Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nutrition > Recap 5 > Flashcards

Recap 5 Flashcards

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

RAG1 et RAG2 genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

CD2
Integrin
CD28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do Treg express, produce?

A

CD25+
Produce IL4, IL10, TGFB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Examples of superantigen

A
  • Chaine VB TCR
  • a CMH II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the R for ligand C3b and C3d?

A

CD21 (CR2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What receptors do monocytes express?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Receptor of white pulp macrophage (corps tingibles)

A

CD68

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Importance of DC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

R for Langerhans

A

CD207

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cytokines in innate and adaptive response

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Autoimmune regulator = AIRE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Agammaglobulinemia :
Clinic
Mutation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Deficiency in C3 complement

A

Most serious
Autosomal recessive
Deletion = stop codon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Deficiency in factor H of complement

A

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
Q

Deficiency in C1 inhibitor

A

Autosomal dominant
Hereditary angioedema

29
Q

Chediak-Higashi syndrome :
Mutation
Defect in

A

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
Q

Detection of ANA via indirect immunofluorescence

A
  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
Q

Acute and chronic graft rejection

A
  • 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
Q

Pathogenesis of hyperacute graft rejection**

A

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
Q

Pathogenesis of acute graft rejection

A

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
Q

Pathogenesis of chronic rejection

A

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
Q

Defects in leucocytes fct

A

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
Q

X-linked SCID
Defects

A

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
Q

Autosomal recessive SCID

A

Deficiency in enzyme adenosine deaminase (ADA) = accumule deoxyadenosine = toxic to rapidly dividing LT

38
Q

HyperIgM syndrome mutation

A

Mutation in CD40L

39
Q

What do senescent cell express?

A

Senescence-associated B-galactosidase

40
Q

Role of mTOR

A

Major inhibitor of autophagy

41
Q

Steps of tumor development

A
  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
Q

By what are encoded tumor specific shared AG

A

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
Q

Tumor immunosuppressive secretory products

A

TGFa = inhibe function/prolif of lympho and macro
FasL = binds Fas-R on LT and trigger apoptosis

44
Q

Epithelial-mensenchymal transition morpho

A

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
Q

By what is facilitated cell migration and vessel penetration

A

By tumor associated macrophages that accompany invading tumor cells

46
Q

Cause of neurological syndrome in cancer

A

HyperCa, hypoglycemia, hyperviscosity

47
Q

Mechanisms of retroviral genomes (replicate after insert in animal genome)

A

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
Q

Cause of amplification mutation

A

DNA polymerase slippage during replication

49
Q

Germline mutations and cancer syndrome :
1. Multiple endocrine neoplasia
2. Hereditary renal cystadenocarcinome

A
  1. Multiple endocrine neoplasia = MEN1, RET
  2. Hereditary renal cystadenocarcinome = BHD locus
50
Q

Effet of DNA methylation ***

A

Add of methyl group to cytosine beside guanine (CpG dinucleotide) = cytosine - phosphate - guanine
HYPOMETHYLATION = gene activation (++ promoter region)
HYPERMETHYLATION = gene silencing

51
Q

Effet acetylation of histone

A

Hausse acetylation = hausse transcription (chromatine lâche)
Deacetylase = baisse transcription

52
Q

Role of mismatch repair enzyme MLH1, MSH2

A

Proof-read DNA to locate and fixe single nucleotide mismatch during normal DNA synthesis

53
Q

Effects of radiation

A

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
Q

Papillomavirus mechanism

A

E6 inhibe p53
E7 inhibe pRb

55
Q

R-tyrosine kinase in cancer

A

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
Q

Mutation of downstream component of tyrosine kinase in cancer

A
  • 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
Q

Functions of MYC***

A
  • 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
Q

Mechanism of p53 after release from inhibitory state of MDM2 in DNA damage/hypoxia and oncogenic stress

A

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
Q

Immunosuppressive factors secreted by cancers

A

TGFB
IL10
PGE2
Metabolites from tryptophan
VEGF

60
Q

What is the hallmark of mismatch repair defects

A

Microsatellite instability

61
Q

What is the most common mechanisms that activate prot-oncogene?

A

Chromosomal translocations

62
Q

Burkitt vs LB lymphoma with epstein barr virus

A

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
Q

What do nasopharyngeal carcinome express?

A

LMP-1 (active NFkB = upregule VEGF, FGF, MMP, COX2) and PD-L1

64
Q

Effects of hepatitis B virus

A

Random integration in genome
Active NFkB blocks apoptosis, dividing hepatocytes undergo genotoxic stress and accumulate mutation
Has some gene that directly promotes cancer

65
Q

Mechanisms of helicobacter pylori

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions