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MMMD 1 - QH > Immunology > Flashcards

Immunology Flashcards

1
Q

1ary vs 2ry lymph tissues?

A

1ary: bone marrow, thymus for maturation
2ary: all other lymphoid tissue: nodes, spleen, tonsils, MALT, GALT

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2
Q

Anatomy of lymph node - where are macrphoages, B, Ts

A
  • medularry cords: macrophages, plasma cells
  • paracortical area: T cells
  • cortical area: B cells and germinal centres
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3
Q

Where are we most prone to infection and what structures are there to help?

A

tracts:

  1. gastrointestinal: tonsils and adenoids; peyer’s oatches, intestines have most lymphocytes in body
  2. resp
  3. urogenital
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4
Q

Macrophages?

A
  • phagocytosis!
  • apc
  • repair
  • secrete pro-inflamm cytokines
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5
Q

Neutrophil?

A

lots in blood; 1st line after epithelial/mast cells

  1. phagocytosis
  2. degranulation to kill
  3. NETs - form net with antimicrobial peptides to kill
  4. signal to recruit others
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6
Q

Eosinophils?

A
  • kill ab-parasites

- in allergic rxns

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7
Q

Basophils?

A
  • unknown
  • similar to mast cells
  • allergic rxns
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8
Q

Mast cells?

A
  • release granules iwith vasoactive amines

- anaphalyxis, type 1 hypersen

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9
Q

What are TLRs?

A

toll like receptors

  • pathogen-associated molecular pattern receptors on cells
  • each TLR recog one type of microbial component
  • can be at membrane surface or intracellular
  • binding > signalling cascade > transcription factor (NF-kB) > protein production to respond > cytokines
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10
Q

Dendritic cells?

A
  • apc
  • migrate to lymph nodes to activate lymphocytes
  • link innate and adaptive
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11
Q

Role of antibodies?

A
  1. neutralization - binds toxin, viruses
  2. opsonization
  3. complement activation via classical pathway
  4. activate other cells
  5. RECOGNIZE specific epitopes not just patterns of antigen protein
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12
Q

How is tolerance obtained?

A
  • delete autoreactive T cells in thymus
  • delete autoreactive B cells in bone marrow
  • anergy of autoreactive cells after development
  • Tregs suppressing fnc
  • immunoinhibitory receptors
  • presence of barriers for priveleged sites
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13
Q

List components of INNATE immune system:

A
  • physical barriers: skin, pH, mucus
  • mast cells
  • neutrophils
  • macrophages
  • NK cells
  • dendritic cells

-non specific recognition (patterns); killing; signals for inflame; activation of adpative immune cells; no memory

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14
Q

How does innate system recog pathogen?

A
  1. TLR recognizing PAMP

2. inflammasome: cytoplasmic proteins send danger signal in presence of PAMPS > IL1 secretion to initiate inflamm

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15
Q

linking bt innate and adaptive

A

Dendritic cells
cytokines (from macrophages)
complement cascade

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16
Q

What are the chemical (non cellular) components of immune system?

A 
4 C's:
Cytokines
Complements
Chemokines
Coagulation
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17
Q

What is phagocytosis? Who does it?

A

-recognition: TLR, Fc, mannose, complement
-pseudopod to surround pathogen
-engulf
-phagolysosomal fusion > digestion
» also lead to antigen presentation, and cytokine release
-neutrophils, macro, B cells, dendritic cells

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18
Q

How does immune system kill?

A
  1. Phagocytosis
  2. complement cascade
  3. ADCC: antibody-dependent cell mediated cytotoxicity
    - ab opsonize for NK cells, neutrophils, eosinophils to relesase granules for killin
  4. Defensins: antimicrobial from neutrophils
  5. Pentraxins; link pathogen adn phagocyte
19
Q

Purpose of complements?

which one is important?

A
  1. direct killing (MAC) - C5b onward
  2. opsonization -C3b
  3. recruiting inflammatory cells -C3a, C5a
20
Q

Role of cytokines?

ex:

A

-activate other cells
-chemotaxis
-activate liver to secrete proteins: complements, opsonization
-on bone marrow to recruit neutrophils
-on hypothalamus, fat, muscle > fever
-on dendtritic cells >migration and link adaptive response
IL1, IL6, IL12, TNFalpha

21
Q

Why is C3 impt?

