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(DIT) Rapid Fire + 4/5 Stars > Immunology > Flashcards

Immunology Flashcards

1
Q

Peyer’s patches

A

unencapsulated
in lamina propria and submucosa of ileum

Overlying epithelium - follicule associated epithelium

  • flattened w/ M (microfold) cells interspersed
  • take up antigens to basal side

Germinal center w/ B cells - IgA

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2
Q

Innate immune system

A

non specific
rapid response
no memory

macrophages
dendritic cells -APC - activate Th cells
neutrophils
mast cells
eosinophils
basophils
NK cells
complement proteins
skin and other barriers
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3
Q

adaptive immune system

A

very specific
memory
takes longer to get activated

T and B lymphocytes
circulating Abs

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4
Q

T cell markers

A

TCR - antigen specific
CD3
CD4 - Th –> MHCII
CD8- Tc –> MCHI

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5
Q

MHCI

A

all nucleated cells (Not on RBCs since no nucleus)

HLA-A, -B, -C

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6
Q

MHCII

A

APCs

HLA-DR, -DP, -DQ

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7
Q

Dendritic cells surface markers

A

MHC I, MHC II
B7 (CD 80/86) - costimulatory
CD40 - interact w/ T cells to further activate the APC

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8
Q

Dendritic cell function

A

Peripheral sentinel - immature or Ag capturing state

  • Phagocytosis
  • receptor-mediated endocytosis via clathrin coated pits
  • pinocytosis

migrate to LN via circulation to present to Th cells

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9
Q

Langerhans cells

A

in epidermal layers of skin

cutaneous associated lymphoid tissue - CALT

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10
Q

Interstitial dendritic cells

A

in interstitial spaces of all organs except brain

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11
Q

Langerhans cell histiocytosis

A

Excessive proliferation of Langerhans Cells
not good at APC

S100+
CD1a

Birbeck granules - tennis racket shape

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12
Q

Thymus organization

A

Outer - cortex - immature T cells

Middle - medulla - mature T cells

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13
Q

T cell positive and negative selection

A

Positive selection:
Cortex has MHC to test binding strength
Too strong or weak –> cell death
-survival signal keeps T cell alive –> specificity. Become only CD4 or CD8, lose the other marker

Negative selection:
Corticomedullary junction
-bind to self antigen –> apoptosis
–> naive T cell

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14
Q

Th0 cytokines to Th1 cells vs Th2 cells

A

Th0 release IL12 –> Th1
Th0 release IL4 –> Th2
Th0 release IL10 inhibits Th1

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15
Q

Th1 cells

A

stimulate macrophages and Tc
IL2 –> stimulate Tc and Th1, T reg prolif
IL3 - stimulate bone marrow stem cells (GM-CSF like)
IFN gamma –> activated Macrophages, suppresses Th2

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16
Q

Th2 cells

A

stimulate plasma cells to make Ab
IL4 - “BEG 4” - stimulates B cell prolif, IgE and IgG; induces Th0 –> Th2
IL5 - promote B cell growth, IgA production, stimulates eosinophils
IL 10 - inhibit Th1 cells and macrophages

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17
Q

B cell activation

A
  1. Th2 activated
  2. B cell endocytoses antigen bound to Ig presents to Th2
  3. Costimulatory signal CD40 on B binds to CD40L on Th2
  4. Th2 secretes IL4, IL5 –> proliferation of B cells and Ig class switching
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18
Q

Th cell activation

A

naive Th0 binds antigen from APC MHCII on TCR w/ CD4

costimulatory signal from B7 protein (CD80/86) bind CD 28

starts T cell producing cytokines

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19
Q

Tc activation

A

Tc binds antigen from APC/virus infected cell MCHI on TCR w/ CD8

CD28-B7 costimulatory

  • -> kills infected cells
  • -> clonal expansion
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20
Q

Cytokines produced by macrophages and dendritic cells

A

IL12

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21
Q

Function of Tc - CD8+ cells

A

bind MHCI on “self” cells
kills virus infected cells
kill cancer cells
kill transplant cells

release perforin and granzyme –> aopotosis

Fas-L activates Fas receptor –> apoptosis

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22
Q

Memory T cells

A

spleen and LN
inactive state
activated against pathogen
Allow live virus vaccines to induce life long immunity

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23
Q

T reg cells

A

inhibit B cells from producing Ab
inhibit Th and Tc cells
produce IL10
produce anti-inflammatory cytokines

