Test your basic knowledge |

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. Which diseases are associated with DR5?
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
Pernicious Anemia and Hashimotos
pentamer
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

2. which of the transplant rejections is antibody mediated? why does it occur?
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)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Inferior mesenteric
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

3. What is the pathogenesis of a hypersensitivity reaction?
MHC I - CD16 - CD56
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
Cyclosporine - OKT3
Anti Ach receptor

4. which antibodies prevent antigens from binding mucosal surfaces?
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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgA
mesenchymal

5. 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?
Cross link
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
...
CD56

6. which cells have more complete tolerance - B or T cells?
T
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
A recomb cytokine of IL 2; RCC and metastatic melanoma
Interferon gamma and IL 2

7. What is the marginal zone of the spleen? what happens there?
opsonizes
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Humoral

8. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Activates Th1 helper cells; Macrophages
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Daclizumab; prevent ACUTE rejection of renal transplant
DM type I and RA

9. What does granulysin do?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 3; supports growth and differentiation of bone marrow stem cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

10. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Carbohydrate
T cell precursor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

11. What is the main function of TNF alpha? How does it do this?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

12. Which disease is associated with HLA A3?
IgM
Hemochromatosis
Its a serine protease that activates apoptosis; NK and CD8
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

13. What are the labs in brutons agammaglobulinemia?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
TGF beta and IL 10
MHC II - B7

14. Which diseases are associated with DR4?
IgG
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Increases expression of MHC I and MHC II and also activates NK cells
DM type I and RA

15. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Antihistone

16. How do you test for type III hypersensitivity?
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
Immunoflourescent staining of tissue biopsies
IgAs in mothers breast milk!
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

17. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Glycoproteins; HLA
Antihistone
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)
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

18. What happens in a deficiency of C3?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Graves
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

19. What are the cell surface proteins on NK cells?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anti TSh receptor
Stimulate the liver to release acute phase reactants
MHC I - CD16 - CD56

20. What is epo used for?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Anemias (esp due to renal failure)
active complement pathway
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

21. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Tetanus - Botulinum - HBV - Rabies
SP infections
Its main effect is a defect in Ab opsonization for killing

22. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Antidote for digoxin intoxication
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
Paracortex
encapsulated

23. What does IgA pick up from epithelial cells before being secreted?
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
pentamer
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
Secretory component

24. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
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
TNF alpha and IL1
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
When you select for which MHC it will have; take out the lymphs that self react

25. What are the autoantibodies for pernicious anemia?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Anti IF

26. What are howell jolly bodies?
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Cytokine IL 10 secreted by Th2
Anti viral and anti tumor

27. Describe the capsular structure of a lymph node; What are the functions of the LN?
Secretory component
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
secondary
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

28. Name two endogenous pyrogens
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IL 1 and IL 6
Anti Jo -1

29. give an example of how influenza does a major antigenic shift.
Bind FcG for antibody dependent cellular cytotoxicity
encapsulated
RNA segment reassortment
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

30. How does the alternative pathway lead to MAC activation?
Negative selection
Anti TSh receptor
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 5

31. what cell surface marker is used for NK cells as it is unique to them?
Superficial inguinal
CD56
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
DM type I

32. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti topoisomerase
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

33. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
MHC II - B7
Glycoproteins; HLA
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

34. What is chronic mucocutaneous candidiasis d/t?
Local infection/inflammation; infection of the ln itself; metastasis
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
T cell dysfunction

35. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Basophils! THey want IG E class switch!
except hyperacute
delayed!

36. IgM can exist as a _______ also
Superior mesenteric
pentamer
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Hemochromatosis

37. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
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
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

38. A lymph node is a ________ lymphoid organ.
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
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
secondary
IgA

39. What is the autoantibody for SLE that is nonspecific? Specific?
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
Bind FcG for antibody dependent cellular cytotoxicity
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Antimicrosomal and antithyroglobulin

40. What links the adaptive and innate immunity?
not Ab mediated
lowest concentration
Recom IL 11; thrombocytopenia
Complement activation (active in both)

41. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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

42. What does IL 4 do?
Cross link
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Acts as second signal on B cells to induce class switching to IgE and IgG
Antimicrosomal and antithyroglobulin

43. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

44. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Th2; Th1
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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

45. which interleukin receptor is required for NK development? activation?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti Ach receptor
IL 15; IL 12 - interferon Beta and interferon alpha

46. What are the autoantibodies for drug induced lupus?
...
TLR ad nuclear receptors
Antihistone
T

47. which antibody activate mast cells - basophils - and eosinophils?
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
SP infections
IgE
Tetanus - Botulinum - HBV - Rabies

48. What can cause a lymph node enlargement?
Local infection/inflammation; infection of the ln itself; metastasis
...
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Barrel hoop basement membrane fenestrations

49. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Cyclosporine - OKT3

50. What is the white pulp of the spleen?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
MS
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Antimicrosomal and antithyroglobulin