and increase body temperature

Bone marrow : scavenger cells, monocytes to increase phagocytosis

Fat: energy metabolism

Dendritic cells: TNF makes them go back to the lymph nodes to make sure a proper response is happening

Front 17

What is another name for maladaptive systemic inflammation?

Back 17

Sepsis

When an infection is in a tissue, systemic inflammation is moderate and adaptive. If the infection gets into the bloodstream, triggers sepsis. Greatly exaggerated response that is fatal

Cytokines also dump reactive oxygen species systemically, which isn't good. Causes drop in blood pressure and septic shock.

Front 18

Why is septic shock dangerous?

Back 18

Less blood flow to all of our organs from drop in BP

Disseminated intravascular coagulation -- paradoxical hemmorage, causing overactivation of clotting cascade

Front 19

Are viruses in ICF?

Back 19

No -- they live in the cells. Host cell has to present

Front 20

How does the host cell know that it is infected?

Back 20

It detects double stranded RNA inside itself -- humans don't do that

Front 21

What 3 things does a host cell do when it detects a virus in it? What does it release to notify these procedures to initiate?

Back 21

Releases cytokines interferon Alpha and Beta to affect host and neighboring cells to:

1) Host cell and neighboring cells to make enzymes to break down RNA

2) MHC1 production increased

3) activate NK cells in innate immune system to release interferon gamma to potentiate alpha and beta as well as destroying the host cells

Front 22

Complete resolution

Back 22

After healing, the tissue looks and functions exactly the same as it did before the damage

Front 23

Puss stage resolution

Back 23

formation of an abscess. Happens with infection of certain bacteria that are difficult to clear. Causes perpetual attraction of neutraphils, which die upon arrival and create the puss.

Puss = collection of neutrophils.

Usually leads to scarring

Front 24

Scar tissue resolution

Back 24

Happens when tissue cannot regenerate the same cells

Happens with myocardial infarction--heart cells cannot replicate. Healing occurs through fibrotic scar tissue remodeling, which is not as functional

Front 25

Chronic inflammation resolution and causes

Back 25

An injury that is not acute--persistent.

Conflicting events of active inflammation and events to repair tissue. Frustrated repair

if chronic inflammation is not interrupted, will make scar tissue

Syphilis does this. Hepatitis. Chronic hyperglycemia and cholesterol. Alcohol
Exogenous or endogenous

Front 26

What happens after neutrophils release reactive O2 and die?

Back 26

Monocytes come and turn into macrophages, cleaning up the mess. Continue inflammatory mediators but also clean up. Phagocytose neutrophils and dead pathogens, escaped proteins.

Front 27

Early vs late macrophages

Back 27

Early in damage: stimulating inflammation and cleaning, leave the tissue

Later in healing: release anti inflammatory cytokines and growth factors for tissue and blood vessels and then leave the tissue

Front 28

frustrated repair

Back 28

Attempts to repair tissue by cytokines but the ongoing inflammation from other cytokines damages the attempts to repair. Happens in chronic inflammation. Debris and cells can't leave tissue/constantly recruited to the area. Macrophages release pro inflammatory and pro healing.

As a result, only fibrotic scar tissue survives. Loss of function

Front 29

Purposes (3) of the complement system

Back 29

Promotes inflammation

direct killing

opsonization/tagging, to increase phagocytosis

Front 30

How is complement activated? (3)

Back 30

Presence of a pathogen

part of systemic response, the liver

Adaptive immune system via antibodies

VIA

CLASSICAL, MBLECTIN OR ALTERNATIVE

Front 31

Classical pathway to complement system

Back 31

C1 starts the cascade (binds to pathogen surface, binds to c reactive protein produced by liver in systemic inflammation, C1 binds to pathogen antibody)

Front 32

MBLectin pathway to complement system

Back 32

MBL, produced in liver during inflammation, acts like C1 -- increases probability of complement action. Binds to pathogen surface and that binds to the second complement and triggers cascade.

Front 33

Alternative pathway to complement system

Back 33

Inactive C3 binds to pathogen surface

Front 34

Outcomes of complement

Back 34

Promotes inflammation

Opsonization

Membrane attack complex (tunnel made from complement protein inserted into pathogen cell wall)

Front 35

4 Outcomes of Kinin system

Back 35

Bradykinin promotes localized vasodilation/cap permeability, enhancing vascular effect of inflammation

Activates pain receptors to make inflammation painful

Chemotaxins for neutrophils

Stimulates complement system

Front 36

The enzyme that activates the kinin system also activates what?

Back 36

Factor 12 clotting system, which results from blood vessel damage.

When neutrophils arrive at inflammation site, they release this factor to start kinin system.

Front 37

What are the two ways the clotting cascade is triggered?

