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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.

1. which of the transplant rejections is antibody mediated? why does it occur?
When you select for which MHC it will have; take out the lymphs that self react
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

2. What is the most common example of passive immunity?
Para aortic
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IgAs in mothers breast milk!

3. What lymph node drains the upper limb?
Para aortic
Axillary
Negative nitroblue tetrazolium reduction test
Anti Jo -1

4. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Anti Jo -1
not Ab mediated

5. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Activates cytotoxic CD 8 T cells as second signal
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Anti topoisomerase
Previous transfusion; pregnant woman whose fetus had paternal antigens

6. What does granzyme do? who secretes it?
T cell activation; no with CD 4 or CD 8
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
Its a serine protease that activates apoptosis; NK and CD8

7. Which cytokines do Th2 release and For what?
Th2; Th1
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Basophils! THey want IG E class switch!

8. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Glycoproteins; HLA
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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

9. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
MS - hay fever - SLE - goodpastures
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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

10. which cells have more complete tolerance - B or T cells?
T
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
S. aureus - E. Coli - aspergillus
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

11. What lymph node drains the testes?
Para aortic
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

12. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
T cell dysfunction
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Macrophages - Dendritic cells - B cells
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

13. The MALT/GALT are not...
Wiskott Aldrich syndrome
Hereditary angioedema; PNH
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
encapsulated

14. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
T
T cell activation; no with CD 4 or CD 8
IL 4 - 5 - 10 - 6

15. What happens in a secondary follicle?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Delayed type hypersensitivity
Antibody mediated cytotoxicity; either complement dependent or complement independent
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

16. The Fc region is found on the...
Yes
carboxy terminal
Daclizumab; prevent ACUTE rejection of renal transplant
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

17. What is the toxicity of azathioprine?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
MHC II - B7
...
Para aortic

18. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Barrel hoop basement membrane fenestrations
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

19. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
...

20. Which helper T cells' development is induced by IL 4? IL 12?
Internal iliac
By transcytosis
Th2; Th1
Remove encapsulated bacateria

21. which antibody is involved in the primary response or immediate response to an antigen?
Activates Th1 helper cells; Macrophages
IgE
IgM
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

22. What lymph node drains the breast?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
IgG
Axillary

23. IgM can fix complement but...
Remove encapsulated bacateria
cannot cross placenta
Macrophages - Dendritic cells - B cells
Antidote for digoxin intoxication

24. What does granulysin do?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Anti viral and anti tumor
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
...

25. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
MHC I; from RER with help of the B2 microglobulin
DM type I and RA
Anti topoisomerase

26. What is the defect in hyper IgM syndrome? What are the lab results?
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
Delayed type hypersensitivity
The patient could become cyanotic in the OR!
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

27. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
heavy chains
Anti TSh receptor
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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

28. A lymph node is a ________ lymphoid organ.
secondary
Para aortic
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in

29. What are the major functions of Antibodies?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Negative selection

30. What does IgA pick up from epithelial cells before being secreted?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Th cells fail to produce interferon gamma; a lot of IgE
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Secretory component

31. What bugs can actually infect the lymph node itself?
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!
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Sinusitis - otitis media - pneumonia
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

32. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Humoral
A - B - C; all the D's

33. give an example of how influenza does a major antigenic shift.
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
RNA segment reassortment
neutrophilia!
Type IV

34. What is three common causes of severe combined immunodef? What is the result of all three?
If there is class switching and plasma cell production (that is when memory cells are produced)
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

35. Name 5 ways Antibody diversity is generated?
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
Antihistone
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Negative nitroblue tetrazolium reduction test

36. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Recom IL 11; thrombocytopenia
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
MHC class molecules bind to KIRS or CD94 to prevent killing
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

37. The two heavy chains of an antibody contribute to the...
Fab portion
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
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T cell activation; no with CD 4 or CD 8

38. What links the adaptive and innate immunity?
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
MS - hay fever - SLE - goodpastures
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Complement activation (active in both)

39. What does IL 4 do?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Acts as second signal on B cells to induce class switching to IgE and IgG
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
No because no peptide fragment!

40. What happens in a deficiency of C3?
Graves
...
IgG
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

41. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IL 5
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

42. What are the autoantibodies for polymyositis and dermatomyositis?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti Jo -1
Activates Th1 helper cells; Macrophages
active complement pathway

43. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Cross link
IgE

44. What are the autoantibodies for Mixed connective tissue disease?
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Anti U1 RNP (ribonucleoprotein)
Th cells fail to produce interferon gamma; a lot of IgE
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

45. what results in symptoms of shock in an acute hemolytic transfusion reaction?
acute phase reactants
opsonizes
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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

46. What are superantigens? give two examples.
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
Popliteal
IgM and IgA
Para aortic

47. What are the autoantibodies for pernicious anemia?
Anti IF
Basophils! THey want IG E class switch!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
MHC I - CD16 - CD56

48. What are the main symptoms of B cell immunodeficiencies?
Active; passive - fast but short half life (3 weeks!)
SP infections
TGF beta and IL 10
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

49. What are the autoantibodies for Celiac disease?
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
...

50. Describe the capsular structure of a lymph node; What are the functions of the LN?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Histamine; post capillary venules - vasodilation
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
Recom IL 11; thrombocytopenia