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Inflammation Block > Inflammation: IMMUNO > Flashcards

Inflammation: IMMUNO Flashcards

1
Q

Cytokines list

A 
IL-1
IL-2
IL-4, IL-5
IL-6
IL-7
IL-10 
IL-12 induces IFN-y

TNF-a

IFN-a
IFN-B
IFN-y

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2
Q

CD list

A

Messengers/ mediators in immune regulation. (Traffic signals that attract cells to site)

CD4+ helper T (Th) (binds MHC II + EC pathogens)
CD8+ cytotoxic/killer T (binds MHC I + IC pathogens)

CD 28

CD80, CD86

CD40L, CD40

CD19, CD20

CD 25

CDR

CD3

CDR3

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3
Q

Antigen presenting cells (APCs)

A

Dendritic cells (hematopoetic, everywhere and present IC pathogen fragments), macrophages, and B-cells

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4
Q

Cells involved in innate immunity

A
  • Phagocytes! Digest particle via phagolysosome
  • First to act are neutrophils in accute inflamm, use chemotaxis to find infection and spit out NET to prevent bacteria prolif
  • Macrophages (monocytes in circ, and become macrophages once they enter tissues), which have many names
  • NK cells (detect stim signal and MHC I to kill cell, but don’t attack RBCs, which is why malaria can hide there)
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5
Q

Complement system

A

Assists antibody activity pathways, serves to recruit phagocytes (combo of complement opsonization and antibody paths are best for getting phagocytes to act).
-C3 splits into C3a and C3b. C3a goes on to be a anaphylotoxin, meaning it recruits phagocytes (esp neutros) (C5a does this too, potent). C3b deposits on bacteria, tagging it (opsonizing it) for destruction (by macros)

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6
Q

Immunoglobulins list

A 
IgG
IgA
IgM
IgE
IgD
(GAMED)
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7
Q

Affinity vs. Avidity

A

AVIDITY is higher for IgM bc pentamer and contains MORE binding sites, but IgG generally has higher affinity bc binds more strongly (must undergo at least ONE rearr to produce IgM, but if single rearr produces clones then will all have same affinity)

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8
Q

Heavy change vs light chain rearrangement

A

H (mu) chain– DJ rearr, then V-DJ rearr via Rag

Light chain: kappa genes rearr, then lambda if needed

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9
Q

IgG

A
  • most abundant, impt in secondary ab response
  • Can cross placenta to give immunity to fetus
  • Can bind to IgG Fc receptors on macrophages when ab bound to antigen to opsonize pathogens
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10
Q

IgA

A
  • Dimer
  • in secretions (saliva, tears, milk, mucus linings)
  • Neutralizes and activates ALT complement pathway (firs to act, makes sense b/c in mucus linings)
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11
Q

IgM

A
  • Pentamer
  • Strong avidity bc many sites for binding
  • Activates classical complement path (along with IgG)
  • First ab made in resp to pathogen
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12
Q

IgE

A
  • Bound to FCE receptors on basophils/mast cells
  • Activating this leads to ASTHMA and ALLERGIC rxn
  • can protect from helminths
  • IL-4 from helper-T celsl helps with isotype switching to IgE
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13
Q

IgD

A
  • can be found on B cell surface etc (can can fxn as B cell rec along with IgM)
  • Express on B-cells during maturation when leaving marrow (mature but naive) before entering lymph nodes
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14
Q

IgG

A
  • most abundant, impt in secondary ab response
  • Can cross placenta to give immunity to fetus
  • Can bind to IgG Fc receptors on macrophages when ab bound to antigen to opsonize pathogens
  • In ab isotype switching, IgM may switch to this
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15
Q

CDR3

A

CDR= complementarity determining region
CDR3 is the part of the B-cell receptor (antibody) that contacts the epitope (antigen) and will send signal to let itself know that pairing between H-chain an surrogate light-chain is productive (still @ pro-b cell stage) (???), mutations here cause somatic hypermutations

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16
Q

PAMPS

A

Immune cells recognize PAMPS on pathogens and respond using PRRs (such as TLRs)
-Example: TLR-4 recognizes LPS in gram(-) bacteria, and then this PRR initiates the inflammatory response

17
Q

Classical vs Alternative complement pathway

A

Classical: activated by antibody-antigen COMPLEX (occurs 3 days later, adapative)
Alternative: First to act, begins at C3 (always on, innate)

18
Q

Th1 vs. Th2 helper T-cells

A

Th1: produce IFN-y which activates macrophages and opposes IL-4

  • makes macrophages better, opsonize antibodies of B-cells
  • high affinity TCR only req low amt of antigen to get activated to Th1

Th2: Produce IL-4 to activate B-cells and oppose IFN-y

  • Makes B cells better, prob made for helminths, and IL-10 to inhib immune resp
  • low affinity TCR req lots of antigen to get acitvated to Tf2
19
Q

Fc region

A

Antibodies bind to microbe, and then Fc receptors on phagocytes usually bind to these antibodies. Fc is the portion of the cytophilic ANTIBODY that binds to FcRs on phagocytes. For example, IgE binds to FcE receptors on mast cells, triggering degranulation and immune repsonse. Fc helps with opsonization and degranulation, but is NOT needed for neutralization in Ig digestion

  • Some pathogens can encode proteins that prevent this, allowing them to live bc their proteins block phagocytes from binding and digesting
  • Fab region is variable
20
Q

