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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. what cell surface marker is used for NK cells as it is unique to them?
CD56
MHC I; from RER with help of the B2 microglobulin
type four
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

2. What are the two signals to kill for NK cells?
2 heavy chains and two light chains
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Activates Th1 helper cells; Macrophages

3. What happens in a secondary follicle?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Histamine; post capillary venules - vasodilation
delayed!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

4. what secretes IL 4?
Basophils! THey want IG E class switch!
Negative selection
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
T cell dysfunction

5. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
If there is class switching and plasma cell production (that is when memory cells are produced)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

6. What are superantigens? give two examples.
Axillary
mesenchymal
S. aureus - E. Coli - aspergillus
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen

7. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
acute phase reactants
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Its a serine protease that activates apoptosis; NK and CD8
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

8. What is the main function of IL 8?
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
A chemotactic factor for neutrophils
CRP - C3b - IgM

9. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Inferior mesenteric

10. which antibodies can bind complement?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Anti topoisomerase
T cell precursor
IgM and IgG

11. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
lowest concentration
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

12. Which cytokines do Th2 release and For what?
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
MS
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

13. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
A chemotactic factor for neutrophils
Immunoflourescent staining of tissue biopsies
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

14. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia

15. What are some sinopulmonary infections?
Tetanus - Botulinum - HBV - Rabies
Chronic granulomatous disease
Sinusitis - otitis media - pneumonia
IL 5

16. What lymph node drains the anal canal (below the pectinate line)?
Superficial inguinal
Acts as second signal on B cells to induce class switching to IgE and IgG
pathogenesis
A j chain

17. What is serum sickness? give an example.
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
except hyperacute
Viral neutralization of igM and IgG!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

18. which cells have more complete tolerance - B or T cells?
T
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 4 - 5 - 10 - 6
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

19. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

20. What do multimeric antibodies require for assembly?
A j chain
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

21. what cell surface proteins are on all APCs?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MHC II - B7
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IL 4 - 5 - 10 - 6

22. How do you test for chronic granulomatous disease?
Anti Jo -1
Fc
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
Negative nitroblue tetrazolium reduction test

23. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
Immunoflourescent staining of tissue biopsies
Acts as second signal on B cells to induce class switching to IgE and IgG
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

24. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
MS - hay fever - SLE - goodpastures
Receiving preformed Antibodies
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti

25. Describe the Mannose Lectin pathway
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Popliteal
IgE
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

26. What is the presentation of Brutons agammaglobulinemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

27. What are the autoantibodies for wegeners granulomatosis?
TGF beta and IL 10
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Wiskott Aldrich syndrome
Recom IL 11; thrombocytopenia

28. What are the autoantibodies for other vasculitides?
Anti alpha subunit 3 of collagen on type IV bm
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule

29. What is the pathogenesis of acute transplant rejection? When does it occur?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a

30. What is the clinical use for azathioprine?
Antihistone
...
cannot cross placenta
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

31. What is the main cytokine that activates eosinophils?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
IL 5
Para aortic
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

32. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Edema and necrosis in that region
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

33. What is the main function of IL 12? other than macrophages who else can release IL 12?
CD56
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IgM and IgA
delayed!

34. which B and T cell disorder presents with specifically low IgM?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
CD56
Wiskott Aldrich syndrome

35. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
cannot cross placenta
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

36. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
The patient could become cyanotic in the OR!

37. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
Antidote for digoxin intoxication
No because no peptide fragment!
Anti TSh receptor

38. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Complement activation (active in both)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
...
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

39. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

40. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Axillary

41. give an example of how influenza does a major antigenic shift.
Previous transfusion; pregnant woman whose fetus had paternal antigens
RNA segment reassortment
Pernicious Anemia and Hashimotos
IgG

42. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
heavy chains
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep

43. What is the toxicity of azathioprine?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
...
Activate macrophages

44. what happens in a deficiency of C1 esterase inhibitor? DAF?
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Hereditary angioedema; PNH
Wiskott Aldrich syndrome
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway

45. What are the cell surface proteins on NK cells?
Chronic granulomatous disease
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
MHC I - CD16 - CD56
IgG

46. What lymph node drains the stomach?
Axillary
Celiac
Barrel hoop basement membrane fenestrations
Inferior mesenteric

47. What does it mean if there are igM in the serum at birth?
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Negative nitroblue tetrazolium reduction test
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

48. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Celiac
Superficial inguinal

49. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Graves
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

50. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
B - T - and NK cells
When you select for which MHC it will have; take out the lymphs that self react
Th cells fail to produce interferon gamma; a lot of IgE

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USMLE Step 1 Immunology

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