Immunity and interferons

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innate inflammatory response

histamine released causes blood vessels to dilate and fluid leaks produce swelling, influx of macrophages and neutrophils fit into PAMPs or pathogen associated molecular patterns

How do B-cells make antibodies?

once bound to the B-cell surface, B cells form plasmablasts, which rapidly produce antibodies that are carried through lymph nodes to blood

How do antibodies work?

bind directly to antigen, neutralizing it by cutting off interactions with other cells AND promote clusterin of antigens AND making the antigen recognizable to phagocytes

How does immunization work?

B cells produce memory cells, and when they encounter the same antigen, they produce plasma cells, which produce antibodies. rapid response due to memory of a past antigenic invasion. the strain is weak enough that it doesn't cause actual infection but still causes antibodies to be produced, creating B memory cells

What are T-cells?

(CD4+ and CD8+) Like B-cells, they are also lymphocytes found in the bone marrow, but then migrate to the thymus "T-thymus". While B-cells are the archers, T-cells are the knights. They attack foreign objects, and lyse infected cells--apoptosis. Produce cytokines, ie interleukin-2. have antibody flag on membrane

double-stranded RNA

guarantees infection, can induce interferon synthesis

mast cells

produces histamine in response to PAMP signals, may be located just under skin surface

macrophages

engulfs invading pathogens, enters interstitial space, recognizes PAMPs, carries fragments of pathogenic organisms on their surface

dendritic cells

engulfs invading pathogens

interferons

induced by virus infection and double-stranded RNA, bind with receptors on target cells, activate Jak kinases, which phosphorylate Stat proteins (JakStat pathway)

ways to block interferon response

make hairpins, cleave PKR and activate it

PKR pathway (induction, mechanism of action)

2 PKRs bind to the same dsRNA and phosphorylate each other, the activated PKRs phosphorylate a protein cascade, and the GDP-GTP interaction eventually inhibits protein synthesis

How does double stranded DNA virus produce RNA?

in dsDNA viruses like adenoviridae, viral DNA enters the host nuclei and replicates, producing more virions that are secreted from the host cell

How do CTLs activate, increase, and recognize pathogen-infected cells?

CTLs are signaled by helper T-cells which help by producing interferon-gamma and interleukins, they recognize pathogen-infected cells by the MHC peptide on the surface of the cell (analogous to the antibody receptor in B-cells). kill cells by lysing them. CTLs have serine proteases that cause apoptosis. apoptosis can also happen when CTLs behind to the Fas transmembrane protein.

How is dsRNA produced?

1) ssRNA produces mRNA which then binds to another ssRNA
2) DNA produces two RNA that complement each other

How do hairpins interfere with PKR pathway?

the PKR binds to the hairpin, but due to the hairpin nature the PKR can't bind to another PKR and can't get phosphorylated, so the protein cascade is never activated and in the end, protein synthesis isn't stopped

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