T-cell maturation steps

A

Recognized processed antigen (as peptide fragments)

  • Thymocytes from marrow enter THYMUS via HEVs and undergo (+) selection in cortex (via cortical thymic epithelial cells, where they acquire a-B TCR and interact w/ thymus hormones), and (-) selection in medulla (via AIRE TF).
  • Had a-B chain rearrangement. Cells were first DN cells, then DP cells (expressing both CD4 and 8), then expressed only one (cytotoxic or helper)
21
Q

T-cell activation steps

A
  • To become an active cell, T cell binds to self antigen,, and there’s co-stimulation of its CD28 to B7 (80 or 86) on an APC and sends signal to move on (B7 is off, but can become turned on under inflammatory state).
  • Once active, undergoes CLONAL EXPANSION via IL-2 (but NOT somatic hypermutation–don’t need the affinity increased)
  • Effector T-cell can become either Th1 or Th2
22
Q

IgM

A
  • Pentamer
  • Strong avidity bc many sites for binding (good complement fixation)
  • Activates classical complement path (along with IgG)
  • First ab made in resp to pathogen
23
Q

MHC I

A

MHC I:

  • on all nucleated cells, trimer with 3 a-chains(???), binds short chain which fits in groove, genes are HLA-A/B/C, presents IC pathogen fragments to CD8 cell (IC means enters INSIDE cell, such as viruses)
  • mech: in ER, calnexin and calreticulin chaperone prots fold chains and bind B2. MHC I binds TAP transport prot via tapasin enz, which peptide binds to and travels thru and binds MHC I, which now exits golgi to be recognized by CD8 cells at cell membrane
24
Q

How HSV affects MHC I

A

HSV prevents its peptide from binding to TAP, so it cannot travel thru TAP to get to the ER, or memb, and remains undetected

25
Q

MHC II

A

-on APCs

26
Q

MHC II

A
  • on APCs, binds longer peptide that hangs out, 2 a and 2 B chains, genes HLA-DP/DQ/DR, presents EC pathogens (eg bacteria, allergens), presents antigen to CD4 cells
  • mech: CLIP (a portion of the invariant chain that was cleaved in an endosome) prevents peptides from binding to MHC II, but once HLA-DM binds MHC II, CLIP is released so the antigen peptides can bind, then travels to cell surface
27
Q

IgG digestion

A
  • Papain: digested into 3 fragments, one Fc and 2 Fab
  • Pepsin: digested into 2 fragments (Fc is degraded, but Fab2 has 2 arms/one seg)
  • Afelimonmab degrades Fc so cant react w macro so can block cytokine rel from macro
28
Q

Activation of B-cells T-cell independent antigens

A

Type 1 mitogen acts via TLRs on B cell surface to prolif

Type 2 polysac cross-link receptors

29
Q

T-cell maturation steps

A

Recognized processed antigen (as peptide fragments)

  • Thymocytes from marrow enter THYMUS via HEVs and undergo (+) selection in cortex (via cortical thymic epithelial cells, where they acquire a-B TCR and interact w/ thymus hormones), and (-) selection in medulla (via AIRE TF, w/ dendritic cells).
  • Had a-B chain rearrangement. Cells were first DN cells, then DP cells (expressing both CD4 and 8), then expressed only one (cytotoxic or helper)
30
Q

Linked recognition in vaccines

A 
A vaccine is a polysaccharide (similar to a sugar that would be on a bacteria etc) conjugated with a peptide protein (any kind). The B-cell specific for that vaccine’s sugar will bind. A helper T-cell specific for the conjugated peptide (can be anything) will also bind in order to activate that B-cell to produce antibodies for the sugar. The peptide type doesn’t matter, as long is it can be recognized by some T cell. the sugar is specific though, and the whole purpose of the peptide is to attract any T-cell, so that the B-cell can proliferate and produce antibodies for the sugar.
-(as sugar gets degraded by B cell, peptide also gets degraded by B cell and is presented in fragments on MHC II. Now a T-cell CD40L binds binds B. Now B-cell can under go class switching, aff maturation and som hypermut)
31
Q

How are most T-cells lost (95%)

A

From failure to bind with self MHC

32
Q

What do macrophages do?

A

Find antigen, then RELEASE CYTOKINES which RECRUIT inflammatory cells to area and increase vascular permeability

33
Q

Initial sensitization to allergen seq:

A

T cell induction, cytokine rel (???), then IgE prod

34
Q

Linked recognition in vaccines

A

A vaccine is a polysaccharide (similar to a sugar that would be on a bacteria etc) conjugated with a peptide protein (any kind). The B-cell specific for that vaccine’s sugar will bind. A helper T-cell specific for the conjugated peptide (can be anything) will also bind in order to activate that B-cell to produce antibodies for the sugar. The peptide type doesn’t matter, as long is it can be recognized by some T cell. the sugar is specific though, and the whole purpose of the peptide is to attract any T-cell, so that the B-cell can proliferate and produce antibodies for the sugar.

  • (as sugar gets degraded by B cell, peptide also gets degraded by B cell and is presented in fragments on MHC II. Now a T-cell CD40L binds binds B. Now B-cell can under go class switching, aff maturation and som hypermut)
  • B cell can bind anything

Inflammation Block (3 decks)

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