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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 is epo used for?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anemias (esp due to renal failure)
Receiving preformed Antibodies

2. The ______ in the BM are DN - the DP are in the cortex of thymus
Complement activation (active in both)
Para aortic
Not thymus - BM
T cell precursor

3. What cytokines to Th2 secrete?
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IL 4 - 5 - 10 - 6
2 heavy chains and two light chains

4. What is Aldesleukin? What is it used for
Negative!
IgA
TGF beta and IL 10
A recomb cytokine of IL 2; RCC and metastatic melanoma

5. What is the presentation of scid? treatment?
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Not thymus - BM

6. what prevents NK cells from killing normal cells if their default is to kill?
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
MHC class molecules bind to KIRS or CD94 to prevent killing
Cells that stil have weird parts of their membrane that macrophages usually bite off
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

7. What lymph node drains the scrotum?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Superficial inguinal
IgA
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

8. 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).
T
Wiskott Aldrich syndrome
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
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!

9. What are the symptoms of serum sickness?
neutrophilia!
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Sinusitis - otitis media - pneumonia
Antimicrosomal and antithyroglobulin

10. other than eat and bite RBCs what else do Macrophages of spleen do>
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
Remove encapsulated bacateria
MHC I - CD16 - CD56
Anti Jo -1

11. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Basophils! THey want IG E class switch!
IgM and IgA
Glycoproteins; HLA
If there is class switching and plasma cell production (that is when memory cells are produced)

12. What does IL 4 do?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Increases expression of MHC I and MHC II and also activates NK cells
Acts as second signal on B cells to induce class switching to IgE and IgG
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

13. What does granzyme do? who secretes it?
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
except hyperacute
Its a serine protease that activates apoptosis; NK and CD8
active complement pathway

14. What are the two signals required for B cell class switching? Which is the second signal?
encapsulated
Interferon gamma; Th1
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Chronic granulomatous disease

15. What are the three types of lymphocytes?
B - T - and NK cells
IL 15; IL 12 - interferon Beta and interferon alpha
When you select for which MHC it will have; take out the lymphs that self react
Sinusitis - otitis media - pneumonia

16. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
The igA found in breast milk
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Local infection/inflammation; infection of the ln itself; metastasis
Superficial inguinal

17. What lymph node drains the sigmoid colon?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Inferior mesenteric

18. What lymph node drains the upper limb?
A - B - C; all the D's
Axillary
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Basophils! THey want IG E class switch!

19. What cytokines are released by Th1 cells?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Interferon gamma and IL 2
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

20. Type Iv hypersensitivity is...
MS
IL 5
delayed!
Yes

21. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
pathogenesis
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Daclizumab; prevent ACUTE rejection of renal transplant
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

22. Which MHC presents intracellular peptides? how so?
Negative selection
MHC I; from RER with help of the B2 microglobulin
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Antidesmoglein

23. How does the alternative pathway lead to MAC activation?
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Active; passive - fast but short half life (3 weeks!)
IL 15; IL 12 - interferon Beta and interferon alpha

24. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Delayed type hypersensitivity
heavy chains
Type IV

25. Which cytokines do Th2 release and For what?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Popliteal
Anti Jo -1
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

26. How is the antigen loaded onto a MHC II?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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

27. where are complements produced?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
DM type I
T
Liver! (they are proteins circulating in the blood)

28. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
cannot cross placenta
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

29. is IgM an opsonizer?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Negative!
active complement pathway
CRP - C3b - IgM

30. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Influenza; antigenic shift; antigenic drift
Antihistone
Histamine; post capillary venules - vasodilation
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

31. 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)?
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
Anti glutamate carboxylase and anti insulin
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Humoral

32. What is hereditary angioedema? What are the C3 levels?
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
heavy chains
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Superficial inguinal

33. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
heavy chains
TGF beta and IL 10
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
Macrophages - Dendritic cells - B cells

34. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Carbohydrate
Activates Th1 helper cells; Macrophages
TNF alpha and IL1
Receiving preformed Antibodies

35. Which is the most abundant antibody in blood?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
IgG

36. The Fc region is found on the...
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
carboxy terminal
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Antidesmoglein

37. What are the autoantibodies for other vasculitides?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

38. What is muromonab - CD3 (OKT3)
Basophils! THey want IG E class switch!
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
MS

39. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Cells that stil have weird parts of their membrane that macrophages usually bite off
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
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

40. What is colostrum?
The igA found in breast milk
Axillary
Anti topoisomerase
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

41. Which disease is associated with HLA A3?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Hemochromatosis
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
MHC class molecules bind to KIRS or CD94 to prevent killing

42. What is the autoantibody for SLE that is nonspecific? Specific?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Daclizumab; prevent ACUTE rejection of renal transplant
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

43. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Kill them because they have CD16 on them that recognize the FcG portion
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

44. which cells have more complete tolerance - B or T cells?
Anti TSh receptor
Barrel hoop basement membrane fenestrations
Glycoproteins; HLA
T

45. The alternative pathway is the only constutively...
active complement pathway
pentamer
Tetanus - Botulinum - HBV - Rabies
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

46. What are some catalase positive organisms?
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
S. aureus - E. Coli - aspergillus
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

47. where do NK cells develop?
IgA
Alternative splicing of mRNA
Not thymus - BM
Activate macrophages

48. What are target cells?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anti topoisomerase

49. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
Local infection/inflammation; infection of the ln itself; metastasis
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
DM type I

50. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Macrophages - Dendritic cells - B cells
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)