A

activation of complement > C3 convertase metabolizing C3 > C3a: ENDO PERM, activation of phagocytes = inflammation
>C3b (bigger piece): opsonization with receptor for phagocytes

def: recurrent infections

22
Q

Early vs late complement cascade?

what if deficiency?

A 
early: binds antigen-ab complexes > C3 activation
def > not so serious b.c of multiple pathways to C3
C4 def in SLE
late: killing via MAC (creates holes in membrane)
def > serious inf (gonorrhea, meningitis)
23
Q

Describe B cell development

A

develops in bone marrow:
>ProBcell: commits to B cell line
>preBcell receptor: heavy chain gene rearrangement. checks for functional heavey chain else apoptosis.
>light chain gene rearrangement
>Bcell receptor. checks for functional else.
=Immature B cell with IgM expression
>exposed to self-antigen. Only those that DO NOT self-recog can leave bone marrow

Home via chemokines in blood > activated when in contact with antigen > diff, proliferate, mature:
IL10 >plasma cells > goes to bone marrow > produce antibodies > IgM first then others
IL4 > Memory B cells > IgG early response next time

24
Q

Antibody structure, production, response

A
  • Fc-constant for binding to receptors on phagocytes
  • Fab-variable for recognition of antigen
  • antibodies: opsonize, neutralize, activate complements, activate cells
25
Q

Antibody isotypes and fncs

A

IgG: in serum, tissue, cross placenta. small. opson & complement activation

IgA: dimeric. in secretions (tracts!). Neutralization - bind and excrete. Week ops and activation.

IgM: first response. pentameric. big so not diffused well. in circulation. CANNOT recruit other cells. activate complements

IgE: trace amounts in serum. bound to mast cells under skin/mucosa > reactions to expel pathogen.
-allergies, parasites

IgD - didn’t mention

26
Q

B cell tolerance

A

Central:

  • immature B cell exposed to self-antigen. If recognize self > negative signal for apoptosis = NEGATIVE SELECTION
  • TOLERANT B cells can leave bone marrow
27
Q

Clonal selection hypothesis?

A

-common precursor cell > remove self-reactive immature lymphocytes > antigen presence would activate proliferation of specific lymphocyte differentiation

28
Q

Describe B cell genetic Recombination

A

*must generate large repertoire of antibodies, but each must only recognize one specific antigen. < done via GENETIC RECOMBINATION > diveristy!
Bone Marrow:
-3 gene segments on antibody VARIABLE region rearranged and assembled:
-heavy chain: random V, then random D+J added to V
-light chain: kappa then lambda
-Heavy and light chain combination
*antigen independent

Lymph node: under specific signals
-isotype switching - recombination of CONSTANT genes

29
Q

Describe B cell activation in lymph nodes.

1ary vs 1ary focus?

A
  • goes to lymph node vis HEV
  • surface antibody-antigen binding + coreceptor binding
  • also helped by Thelper cells that recogn same antigen> express CD40L to CD4 on B cell + cytokine binding
  • PRIMARY FOCUS: clonal expansion adn IgM in medullary cords
  • 2ary FOCUS: B cell move to cortical area > germinal center > later better response. Needs presence of Thelper cell, follicular dendritic cells, activated B cells
30
Q

What occurs in a germinal centre?

A

-activated B cells under strong cytokine signalling and interaction with dendritic cell, antigen, Thelper > rapid proliferation
-SOMATIC HYPERMUTATION occurs > B cells with higher affinity for antigen selected for = AFFINITY MATURATION
-ISOTYPE SWITCHING: recombination of CONSTANT genes expressed for same V region
»swollen lymph nodes. 1 wk post infection

31
Q

T cell development

A

-Precursor formed in bone marrow
> arrive thymus: VJ rearrganement of TCR + positive selection + negative selection:
-Rearrange B chain - DJ then VDJ. CHECK PreT cells
-proliferate as DOUBLE NEGATIVE PreTcell. CHECK
-DOUBLE POSITIVE Immature T cell
-Rearrage alpha chain - VJ. CHECK. Now DOUBLE POSITIVE mature T cell (have both CD4 and CD8 receptors)
-positive selection- keep those that can recog self MHC and only express one CD coreceptor
-negative selection-rid those that can recog self antigen

