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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. are Th cells involved in trapping of antigens of endotoxin/LPS?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Popliteal
No because no peptide fragment!
T cell precursor

2. __________ are a part of the innate system.
Superficial inguinal
IgE
NK cells
IL 5

3. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Antidote for digoxin intoxication
Th2; Th1
except hyperacute
Graves

4. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Activate macrophages
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
mesenchymal

5. 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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
IgM and IgG
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

6. What are the three types of lymphocytes?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
B - T - and NK cells

7. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
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
T cell precursor
CD21 on B cells (although there is T cell lymphocytosis in EBV)

8. 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
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
Anti Ach receptor
Anti viral and anti tumor

9. What lymph node drains the breast?
By transcytosis
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!
Inferior mesenteric
Axillary

10. in which immunodef order do you see a lot of pus? no pus?
T cell dysfunction
Superficial inguinal
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IL 1 and IL 6

11. Which is the most abundant antibody in blood?
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
IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
In the germinal center of secondary follicles (In the paler center)

12. Describe the capsular structure of a lymph node; What are the functions of the LN?
IL 5
The patient could become cyanotic in the OR!
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
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

13. How is sirolimus different from tacrolimus?
Viral neutralization of igM and IgG!
Humoral
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
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

14. What bugs can actually infect the lymph node itself?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
A recomb cytokine of IL 2; RCC and metastatic melanoma

15. What are the labs in brutons agammaglobulinemia?
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
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Immunosuppression after kidney transplantation
Cyclosporine - OKT3

16. How does the alternative pathway lead to MAC activation?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IL 4 - 5 - 10 - 6
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

17. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
not Ab mediated
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
neutrophilia!

18. What is recomb beta interferon used for?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
MS
Wiskott Aldrich syndrome
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

19. What lymph node drains the anal canal (below the pectinate line)?
Anti topoisomerase
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
Its a serine protease that activates apoptosis; NK and CD8
Superficial inguinal

20. What lymph node drains the scrotum?
Superficial inguinal
TNF alpha and IL1
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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)

21. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
Anti U1 RNP (ribonucleoprotein)
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

22. What does IL 10 do? who is secreted by?
Graves
Alternative splicing of mRNA
Negative nitroblue tetrazolium reduction test
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

23. describe the pathogenesis of delayed type IV hypersensitivity
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)

24. IgE has the ___________ in the serum
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IL 15; IL 12 - interferon Beta and interferon alpha
Receiving preformed Antibodies
lowest concentration

25. The secondary follicles have __________; primary follicles are dense
IL 4
pale central germinal centers
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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

26. What is muromonab - CD3 (OKT3)
Antidesmoglein
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
When you select for which MHC it will have; take out the lymphs that self react
Cyclosporine - OKT3

27. What are the autoantibodies for Mixed connective tissue disease?
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
Steroid responsive nephrotic syndrome
Anti U1 RNP (ribonucleoprotein)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

28. What cytokines are released by Th1 cells?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
Cells that stil have weird parts of their membrane that macrophages usually bite off
Interferon gamma and IL 2

29. What do mature naive B lymphocytes express?
NK cells
IgM and IgD
...
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

30. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Glycoproteins; HLA
Cross link
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

31. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Axillary
Anti IF

32. How do you test for type III hypersensitivity?
A j chain
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Immunoflourescent staining of tissue biopsies
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

33. What lymph node drains the testes?
Antidesmoglein
active complement pathway
Para aortic
carboxy terminal

34. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Anti glutamate carboxylase and anti insulin
T cell precursor
Paracortex; viral infection
Antihistone

35. What are the autoantibodies for pemphigus bulgaris?
Anti Jo -1
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
Antidesmoglein
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)

36. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Negative nitroblue tetrazolium reduction test
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
All MHC 1/CD8
Inferior mesenteric

37. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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
...

38. What is the presentation of scid? treatment?
Hemochromatosis
T
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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

39. How is i Th1 helper cell inhibited?
T cell activation; no with CD 4 or CD 8
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
Basophils! THey want IG E class switch!
Cytokine IL 10 secreted by Th2

40. What lymph node drains the stomach?
Secretory component
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
Celiac
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

41. What is hereditary angioedema? What are the C3 levels?
IgAs in mothers breast milk!
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
Glycoproteins; HLA
pentamer

42. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Lymphocytes
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

43. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
Th cells fail to produce interferon gamma; a lot of IgE
IgAs in mothers breast milk!
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Internal iliac

44. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
DM type I
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
lowest concentration
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

45. which antibodies prevent antigens from binding mucosal surfaces?
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
IgA
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

46. is IgM an opsonizer?
Anti glutamate carboxylase and anti insulin
Negative!
acute phase reactants
Inferior mesenteric

47. which antibody activate mast cells - basophils - and eosinophils?
IgE
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
Antidote for digoxin intoxication
IL 15; IL 12 - interferon Beta and interferon alpha

48. Which cytokines do Th2 release and For what?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

49. what will NK cells do to cells covered in IgG Ab? why?
Superior mesenteric
DM type I
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Kill them because they have CD16 on them that recognize the FcG portion

50. Complements are...
acute phase reactants
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)