Inate vs adaptive
This arm of the immune system mounts a defense within minutes to hours but doesn't distinguish one pathogen from another.
Innate immunity
note: fast and general, not antigen specific
Based on its thick peptidoglycan cell wall, MRSA is this type of bacteria on Gram stain.
Gram positive
This complement pathway is triggered when IgM or IgG antibody is already bound to the pathogen.
Classical pathway
note: because it needs pre-formed antibody, it can't help on first exposure, so early defense relies on the other two pathways (hint hint)
This antigen-presenting cell captures MRSA at the infection site, processes it, and migrates to the draining lymph node to prime naive T cells
The dendritic cell
note: DC has to be activated by PAMP sensing to do this
This arm of the immune system takes days to fully mount but leaves behind long-lived memory cells for faster response on re-exposure.
Adaptive immunity
also note: Memory B and T cells are why vaccines work
Any second exposure triggers a faster, stronger response of the immune system
This chemokine, also known as CXCL8, is released by macrophages specifically to recruit neutrophils toward the site of infection.
IL-8
This complement pathway is triggered when MBL binds mannose residues on a microbial surface.
hint: what does MBL stand for
MBL= manose binding lectin and it triggers the lectin pathway
Dendritic cells load processed bacterial peptides onto this molecule before presenting them to CD4+ T cells.
MHC class 2
note: CD4+ T cells are restricted to MHC II and CD8+ T cells are restricted to MHC I, which is why CD8+ T cells target intracellular pathogens (with MHC1), not extracellular ones like MRSA.
What tells the innate immune system that there is something here that shouldn't be here. a conserved microbial structure
PAMPs and DAMPs
note: PAMP = pathogen-associated molecular pattern (peptidoglycan, LPS). DAMP = damage-associated molecular pattern
These three cytokines are released by activated macrophages and are the classic drivers of local and systemic inflammation.
TNF-alpha, IL-1, and IL-6
This complement pathway is triggered spontaneously, when C3b binds directly to a microbial surface and recruits Factor B.
The alternative pathway
note: this happens at low levels to C3 constantly in plasma but it only amplifies once C3b lands on a microbial not host surface
bonus 50 points since i think this one is a bit hard:
Full T cell activation needs two signals, TCR binding peptide-MHC II, plus what costimulatory pairing
CD28 binding B7 (CD80/86)
note: Signal 1 without signal 2 doesn't activate the T cell and aditionally sends it to anergy, meaning it will NEVER be responsive again (to prevent cells from reacting when they shouldn't)
These two lymphocyte populations carry out humoral and cell-mediated adaptive immunity, respectively.
include where they are made and where they mature
B cells mature in the Bone marrow. T cells mature in the Thymus. Both are made in the bone marrow
What does V(D)J recombination cause and in which cells?
V(D)J recombination creates diverse, antigen-specific receptors in developing B cells (BCR/antibodies) and T cells (TCRs)
note: it causes the variation on the variable region of the receptors
All three complement pathways converge to form this enzyme complex, whose job is to cleave C3 into C3a and C3b
200 for the answer, and 200 for what the percise enzyme is for each pathway
C3B convertase
C3bBb for the alternative pathway
C4b2a for the classical and lectin pathway (C4b2b based on the anki- will accept either answer since this is silly)
note: C3b opsonizes the pathogen for phagocytosis AND feeds into forming C5 convertase to continue the cascade.
Driven by dendritic cell signals, naive CD4+ T cells differentiate into this helper subset, Th-??, which releases IL-?? to ramp up neutrophil production and recruitment against MRSA.
Th17, IL-17
note: IL-17 also stimulates keratinocytes to produce antimicrobial peptides directly in the skin (MRSA classically enters through a skin break)
what recognizes lipopolysacharides (from gram negative bacteria), and where is it found
TLR4s found on innate immune cells (such as macrophages, monocytes, and dendritic cells)
Once neutrophils reach MRSA and engulf it, this oxygen-dependent killing mechanism uses NADPH oxidase to generate reactive oxygen species inside the phagosome.
The respiratory burst (oxidative burst)
note: The oxidative burst occurs when neutrophils use NADPH oxidase to generate reactive oxygen species (ROS) inside the phagolysosome, which help kill engulfed bacteria.
This terminal complex, assembled from C5b plus C6 through C9, inserts into the pathogen membrane and causes lysis
The Membrane Attack Complex (MAC)
This helper T subset engages B cells via CD40L-CD40 and, through IL-4, IL-5, and IL-13, drives antibody class switching and plasma cell formation.
200 to answer which helper T cell
100 to answer what IL-4 triggers
100 to answer what IL-5 triggers
100+ 50 to answer what IL-13 triggers (this one is hard!)
helper t cell- Th2
IL4 triggers B cell class switching to IgE (allergic reaction)
IL-5 triggers B cell class switching to IgA and eosinophil activation
IL-13 triggers IgE production, mucus secretion, and alternative macrophage activation (will accept any one of these as correct)