If not working properly –> autoimmunity - atopic dz

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24
Q

FOXP3

A
  • on X Chr
  • transcription factor - controls development and function of Treg cells

mutations –> cant control immune system

IPEX syndrome

  • Immune dysreg: eczema
  • Polyendocrinopathy: T1DM, thyroiditis
  • Enteropathy - severe D, failure to thrive
  • X-linked
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25
Q

NK cell

A

innate immune
induce apoptosis in cells not expressing MHCI - down reg in virus infected and cancer cells

activity enhanced by:
IL12
IL2
IFN alpha and beta - secreted by virus infected cells

Secrete IFN-gamma –> macrophage activation

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26
Q

NK cell surface markers

A

CD56
CD16 –> Ab dependent cell mediated cytotoxicity (ADCC)
MHC I

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27
Q

CD16

A

NK cells

  • binds AB at constant region
  • -> ADCC

also found on macrophages, neutrophils, monocytes

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28
Q

B cell surface markers

A 
CD19
CD20
CD21
IgM
IgD
MHCI, MHC II
B7 (CD80/86)
CD40 --> activate B cell
29
Q

B cell stimulation

A

stimulated by IL4, IL5

activated B cells

  1. plasma cells –> Ab
  2. memory B cell –> dormant
30
Q

Macrophage surface markers

A 
CD14 - binds LPS endotoxin on gram - (--> activation)
CD16
MHC I, MHC II
B7
CD40 --> more sensitive to IFN gamma
31
Q

Passive immunity

A

preformed Abs - immediate immunity
IgA in breast milk
21 day t1/2

-RSV - Palivizumab - Ab against RSV
Rabies - rabies Ig shots

32
Q

Active immunity

A

exposure to foreign Ag
takes weeks to develop
–> memory T/B cells

Tetanus
influenza
MMR
pneumococcal

33
Q

Live vaccine

A

weak, attenuated
infect cells to present to Tc

  • -> cellular immunity
  • -> memory Tc cells
34
Q

Inactivated (Killed) vaccine

A

Ag to be presented

  • -> humoral immunity
  • -> memory Th cells
  • need booster doses
35
Q

Attenuated virus vaccines

A

“ATTENtion! Please Vaccinate Young Infants w/ MMR Regularly”

Attenuated virus vaccines (live)
Polio vaccine (sabin - oral)
Varicella
Yellow fever
Intranasal Influenza
MMR
Rotavirus

avoid in immunocompromised or those close to them
CD4>200 can give MMR, varicella, yellow fever

36
Q

Inactivated virus vaccines

A

IM influenza
HAV
Rabies
Salk polio -inected form

37
Q

Egg based vaccines

A

influenza
yellow fever

(MMR - very small amount)

38
Q

Thymus-dependent Ag

A

present peptides via MHC to T cells in thymus –> B cell activation

better immune response and immunologic memory

39
Q

Thymus independent Ag

A 
LPS
-non peptide Ag
-cannot present to T cells in thymus
no T cell response
B cell response weaker --> weaker immune memory
boosters needed
40
Q

Bacterial vaccines

A

Toxins - tetanus toxoid

Capsular polysaccharides
-S pneumo, H flu

killed bacteria - vibrio cholerae

Live attenuated bacteria

  • Typhoid vaccine
  • BCG vaccine

–> humoral response to T cell response since not infecting cells

41
Q

C1 inhibitor

A

aka C1 esterase inhibitor

inhibits cleavage of C1 starting point of classical pathway

42
Q

Classic pathway of compliment activation

A

IgG or IgM bind Ag then binds C1 complement protein

43
Q

Alternate pathway of compliment activation

A

molecules on surface microbe or spontaneously

44
Q

Lectin pathway of compliment activation

A

mannose binding lectin binds mannose on surface of microbe

45
Q

Membrane attack complex

A

C5b, C6-C9

46
Q

Oposonizing proteins

A

C3b

IgG

47
Q

Anaphylaxis complement

A

C3a, C5a

48
Q

Complement stimulating mast cells and basophils

A

C3a

49
Q

Complement responsible for neutrophil chemotaxis

A

C5a

50
Q

Paroxysmal nocturnal hemoglobinuria (PNH)

A

Complement mediated damage of RBCs by MAC complex

  • deficient in Glycosylphosphotidylinositol (GPI) which anchors decay accelerating factor (DAF) (CD55) to plasma membrane
  • deficient MAC-inhibitory protein (CD59)

Present with:

