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Recap 5 Flashcards

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1
Q

Examples of PRR (recognize DAMP, PAMP)

A
  • Collectin = active complement
  • Pentraxin = active complement (include C-reactive protein)
  • TLR
  • Cytosolic PRR
    RIG (viral nucleic acid)
    NLR (microbial DNA, activate STING pathway -> IFNy)
  • C-type lectin-R (fungi)
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2
Q

Signaling of TLR

A
  1. Binding of PAMPs active TIR (TLR1) which forms complex MyD88 (IL1-R associated kinase - IRAK) and TRAF6 -> activated TRAF activates MAPK cascade -> active NFkB (cytokines and adhesion molecules and interferon-regulatory factors IRF (antiviral cytokine, type 1IFN)
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3
Q

What are the enzymes mediating recombination of AG receptors for lymphocytes?

A

RAG1 et RAG2 genes

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4
Q

What are innate lymphoid cells (ILC)?

A

Heterogenous population of nonB nonT lympho not AG-Sp
Tissue resident lympho that lack LT-AG-R = can’t respond to AG but activated by cytokines produced at sites of damage

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5
Q

Groups of ILC***

A

GROUP 1
Transcription regulated by T-bet, IL7, IL15
Produce IFNy and TNF
IC bacteria and parasites
GROUP 2
Transcription regulated GATA-3, NOTCH, IL25, IL33, TSLP, TL1A
Produce IL4, IL5, IL9, IL13, Areg
Helminths, asthma, allergy
GROUP 3
Regulated by RORyt
Produce IL17, IL22, GM-CSF
Stimulated by AHR ligand, IL18, IL23

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6
Q

LT receptors (TCR)

A

1- aB-TCR (most peripheral blood lymphocytes) - covalently linked to 5 polypeptide chains = 3 CD3, 2 B-chain -> act as signal transduction after binding
- CD4+, CD8+
2- yd-TCR (intraepithelial lympho) - recognize peptides, lipides and small molecules without CMH - produce cytokines, CTL, induce/suppress CD4+, present AG
- early cell mediated immune response in neonates (CD3+)
3. NK-T lymphocytes - recognize glycolipids associated with CD1 (CMH-like molecule)
Genes for a, B, y, d chain undergo somatic rearrangement in thymus

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7
Q

Other molecules expressed on the surface of LT that assist TCR complex

A

CD2
Integrin
CD28

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8
Q

What do Treg express, produce?

A

CD25+
Produce IL4, IL10, TGFB

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9
Q

Examples of superantigen

A
  • Chaine VB TCR
  • a CMH II
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10
Q

What is the R for ligand C3b and C3d?

A

CD21 (CR2)

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11
Q

Function of Thelper

A

CD4+ LT recognixe AG displayed on APC, LT express CD40L engages CD40 on macrophages or LB = active these cells
Combination of CD40 and IFNy mediated activation = M1 macro

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12
Q

Types of activation of humoral activity

A
  1. T-dependent activation : LB recognize AG by Ig-R -> endocytosis -> degrade -> display peptides bound to CMH II for recognition by Th (CD40L, Ig isotype switching need LThelper)
  2. T-independent : polysaccharide and lipid AG can’t be rexognized by LT bc can’t bind to CMH, but have many epitopes that engage AG-R on LB -> LB activation -> stimule IgM production
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13
Q

What receptors do monocytes express?

A

CSF-1 (CD115)
CX3CR1
Blood monocytes = CD14, CD16

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14
Q

Receptor of white pulp macrophage (corps tingibles)

A

CD68

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15
Q

Importance of DC

A

Important for negative selection (thymus) and maintenance of peripheral tolerance

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16
Q

R for Langerhans

A

CD207

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17
Q

Molecules expressed by NK
Activation
Effectors

A

CD16 (R for IgG Fc tail)
CD56
CD2 (IL2-R)
Activated by IFNy, IFNB, IL12-15-18
Effectors = perforin, TNF

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18
Q

Cytokines in innate and adaptive response

A

Innate = TNF, IL1, IL12, IFN 1, IFNy, chemokines
Adaptive = IL2, IL4, IL5, IL17, IFNy

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19
Q

Phase of hyperS I

A

Sensitization phase = binding of AG-Sp IgE to Fce on mastocytes
Effector phase = binding of AG to IgE on mast cells
Immediate phase = release vasoactive amine
Late phase = intense inflammation ; eosino, neutro, baso, macro, CD4+ -> tissue damage

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20
Q

Major cytokines released from mast cells during hyperS I

A

IL4, IL5 = contribute to LB activation, IgE synthesis
IL5 = chemotactic for eosino
IL6, TNFa = shock

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21
Q

By what is the expression of peripheral AG in thymus regulated?

A

Autoimmune regulator = AIRE

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22
Q

Mechanisms of autoimmunity

A
  1. Genetic factors
    - +++CMH
    - Defects Fas or FasL, lack of AIRE, defect in CTLA-4 (LT anergy), IL2-R (Treg)
    - HLA alleles
    - Association of non CMH genes
    PTPN22 = encode tyrosine phosphatase -> mutation = excessive lympho activation
    NOD2 = cytoplasmic sensor of microbes -> mutation = entry and chronic inflamm of commensal bact
  2. Microbial agent
    - some cells induced by IFNy increase expression of CMH during inflamm
    - molecular mimicry
    - some virtus cause polyclonal LB activation with prod of autoAC
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23
Q

SCID in horse ;
Mutation

A

Autosomal recessive
Spontaneous mutation in gene encoding catalytic subunit of a DNA-dependent protein kinase
- required for recombination of Ig heavy chain and TCR genes during developement
- defect in DNA repair mechanisms

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24
Q

SCID in dogs
Clinic
Mutation

A

Lymphopenia, increase B, fewer to no T
Hypogammaglobulinemia, normal IgM, decrease IgG, IgA
Mutation in the common gamma subunit of IL2-4-7-9-15 receptor = LT nonfct because can’t express functional IL2-R

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25
Agammaglobulinemia : Clinic Mutation
Inability to produce Ig and absence of mature LB and plasma cells Probably Xlinked Mutations BTK = encoded tyrosine kinase that arrest LB development at pre-B stage EC bacterial infection
26
Deficiency in C3 complement
Most serious Autosomal recessive Deletion = stop codon
27
Deficiency in factor H of complement
Regulatory component of complement activation = block formation of C3 convertase and cofactor of C3b cleavage by factor I = unregulated elaboration of C3b on activation
28
Deficiency in C1 inhibitor
Autosomal dominant Hereditary angioedema
29
Chediak-Higashi syndrome : Mutation Defect in
Mutation in Lyst gene (regulates IC protein trafficking) Defects : Lysosome Melanosome (hypopigmentation) Platelet dense granules = excessive bleeding Cytolytic granules (neutro) = recurrent infections Defect in NK cells Ocular abnormalities
30
Detection of ANA via indirect immunofluorescence
1. Homogenous or diffuse nuclear staining = AC chromatin, histone, double-stranded DNA 2. Rim or peripheral staining = double stranded DNA, nuclear envelope 3. Speckled = Ac to non-DNA nuclear constituents 4. Nucleolar pattern = AC to RNA 5. Centrometric pattern = AC to centromeres
31
Acute and chronic graft rejection
- Direct pathway = graft AG presented directly to LT by graft APC = CTL mediated ACUTE rejection - Indirect pathway = graft AG picked by host APC and presented to LT = CHRONIC rejection
32
Pathogenesis of hyperacute graft rejection**
Preformed AC linked to endothelial cells -> activation of complement -> endothelial injury, thrombosis, ischemic necrosis, arterioles fibrinoid necrosis Rare because cross-match and blood type testing
33
Pathogenesis of acute graft rejection
Mediated by LT and AC (days/weeks) - Acute cellular rejection = CTL directly destroys graft, CD4+ secrete cytokines -> damage - Acute AC-med rejection = AC bind to vascular endothelium -> complement via classical pathway -> damage
34
Pathogenesis of chronic rejection
Months/years LT reacts against graft alloAG and secrete cytokines stimule prolif of fibroblasts and vascular smooth muscle cells Refractory to most tx, principal cause of graft failure Depletion of donor LT before transfusion eliminate dz but recurrence of leukemia, graft failure and LB lymphoma increase
35
Defects in leucocytes fct
1- defect adhesion type 1 = B2 chain (LFA, MAC1) 2- defect adhesion type 2 = absence Sialyl-Lewis X bc of defect in fucosyl transferase 3- chediak-higashi syndrome = defect fusion phagosome et lysosome
36
X-linked SCID Defects
Defects in y-chain subunit of cytokokines-R = IL11, IL15, IL21 IL7 = prolif lymphoid progenitor IL15 = prolif NK LT reduced, LB normal but reduced synthesis of AC
37
Autosomal recessive SCID
Deficiency in enzyme adenosine deaminase (ADA) = accumule deoxyadenosine = toxic to rapidly dividing LT
38
HyperIgM syndrome mutation
Mutation in CD40L
39
What do senescent cell express?
Senescence-associated B-galactosidase
40
Role of mTOR
Major inhibitor of autophagy
41
Steps of tumor development
1. Initiation = cell morphologically normal with irreversible genetic changes = provide growth advantage under some conditions 2. Promotion = not mutagenic = reversible = create proliferative environment End of promotion phase = BENIGN TUMOR 3. Progression = irreversible, genetic/epigenetic changes, alteration in tumor environment
42
By what are encoded tumor specific shared AG
