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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can study here.
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 happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
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
B - T - and NK cells
Barrel hoop basement membrane fenestrations
The patient could become cyanotic in the OR!

2. What happens in a deficiency of C3?
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
not Ab mediated

3. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
T cell dysfunction
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

4. What is the marginal zone of the spleen? what happens there?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Sinusitis - otitis media - pneumonia
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
Type IV

5. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Rheumatic arthritis
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
SP infections
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

6. Which disease is associated with B8?
Basophils! THey want IG E class switch!
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Graves
carboxy terminal

7. What is the common variable immunodeficiency ? How is it different from Brutons?
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
Activates Th1 helper cells; Macrophages
Negative!
A recomb cytokine of IL 2; RCC and metastatic melanoma

8. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
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
If there is class switching and plasma cell production (that is when memory cells are produced)
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

9. What is oprelevkin? and What is it used for?
IgG
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
Interferon gamma; Th1
Recom IL 11; thrombocytopenia

10. What happens in a secondary follicle?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

11. other than C3a - what other complement acts as an anaphyloxin?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
T cell dysfunction
C5a
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

12. What does CD16 on NK cells do?
T cell dysfunction
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
...
Bind FcG for antibody dependent cellular cytotoxicity

13. give an example of how influenza does a major antigenic shift.
TNF alpha and IL1
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
lowest concentration
RNA segment reassortment

14. Other than stimulating fever - what else does IL 6 do?
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Stimulate the liver to release acute phase reactants
IgG

15. What is the pathogenesis of HyperIgE syndrome? What are the labs?
When you select for which MHC it will have; take out the lymphs that self react
Tetanus - Botulinum - HBV - Rabies
Th cells fail to produce interferon gamma; a lot of IgE
Its a serine protease that activates apoptosis; NK and CD8

16. 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).
Graves
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!
encapsulated
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

17. What lymph node drains the lateral side of the dorsum of the foot?
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Popliteal
Anemias (esp due to renal failure)

18. What is the general structure of an Ab?
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
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
pentamer
2 heavy chains and two light chains

19. Type IV hypersensitivity is i...
Anti Jo -1
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
not Ab mediated
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

20. What are the autoantibodies for goodpastures syndrome?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Anti alpha subunit 3 of collagen on type IV bm
S. aureus - E. Coli - aspergillus
Internal iliac

21. what prevents NK cells from killing normal cells if their default is to kill?
Anti Ach receptor
IgM and IgA
Viral neutralization of igM and IgG!
MHC class molecules bind to KIRS or CD94 to prevent killing

22. what mediates the type II hypersensitivity? What are the two different methods?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
dimer
Antibody mediated cytotoxicity; either complement dependent or complement independent
CRP - C3b - IgM

23. What lymph node drains the sigmoid colon?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Inferior mesenteric
Sinusitis - otitis media - pneumonia

24. What is the toxicity of azathioprine?
Carbohydrate
Stimulate the liver to release acute phase reactants
IL 1 and IL 6
...

25. ________ regulate the cell mediated response.
Axillary
Humoral
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Antidote for digoxin intoxication

26. What is the pathology in hyperacute transplant rejection?
Axillary
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Macrophages - Dendritic cells - B cells
...

27. The lymphocytes are ________ origin
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Axillary
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
mesenchymal

28. What are the major functions of Antibodies?
IL 4 - 5 - 10 - 6
Paracortex
T cell activation; no with CD 4 or CD 8
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

29. which antibodies can bind complement?
2 heavy chains and two light chains
IgM and IgG
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Fab portion

30. Describe the complement independent Type II hypersenstivity reaction. Give an example.
Alternative splicing of mRNA
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Anemias (esp due to renal failure)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

31. what will NK cells do to cells covered in IgG Ab? why?
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
Kill them because they have CD16 on them that recognize the FcG portion
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!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

32. What does IgA pick up from epithelial cells before being secreted?
Secretory component
Negative!
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
Fc

33. Which disease is associated with DR7?
Steroid responsive nephrotic syndrome
MHC II - B7
IL 4
Barrel hoop basement membrane fenestrations

34. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
IgG
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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
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

35. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
except hyperacute
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IL 4 - 5 - 10 - 6

36. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Th cells fail to produce interferon gamma; a lot of IgE
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
S. aureus - E. Coli - aspergillus

37. In thymic development - What is the positive selection? negative selections?
When you select for which MHC it will have; take out the lymphs that self react
mesenchymal
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

38. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
TNF alpha and IL1
Anti SS- A (anti RO) and Anti SS- B
CRP - C3b - IgM
SP infections

39. 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?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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
TGF beta and IL 10
Anti mitochondrial

40. What are the cell surface proteins on NK cells?
The igA found in breast milk
MHC I - CD16 - CD56
Pernicious Anemia and Hashimotos
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

41. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Acts as second signal on B cells to induce class switching to IgE and IgG
Complement activation (active in both)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti Jo -1

42. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Delayed type hypersensitivity
Interferon gamma and IL 2
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the

43. What does Interferon alpha and beta do? how?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
type four
Superficial inguinal
not Ab mediated

44. What is serum sickness? give an example.
...
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Activates Th1 helper cells; Macrophages
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

45. which of the transplant rejections is antibody mediated? why does it occur?
...
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs

46. What is the main cytokine released by T cells? What does it do
Carbohydrate
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
IL 3; supports growth and differentiation of bone marrow stem cells
Tetanus - Botulinum - HBV - Rabies

47. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Humoral
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

48. What is Aldesleukin? What is it used for
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
A recomb cytokine of IL 2; RCC and metastatic melanoma
Type IV

49. IgE has the ___________ in the serum
IgG
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
lowest concentration
delayed!

50. other than mediating shock - what else does TNF alpha do? who releases it mainly?
opsonizes
Activates Th1 helper cells; Macrophages
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
TLR ad nuclear receptors