  • chronic intravascular hemolysis
  • hemosiderinuria - red urine
  • thrombosis

Dx: Ham’s test - RBC in acid lyse in low pH - diagnostic
-Flow cytometry - CD55/CD59 not present

Tx:
transfusion
warfarin
Eculizumab - inhibits complement

51
Q

Deficiency of C1 esterase inhibitor

A

Hereditary angioendema
increased bradykinin
never take ACEI with these –> higher bradykinin

52
Q

Deficiency of C3

A

recurrent pyogenic sinus infections and respiratory tract infections
-S. pneumo, H. flu

increased susceptibility to type III hypersensitivity
-esp glomerular nephritis - can’t clear out immune complexes

53
Q

Deficiency in any of the MAC complement components

A

susceptible to Neisseria bacteremia

54
Q

Deficiency in Decay accelerating factor (DAF) - CD55

A

protects self from spontaneous activated complement

–> Paroxysmal nocturnal hemoglobinuria (PNH)

55
Q

Function of spleen

A

Macrophages remove damaged RBCs and encapsulated bacteria

sequesters and stores platelets and RBCs
-Thrombocytopenia in splenomegaly - more platelets sequestered in larger spleen

56
Q

Asplenia

A

risk recurrent infections

sickle cell - autoinfarct
Trauma
hereditary spherocytosis - splenectomy to tx hemolytic anemia

57
Q

Macrophage secreted cytokines

A

IL1, IL6, TNF alpha - acute phase reactants

  • mediate fever, ramp up immune system
  • TNFa - septic shock, recruit leukocytes

IL12: Th0 –> Th1; activate NK cells

IL8: neutrophil chemotaxis

58
Q

Macrophage function

A 
present Ag to T cells
secrete cytokines
Phagocytosis of bacteria opsonized w/ IgG or C3b
-digests in lysosome
-NADPH oxidase --> free radicals

Kill w/o phagocytosis via Ab-dependent cell mediated cytotoxicity (ADCC)

Form granulomas - combine to form multinucleated giant cells
-secrete Vit D

59
Q

Mast cells

A

mucosa o fskin

granules: histamine –> type I HSR

Cromoyn blocks mast cell degranulation

  • asthma tx- inhaled
  • allergy nasal spray
60
Q

Monocytes

A

Leave bone marrow for blood –> circulate 8-12 hours to mature –> migrate into tissues

Skin, connective tissue: dendritic cells (histiocytes) –> LN

Alveoli, intestines, spleen: macrophages - stay put

Liver - kupffer cells
Brain - microglia
Bone - osteoclasts
Joints - type A synoviocytes - clean synovial fluid
(type B similar to fibroblasts, secrete hyaluronic acid)

61
Q

Differential diagnosis for eosinophila

A

“CANADA-P”

Collagen vascular disease (PAN, dermatomyositis)
Atopic dz (allergies, asthma, Churg-Strauss, allergic bronchopulmonary aspergillosis)
Neoplasm
Adrenal insufficiency (addison dz)
Drugs (NSAIDs, PCN, cephalosporins)
Acute interstitial nephritis
Parasites (Strongyloides, Ascaris –> Loeffler eosinophilic pneumonitis)

Other causes: HIV, hyper IgE syndrome, coccidioidomycosis

62
Q

IL1-IL5 function

A

“Hot T-Bone stEAk”

IL1: fever
IL2: stimulates T cells
IL3: stimulates Bone marrow
IL4: stimulates switch to IgE and IgG
IL5: stimulates switch to IgA, eosinophils
63
Q

IFNa and IFNb as antiviral

A

help neighboring cells avoid virus infeciton

inhibit cell protein synthesis
encourage activation of ribonuclease that degrades viral mRNA

activates NK cells

64
Q

IFN gamma as antiviral

A

stimulate macrophages

65
Q

Hyperacute rejection

A

within minutes to hours
type II HSR
-preformed Ab in host to donor Ag

66
Q

Acute rejection

A

within 3 mo
cell mediated
Tc recognize foreign MHCI

give immunosuppressants to block IL2

67
Q

Chronic rejection

A

months to years
T cell and Ab mediated

Th cells generate inflammation via interleukins –> vascular damage and fibrosis

Irreversible

68
Q

Graft vs host disease

A

transplanted immune cells via bone marrow graft

graft T cells proliferate and attack host as foreign

maculopapular rash on neck, shoulders, ears, hands, trunk
-can blister

hemolysis, jaundice
HSM
Abd pain, N/V/D

(DIT) Rapid Fire + 4/5 Stars (162 decks)

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