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Immunology Flashcards

1
Q

LN drainage: what does the celiac LN cluster drain?

A 
Liver
Stomach
Spleen
Pancreas
Upper duodenum
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2
Q

LN drainage: what does the superior mesenteric LN cluster drain?

A

Lower duodenum
Jejunum
Ileum
Colon to splenic flexure

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3
Q

LN drainage: what does the inferior mesenteric LN cluster drain?

A

Colon from splenic flexure to upper rectum

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4
Q

LN drainage: what does the internal iliac LN cluster drain?

A 
Lower rectum to anal canal (above pectinate line)
Bladder
Vagina (middle third)
Cervix
Prostate
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5
Q

LN drainage: what does the para-aortic LN cluster drain?

A

Testes
Ovaries
Kidneys
Uterus

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6
Q

LN drainage: what does the superficial inguinal LN cluster drain?

A

Skin below umbilicus (except popliteal area)
Anal canal below pectinate line
Scrotum
Vulva

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7
Q

LN drainage: what does the popliteal LN cluster drain?

A

Dorsolateral foot

Posterior calf

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8
Q

LN drainage: what does the axillary cluster drain?

A

Upper limb
Breast
Skin above umbilicus

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9
Q

Where are B cells found in the spleen? T cells?

A

B: follicles
T: PALS

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10
Q

What findings might you see in RBCs post-splenectomy?

A

Howell-Jolly bodies (nuclear remnants)
Target cells
Thrombocytosis (lack of removal/sequestration)
Lymphocytosis (lack of sequestration)

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11
Q

What is the thymus derived from?

A

3rd pharyngeal pouch (DeGeorge)

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12
Q

Lymphocytes are of ______________ origin.

A

mesenchymal

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13
Q

What cytokines enhance killing by NK cells?

A

IL-2, IL-12, IFN-alpha, IFN-beta

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14
Q

What types of cells express CD3, CD4, CD25, and FOXP3?

A

Tregs

anti-inflammatory, produce IL-10 and TGF-beta

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15
Q

What binds MHC?

A

TCR + co-receptor (CD4/8)

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16
Q

What cell contains B7 and what cell contains B28?

A

B7 (AKA CD80/86) = APC

CD28 = naive T cell (being activated by APC

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17
Q

While B7 to CD28 interaction is important for naive T cell activation, what is the analogous signal of CD40/CD40L used for?

A

CD4+ = CD40L

B cell = CD40 (B cell being activated by CD4+)

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18
Q

What Ig crosses placenta and provides infants w/passive immunity?

A

IgG

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19
Q

Which of the following does NOT fix complement:
IgG
IgA
IgM

A

IgA (dimer)

  • J chain from secretory cells, protects Fc portion from luminal proteases
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20
Q

What is a thymus-independent antigen?

A

Lacks a peptide component (eg LPS)

  • Cannot be presented by MHC
  • Weakly immunogenic
  • Vaccines often require boosters/adjuvants

There are two classes of antigens for B cells, T cell‐dependent (thymus‐dependent, TD) and T cell‐independent (TI) antigens. The former require the presence of cognate T‐helper (TH) cells to trigger a B‐cell response, whereas the TI antigens can mount an antibody response in the absence of TH.

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21
Q

What is CD25?

A

IL-2R

eg found on Tregs

22
Q

What protein causes anemia of chronic disease?

A

Hepcidin

  • Degrades ferroportin to decrease Fe absorption. (less Fe for microbes)
  • Decreases Fe release from macrophages (less for microbes)
23
Q

What protein binds/sequesters Fe to inhibit microbial Fe scavenging?

A

Ferritin

24
Q

Def. of DAF (CD55) would cause what disease and why?

A

Paroxysmal nocturnal hemoglobinuria

  • DAH inhibits complement for RBCs, so you see lysis without it during low O2 at night time
25
Q

What does Hot T-bone stEAK help us remember?

A 
IL-1 = fever (hot)
IL-2 = T cells
IL-3 = bone marrow
IL-4 = IgE
IL-5 = IgA
IL-6 = aKute phase protein production
26
Q

IL-4 promotes class-switching to Ig__, while IL-5 promotes class-switching to Ig__.

A

IL-4: IgE (+ IgG, also induces Th2 differentiation and B cell growth)

IL-5: IgA (+growth/differentiation of eosinophils, B cells).

27
Q

Def. in NADPH oxidase would result in what disease?

A

CGD

Risk of infections w/catalase+ organisms (because they can neutralize their own H2O2; esp. pseudomonas).

