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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.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.

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. What is the main function of TNF alpha? How does it do this?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Chronic granulomatous disease
No because no peptide fragment!
Its a serine protease that activates apoptosis; NK and CD8

2. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Antimicrosomal and antithyroglobulin
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Inferior mesenteric

3. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Hemochromatosis
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 :(

4. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IL 4 - 5 - 10 - 6

5. Which type of selection of thymic development provides central tolerance?
Negative selection
CD56
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

6. What are the autoantibodies for goodpastures syndrome?
Th2; Th1
TGF beta and IL 10
Anti alpha subunit 3 of collagen on type IV bm
Cyclosporine - OKT3

7. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
pale central germinal centers
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

8. What lymph node drains the lateral side of the dorsum of the foot?
T cell activation; no with CD 4 or CD 8
IL 1 and IL 6
Popliteal
Steroid responsive nephrotic syndrome

9. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
secondary
IL 1 and IL 6
When you select for which MHC it will have; take out the lymphs that self react

10. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Viral neutralization of igM and IgG!
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
isotype

11. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IgE
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
A recomb cytokine of IL 2; RCC and metastatic melanoma

12. What is passive immunity?
isotype
Receiving preformed Antibodies
Antidesmoglein
Remove encapsulated bacateria

13. What type of side chains are found on Fc region of an antibody?
Carbohydrate
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
Edema and necrosis in that region
Anti alpha subunit 3 of collagen on type IV bm

14. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
If there is class switching and plasma cell production (that is when memory cells are produced)
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Yes
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

15. Which disease is associated with DR3?
A - B - C; all the D's
IgAs in mothers breast milk!
acute phase reactants
DM type I

16. IgE has the ___________ in the serum
lowest concentration
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
Anti IF
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

17. IgG...
opsonizes
IgAs in mothers breast milk!
Bind FcG for antibody dependent cellular cytotoxicity
isotype

18. How fast does it occur?
Histamine; post capillary venules - vasodilation
Type IV
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
The patient could become cyanotic in the OR!

19. What does it mean if there are igM in the serum at birth?
acute phase reactants
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Pernicious Anemia and Hashimotos
Cells that stil have weird parts of their membrane that macrophages usually bite off

20. What is thrombopoietin used for?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Thrombocytopenia
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Anti smooth muscle

21. What is the pathology of acute transplant rejection? is it reversible?
Acts as second signal on B cells to induce class switching to IgE and IgG
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IL 1 and IL 6
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

22. which B and T cell disorder presents with specifically low IgM?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Wiskott Aldrich syndrome
Anti Jo -1
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop

23. What is the toxicity of azathioprine?
Th cells fail to produce interferon gamma; a lot of IgE
...
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Local infection/inflammation; infection of the ln itself; metastasis

24. What is a type I hypersensitivity reaction? What is atopic?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Anti topoisomerase
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Superficial inguinal

25. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
except hyperacute
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Anti smooth muscle
Basophils! THey want IG E class switch!

26. What is the pathology seen in chronic transplant rejection?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Fc

27. What are the two signals required for Th1 cells? what happens after then activated?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Interferon gamma and IL 2
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

28. Which MHC presents intracellular peptides? how so?
Superior mesenteric
MHC I; from RER with help of the B2 microglobulin
IL 15; IL 12 - interferon Beta and interferon alpha
Not thymus - BM

29. What are the PALS?
Anti U1 RNP (ribonucleoprotein)
If there is class switching and plasma cell production (that is when memory cells are produced)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Superficial inguinal

30. what secretes IL 4?
Basophils! THey want IG E class switch!
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T cell precursor
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

31. The MALT/GALT are not...
Antidote for digoxin intoxication
NK cells
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
encapsulated

32. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
T cell precursor
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
Carbohydrate
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

33. What is the autoantibody for SLE that is nonspecific? Specific?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Axillary
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

34. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IgG
Tetanus - Botulinum - HBV - Rabies
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM

35. what will NK cells do to cells covered in IgG Ab? why?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Activate macrophages
Kill them because they have CD16 on them that recognize the FcG portion
...

36. what cytokine does basophils secrete?
Cytokine IL 10 secreted by Th2
IL 4
Local infection/inflammation; infection of the ln itself; metastasis
Its main effect is a defect in Ab opsonization for killing

37. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
NK cells
IgE; by activating eosinophils

38. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Secretory component
T

39. What is the main function of IL 12? other than macrophages who else can release IL 12?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
heavy chains

40. What are the mediators that mast cells release?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Histamine; post capillary venules - vasodilation
T cell precursor
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

41. What are the cell surface proteins on NK cells?
All MHC 1/CD8
Secretory component
MHC I - CD16 - CD56
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

42. 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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 1 and IL 6
Yes

43. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Complement activation (active in both)
Histamine; post capillary venules - vasodilation
Influenza; antigenic shift; antigenic drift
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

44. hat is the presentation of Jobs syndrome or Hyper IgE?
Activate macrophages
C5a
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Axillary

45. Describe complement dependent Type II hypersensitivity. Give an example.
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
IL 4
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
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

46. What are the autoantibodies for type I diabetes mellitus?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Its a serine protease that activates apoptosis; NK and CD8
Anti glutamate carboxylase and anti insulin

47. What are target cells?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Cells that stil have weird parts of their membrane that macrophages usually bite off

48. IgM can exist as a _______ also
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
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Secretory component
pentamer

49. What is the presentation of common variable immunodef? and What are the labs?
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
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
Sinusitis - otitis media - pneumonia

50. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Previous transfusion; pregnant woman whose fetus had paternal antigens
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Macrophages - Dendritic cells - B cells
Cells that stil have weird parts of their membrane that macrophages usually bite off