  • mature, self-restricted, self-tolerant, single positive NAIVE Ts migrate to 2ry lymphoid
  • becomes effector cells after antigen exposure > proliferation and differentiation
32
Q

CD4T vs CD8 T?

binds which MHC

A

*a:B TCRs
CD4
-help other cells; extracellular pathogens
-binds MHC 2

CD8

  • kill cells with virus/intracellular pathogens
  • binds MHC1
33
Q

T cell tolerance

A
  • Positive selection - can T cell bind self MHC? Yes - keep.
  • Negative selection - can T cell bind MHC with self antigen? Yes - RID!
  • test in medulla of thymus with APCs presenting peptides made by apcs, from macrophages, from extracellular fluid, and peptides of things outside thymus transcribed by AIRE gene
  • priveleged sites
  • Peripheral tolerance mechanisms:
  • Treg suppression of naive autoreactive cells (natural in thymus; inducible in periphery); foxp3 transcription factor
  • anergy of autoreactive cells
34
Q

Immunological memory?

A

-2ry immune response
-B cells, T cells, antibodies of previous infection remain
>faster, stronger response next time
-long lived cells maintained by cytokines

35
Q

What is B-T cognate interaction?

A

-antigen recogn > induce expression of CD40L and cytokines from Th2 cells > activate B cells

36
Q

What is MHC?
What is MHC Restriction?
How is MHC diversity achieved?

A
  • major histocompatibility complex
  • antigen protein needs to be fragmented and specific epitope presented on MHC for TCR to recognize
  • can bind many different aa sequences (motif)
  • T cell is specific to that antigen on that MHC
  • no recombination
  • diveristy is inherited from each parent
37
Q

MHC 1 vs 2? which cells have which?

binds to which T cells?

A

MHC I: on all nucleated cells
-binds CD8T for intracellular infections

MHC II: on apcs
-binds CD4T for extracellular infections

38
Q

How are antigens presented?

A

-APCs take up: endocytosis or comes in
-degrade: phagolysosomes or proteasomes
-proteins unfolded adn cut
-specific peptide bind to MHC adn brought to surface
MHC II: produced and fuse with vesicle containing antigen while MHC I: have peptides brought to ER and packaged together
-T cell comes by and bind…

39
Q

How are T cells activated?

A

-from APCs: dendritic cells, macrophages, B cell
1. TCR bind MHC with specific antigen
2. Co-stimulation: CD28 with CD80 (B7) ligand on APC
»gene transcription > cytokines > effects on other immune cells
ex: IL2 > further proliferation of T cells

> > effector T cells don’t need costimulation to respond!

40
Q

What is anergy? How?

A
  • T cell can’t be activated
  • MHC and antigen signal but NO costimulation
  • helps to prevent activation to self-antigen
41
Q

Type of CD4 Helper T cells?

which cytokines are impt?

A

Naive CD4 T cells can differentiate to diff effectors under diff cytokines:

  • Th1 - activate macrophage (IFN-gamma)
  • Th2 - activate B cells (IL4, IL5)
  • Tfh - activate B cells to form germinal centre (IL21, IL4)
  • Th17 - enhance neutrophil response where Th1 and Th2 not enough; autoimmune. (IL17, IL6)
  • Treg - suppressor T (TGF-beta, IL10)
42
Q

How does TB hide from immune system?

A
  • hides from lysosomal degradation > can’t be presented by MHCII
  • does not enter cytoplasm > can’t be proteasased > can’t be presented by MHCI
  • T cells can’t recognize.
  • T cells surround the APCs with TB = granuloma
43
Q

How does leprosy present differentially depending on host response?

A

cytokine levels > certain cell differentiation

  • bias toward Th1 response > cell mediated presentation: macrophages can suppress > slow > damage to skin and nerves
  • bias toward th2 > antibodies can’t access bacteria in macrophages > bacteria grow > severe destruction!

MMMD 1 - QH (7 decks)

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