Back 37

Damage to the blood vessel surface, releasing activating 12

Damage to the tissue outside of the vessel, producing mediator tissue factor and activates further down the cascade at 10

Front 38

What is the outcome of the clotting cascade? What is the key step

Back 38

a clot.

Prothrombin, precurser, turns into active thrombin.

Thrombin is the key enzyme that makes the clot, converting fibrinogen into fibrin, which cross link and makes a net for RBCs

Front 39

First thing that happens in an adaptive immune response?

Back 39

After clonal diversity, antigen presenting

Front 40

Antigen Presenting Cells (3)

Back 40

Dendritic cells

Macrophages

RARELY Mature but naive B lymphocytes, while making migration.

Front 41

How is the dendritic cell best for antigen presenting?

Back 41

It is the only antigen presenting cell whose sole purpose is presenting

Front 42

What do B cells mainly respond to?

Back 42

Extracellular bacteria/fungi/paracites like (pneumonia tetanus sleeping sickness)

Front 43

What do adaptive T cell responses tend to target?

Back 43

Intracellular infections (malaria, leprosy)

Front 44

Cell mediated immunity

Back 44

T cell responses. What you are getting to act and fight are affecter cells. TH1

Front 45

Antibody mediated immunity

Back 45

B cell responses are also called, TH2

Front 46

What do intracellular infections tend to infect?

Back 46

Macrophages after phagocytosis. Bacteria shut down the process of breaking them down.

TH1 has to come along, sees the antigen on the surface of the macrophage, and fuses lysozymes and bacterial pockets

Front 47

Interleukin 2 4 5 6

Back 47

Released from CD4 cell after macrophage presents via MHC2 to CD4 T cell onto CD8 cell and causes cell division and proliferation

a set of memory and a set of effector cells are created

Front 48

neutralization

Back 48

Antibody attaches to pathogen and blocks replication/infection of cells

Front 49

Effects of complement

Back 49

inflammation, Neutralization, opsonization membrane attack complex

Front 50

IgG

Back 50

Monomer, tags for opsonization and neutralization

Sticks around for the next time exposed to antigens ready to neutralize. Number doesn't go down as much

Front 51

IgM

Back 51

Activates Complement

Forms B cell receptor with IgD

First wave of antibodies produced after initial infection, but returns. Initial inflammation

PENTAMER, ten binding sites, what it lacks in affinity it makes up for in avidity (number of sites, greater chance to connect

Front 52

IgA

Back 52

Neutralization

Front 53

IgE

Back 53

Sensitization of Mast Cells and allergic reactions

Front 54

IgD

Back 54

Forms B cell receptor with IgM

Front 55

Class switching

Back 55

Varies attack for a single pathogen to be more effective

Front 56

Affinity Maturation

Back 56

How tightly the bind between antigen and binding site.

Initial exposure has low affinity binding with antigen. The waves of IgG has a higher affinity and all of the antigens in the second infection are highest.

Given more experience, we produce antibodies of higher affinity

Front 57

Vaccine

Back 57

initiates antigen in the system without the pathogen. Need boosters, though, because antibody titers get low and you won't have immediate protection. Time is key

Front 58

Allergy

Back 58

Immune response to a non harmful environmental antigen

Front 59

Alloimmunity

Back 59

Reacting to someone else's self antigen

Usually T Cell mediated 4

Front 60

Type 1 - immediate hypersensitivity

Back 60

Anaphylaxis -- true allergies

Mast Cell Sensitization - We are producing IgE to sensitize Mast cells--degranulate and cause inflammation. IL1 also does this

Front 61

Type 2 -- antibody mediated hypersensitivity

Back 61

Looks appropriate -- has the IgM and IgG

Often autoimmune, anemia, tags and kills RBCs

Same as any antibody mediated response except against non harmful antigen

Front 62

Type 3 -- immune complex mediated

Back 62

Antibodies attached to chunks of destroyed pathogens get stuck in tissue -- such as capillary filter in kidneys.

When this gets stuck, triggers complement and inflammation, damaging tissue.

Front 63

Type 4 - cell mediated hypersensitivity

Back 63

Antigen activation of T cells, which causes direct killing and inflammation

Front 64

hyperacute rejection/humoral

Back 64

Very fast -- before patient gets off the table. Alloimmunity already exists

Front 65

Acute rejection

Back 65

most common form of rejection. within 6 months

t cell response on cells in organ, antibodies on blood vessels in organ

usually t cell mediated

Front 66

chronic rejection

Back 66

harder to control -- organ just diminishes in function over time

Front 67

GVH

Back 67

Graft vs Host

immune competent cells in immune compromised person. Donor attacks recipient.
Acute or chronic