Encoded by genes that have a very limited expression in adult tissue but that are expressed by many types of tumor tissues Ex : MAGE
43
Tumor immunosuppressive secretory products
TGFa = inhibe function/prolif of lympho and macro FasL = binds Fas-R on LT and trigger apoptosis
44
Epithelial-mensenchymal transition morpho
Loss of intercellular adhesion (= little to no E-cadherin) Enhance expression of protease Mirgatory capabilities Reduced expression of cytokeratine De novo expression of vimentin
45
By what is facilitated cell migration and vessel penetration
By tumor associated macrophages that accompany invading tumor cells
46
Cause of neurological syndrome in cancer
HyperCa, hypoglycemia, hyperviscosity
47
Mechanisms of retroviral genomes (replicate after insert in animal genome)
Interrupt coding sequence of animal genes, abrogating their expression -> abnormal gene products Juxtaposition of viral promoter elements adjacent to cellular coding sequences of host -> dysregulated expression of gene (often increase)
48
Cause of amplification mutation
DNA polymerase slippage during replication
49
Germline mutations and cancer syndrome : 1. Multiple endocrine neoplasia 2. Hereditary renal cystadenocarcinome
1. Multiple endocrine neoplasia = MEN1, RET 2. Hereditary renal cystadenocarcinome = BHD locus
50
Effet of DNA methylation ***
Add of methyl group to cytosine beside guanine (CpG dinucleotide) = cytosine - phosphate - guanine HYPOMETHYLATION = gene activation (++ promoter region) HYPERMETHYLATION = gene silencing
51
Effet acetylation of histone
Hausse acetylation = hausse transcription (chromatine lâche) Deacetylase = baisse transcription
52
Role of mismatch repair enzyme MLH1, MSH2
Proof-read DNA to locate and fixe single nucleotide mismatch during normal DNA synthesis
53
Effects of radiation
All forms are carcinogens = initiate and promote tumorigenesis Direct DNA damage by ionizing radiation = single or double stranded breaks and base elimination Absorbe UV by DNA -> forms pyrimidine dimers (mutagenic) Generate ROS (DNA damage = altered base, strand break, cross-link)
54
Papillomavirus mechanism
E6 inhibe p53 E7 inhibe pRb
55
R-tyrosine kinase in cancer
Most important in cancer Normally : bind GF -> dimeric state -> autophosphorylate tyrosine residues on IC tail = recruit other signaling molecules RAS,m PI3K In cancer = doesn’t need GF for activity
56
Mutation of downstream component of tyrosine kinase in cancer
- Point mutation of RAS - MAPK activating mutation of BRAF = active transcription factor - Gain of fct of PI3K or loss of fct of PTEN (regulator)
57
Functions of MYC***
- Some targets (cyclin D) involved in cell cycle progression - Upregulates expression of rRNA = enhance assembly of proteins in ribosome - Upregulate gene expression needed for metabolic reprogramming and Warburg effect - Sometimes upregulate expression of telomerase - Rare transcription factor contributing to reprogramming somatic cells into pluripotent cells Mutation of RAS/MAPK, Notch, hedghog -> upregulate MYC
58
Mechanism of p53 after release from inhibitory state of MDM2 in DNA damage/hypoxia and oncogenic stress
DNA/hypoxia -> ATM and ATR stimule phospho of p53 and MDM2 -> disrupt binding and degradation of p53 = p53 accumule Oncogenic stress -> active RAS -> sustained growth signal (MAPK, PI3K/AKT) -> cellular stress -> increase expression of p14/ARF = binds to MDM2 and displace p53 -> p53 accumulate
59
Immunosuppressive factors secreted by cancers
TGFB IL10 PGE2 Metabolites from tryptophan VEGF
60
What is the hallmark of mismatch repair defects
Microsatellite instability
61
What is the most common mechanisms that activate prot-oncogene?
Chromosomal translocations
62
Burkitt vs LB lymphoma with epstein barr virus
Burkitt = don’t express LMP-1, EBNA-2 and other EBV proteins (EBV not directly oncogenic act as mitogen) LB = express LMP-1, EBNA-2 are antigenic and would be recognize by CTL in normal people
63
What do nasopharyngeal carcinome express?
LMP-1 (active NFkB = upregule VEGF, FGF, MMP, COX2) and PD-L1
64
Effects of hepatitis B virus
Random integration in genome Active NFkB blocks apoptosis, dividing hepatocytes undergo genotoxic stress and accumulate mutation Has some gene that directly promotes cancer
65
Mechanisms of helicobacter pylori
Gastric adenocarcinoma : Pathogenicity island that contains cytotoxin-associated A (CagA gene) penetrate epithelial cells and initiae signaling cascade that mimics upregulated growth factor stimulation Gastric LB lymphoma : H.pylori reactive LT stimule polyclonal LB prolif to grow into monoclonal MALToma dependent on LT stimulation Early stage = ATB cure by removing AG stimulation Later = no because of additional mutations

Nutrition (13 decks)

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