Immuno: Innate & Adaptive

Question 1

Discuss PRR, TLR, PAMP, DAMP

Answer 1

PRR = recognize patterns of bad stuff
TLR = type of PRR, recognize PAMPS
PAMP = Patho assoc. molecular pattern (recognize: flagella, cell wall of bacteria, dsRNA)
DAMP = Damage assoc molecular pattern (damage indicator on host cells)

Question 2

Name some common foreign patterns recognized by TLR.

Answer 2

10 TLRs in humans:
TLR4 binds LPS on gram (-)
TLR2 binds peptidoglycan on gram (+)
TLR3 binds dsRNA,

Question 3

Identify the final transcription factor that is most commonly activated in inflammation.

Answer 3

All TLRs (except #3) activate IRAK pathway to make NFkB

Question 4

Define cytokine and chemokine

Answer 4

Both factors that cause inflammation (produced in response to TLR binding foreign pattern). Some chemokines are chemotactic for phagocytic WBCs

Question 5

Describe the function of the innate immune response.

Answer 5

The innate system is fast and responds to established molecular patterns common to pathogens. It also causes local inflammation to boost immune response.

Question 6

Name the cell that forms the bridge between innate and adaptive immunity.

Answer 6

Dendritic cell. In wounded area, immature DC gets activated by the cyto/chemokines and eat anything they can (including parts of invaders. The activated DC leaves the local area and travel in the lymphatics to the nearest LN where they ‘show’ what they’ve eaten to lymphocytes
NOTE: Innate response is NECESSARY for a good adaptive response to cause inflammation & “prime the pump”

Question 7

Discuss in principle the role T cells play in immunity.

Answer 7

They recognize Ag, activate & proliferate, then circulate through the body to get to affected area. Once there, they can use cytokines called lymphokines to attract macs to do their work (Th), or they can directly target the antigen-showing cells for destruction (killer T). Some T cells (Th2) can activate B cells for antibody production.
T CELLS MOSTLY FOR INTRACELLULAR ENVIRONMENT

Question 8

Discuss in principle the role B cells play in immunity.

Answer 8

B cells also arrange for the phagocytosis and destruction of foreign materials. Like T cells, they recognize antigens via surface receptors, and become activated and proliferate. They then release antibodies, which go out to do the work.
B CELLS MOSTLY FOR EXTRACELLULAR ENVIRONMENT

Question 9

Describe some of the functions of antibodies.

Answer 9

IgG: most abundant in blood, PASSES THRU PLACENTA. Two adjacent IgG molecules, binding an antigen such as a bacterium, cooperate to activate complement (which can lyse cell, attract neutrophils, etc).

IgM: is a large polymeric immunoglobulin. Better at activating complement, first one made (replaced by IgG in a week or two)

IgD: located on B-cell surface membrane

IgA: found in mucosa, so saliva, tears, genitourinary and intestinal fluids, and milk. In these secretions it’s associated with another chain called Secretory Component, which it acquires from epithelial cells during the process of being secreted. SC makes it resistant to digestive enzymes. First line of defense against microorganisms trying to gain access to the body through the mucous membranes.

IgE is designed to attach to mast cells in tissues. Causes the mast cell to make prostaglandins, leukotrienes, and cytokines, and release its granules which contain powerful mediators of inflammation like histamine –> allergy. The real role of IgE is in resistance to parasites, such as worms.

Question 10

Give examples of immunopathology.

Answer 10

• Type I: Immediate hypersensitivity (allergic run; big IgE response to environmental Ag)
• Type II: Autoimmune rxn from Ab
• Type III immunopathology: Ab against a soluble antigen. Ab+Ag complexes are sometimes too small to be eaten by macs and get trapped in the basement membranes of capillaries they circulate through (occurs where there is net outward movement of fluid to tissues, e.g. kidneys, joints, pleura and skin). The trapped complexes activate complement and the usual inflammatory response occurs, with the tissue damaged as an innocent bystander. No matter what the antigen is, the symptoms tend to be the same: arthritis, glomerulonephritis, pleurisy, rash.
• Type IV: T-cell “collateral damage” after they activate macs
• Chronic frustrated immune responses: immune response to something you can’t get rid of but not self (gut flora, gluten, etc)
• HIV infection / AIDS