28
Q

Unique CD marker for macrophages?

A

CD14 (receptor for PAMPs, eg *LPS, binds TLR4)

recall: they have CCR5

29
Q

Unique CD marker for NK cells?

A

*CD56 (unique to NK cells)

CD16 (binds Fc of IgG)

30
Q

Unique CD marker for HSC’s?

A

CD34

31
Q

In what infections are pts given pre-formed AB’s?

A

Tetanus, botulism, HBV, varicella, or rabies

32
Q

What is the only live-attenuated vaccine given to HIV+ people?

A

MMR

33
Q

What does BCG vaccine protect against?

A

TB (live-attenuated)

Note: yellow fever is live attenuated as well

34
Q

What type of hypersensitivity rxn’s are serum sickness and Arthus rxn?

What’s the difference b/w them?

A

Both T3HS

Serum sickness takes 5 days because you make AB’s, then complexes form. Arthus is faster, you have pre-formed AB’s and they form complexes upon exposure to foreign substance.

35
Q

What are the 4 T’s of T4HS rxns?

A

T cells
Transplant rejections
TB skin tests
Touching (contact dermatitis)

36
Q

What is defective in X-linked agammaglobulinemia?

A

Bruton tyrosine kinase (BTK)

37
Q

Most common Ig immunodeficiency?

A

IgA

38
Q

What is the defect in common variable immunodeficiency?

A

Defect in B cell differentiation (many causes)

39
Q

An IL-12 def. (AR) would cause decreased response of what cell type?

A

Th1 (therefore decreased IFN-gamma)

40
Q

Someone w/chronic mucocutaneous candidiasis would likely have a dysfunction of what cell type?

A

T cells (normally fights of fungus)

41
Q

What’s another way to get SCID besides ADA def. (AR)?

A

IL-2R gamma chain defect (X-linked)

*Unique to SCID: no concern for rejection of bone marrow xplant

42
Q

What is the problem in ataxia-telangiectasia?

What protein would be elevated?

A

ATM gene: failure to repair ds-breaks

^ AFP
ataxia due to cerebellar defects

43
Q

What usually causes hyper-IgM syndrome?

A

Defective CD40L on Th cells (can’t class switch by binding CD40 of B cells, *but B cells can still be activated by directly binding pathogens).

44
Q

What is defective in Leukocyte adhesion def. (type 1)?

A

Defect in LFA-1 integrin on phagocytes, leading to impaired migration and chemotaxis (AR). Leads to increased infections/poor wound healing, delayed separation of umbilical cord, neutrophilia (*in blood, but none at infection site!).

45
Q

What is dysfunctional in Chediak-Higashi syndrome?

A

Defect in lysosomal trafficking gene regulator (AR). MT disfuction, can’t fuse phagosomes w/lysosomes (see giant granules in cells). Also pancytopenia (can’t divide) leading to recurrent pyogenic infections (staph, strep).

46
Q

What has replaced the nitroblue tetrazolium test for CGD?

A

See abnormal dihydrorhodamine (flow cytometry) test, decreased green fluoresnce.

47
Q

What fungal infections are those w/low T cells prone to?
B cells?
Granulocytes?

A

T cells def: candida, PCP
B cells def: GI giardiasis (no IgA)
Granulocyte def: candida, aspergillus

48
Q

Def. of what types of immune cells renders someone susceptible to encapsulated organisms?

What are 2 encapsulated organisms that don’t have obvious capsules on sketchy?

A

B cells

Klebsiella
Strep pneumo

49
Q

How long until onset of hyperacute rejection?

What causes it?

A

W/in minutes

Pre-existing AB’s

50
Q

How long until onset of acute rejection?

What causes it?

A

Weeks to months

CD8+ response vs. donor MHC (T4HS).
AB development.
*Prevent acute rejection w/immunosuppressants

51
Q

How long until onset of chronic rejection?

What causes it?

A

Months to years

CD4+ T cells respond to recipient APC’s presenting foreign peptide (which is the host’s body), T2&4HS. T cells secrete cytokines: proliferation of vascular smooth muscle, parenchymal atrophy, interstitial fibrosis (bronchiolitis obliterans, accelerated atherosclerosis, chronic graft nephropathy, vanishing bile duct syndrome).

52
Q

What types of transplants more commonly result in GVH dz?

A

Bone marrow and liver (rich in grafted lymphocytes, T4HS).

but may benefit leukemia pts (might attack the cancer).

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