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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. which of the transplant rejections is antibody mediated? why does it occur?
Wiskott Aldrich syndrome
Hereditary angioedema; PNH
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

2. What is the pathology of acute transplant rejection? is it reversible?
SP infections
The patient could become cyanotic in the OR!
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Anti mitochondrial

3. What are the T cell functions?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

4. What are the autoantibodies for pernicious anemia?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Anti IF

5. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

6. What does granulysin do?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Sinusitis - otitis media - pneumonia
Anti Jo -1
Receiving preformed Antibodies

7. Which diseases are associated with DR5?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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
Pernicious Anemia and Hashimotos

8. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Local infection/inflammation; infection of the ln itself; metastasis
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
No because no peptide fragment!

9. What is filgrastim and sargramostim? and What is it used for?
T cell dysfunction
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
No because no peptide fragment!
Lymphocytes

10. What are the main cell surface proteins on B cells?
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
Complement activation (active in both)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
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

11. Describe the Mannose Lectin pathway
Its main effect is a defect in Ab opsonization for killing
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
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

12. What are the mediators that mast cells release?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgE; by activating eosinophils
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
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

13. How do you test for type III hypersensitivity?
secondary
type four
Immunosuppression after kidney transplantation
Immunoflourescent staining of tissue biopsies

14. Leukocyte adhesion defect presents with...
Active; passive - fast but short half life (3 weeks!)
neutrophilia!
Anti U1 RNP (ribonucleoprotein)
Negative nitroblue tetrazolium reduction test

15. What does IL 5 do?
The patient could become cyanotic in the OR!
MHC class molecules bind to KIRS or CD94 to prevent killing
T cell dysfunction
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

16. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Carbohydrate
carboxy terminal
When you select for which MHC it will have; take out the lymphs that self react
Influenza; antigenic shift; antigenic drift

17. The ______ in the BM are DN - the DP are in the cortex of thymus
Cytokine IL 10 secreted by Th2
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Hereditary angioedema; PNH
T cell precursor

18. What is the general structure of an Ab?
2 heavy chains and two light chains
pathogenesis
Anti U1 RNP (ribonucleoprotein)
Antidote for digoxin intoxication

19. 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
Basophils! THey want IG E class switch!
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

20. What is muromonab - CD3 (OKT3)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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

21. IgG...
False! B cell class switching requires a second signal
opsonizes
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

22. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
IL 5
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

23. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Anti SS- A (anti RO) and Anti SS- B
except hyperacute
Receiving preformed Antibodies

24. What is passive immunity?
Carbohydrate
Receiving preformed Antibodies
DM type I and RA
Antidesmoglein

25. describe the classic complement pathway.
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Immunosuppression after kidney transplantation

26. What lymph node drains the rectum (above the pectinate line)?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
The igA found in breast milk
Internal iliac
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

27. What lymph node drains the anal canal (below the pectinate line)?
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
Pernicious Anemia and Hashimotos
Superficial inguinal
IgE

28. Which are the only two antiinflammatory cytokines?
Fc
IgG
Local infection/inflammation; infection of the ln itself; metastasis
TGF beta and IL 10

29. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Thrombocytopenia
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Paracortex; viral infection
Steroid responsive nephrotic syndrome

30. What are some catalase positive organisms?
Yes
Paracortex
S. aureus - E. Coli - aspergillus
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

31. Give three examples of bacteria that use antigenic variation and how.
IgE; by activating eosinophils
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
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

32. What kinds of receptors activate innate immunity?
TLR ad nuclear receptors
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
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

33. What is hereditary angioedema? What are the C3 levels?
IgAs in mothers breast milk!
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
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
The igA found in breast milk

34. What is the toxicity of muromonab?
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Tetanus - Botulinum - HBV - Rabies

35. What is the clinical use for azathioprine?
Immunoflourescent staining of tissue biopsies
Cytokine IL 10 secreted by Th2
...
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

36. What are the autoantibodies for polymyositis and dermatomyositis?
Anti Jo -1
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
IgG
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

37. What lymph node drains the sigmoid colon?
Inferior mesenteric
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
heavy chains
Antibody mediated cytotoxicity; either complement dependent or complement independent

38. what results in symptoms of shock in an acute hemolytic transfusion reaction?
S. aureus - E. Coli - aspergillus
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
MHC II - B7
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

39. To what portion of the Antibody do the complements bind?
Para aortic
DM type I and RA
Lymphocytes
Fc

40. What are the main symptoms of B cell immunodeficiencies?
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
T cell precursor
SP infections
Edema and necrosis in that region

41. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Stimulate the liver to release acute phase reactants
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
Anti glutamate carboxylase and anti insulin

42. What is the main cytokine that activates eosinophils?
IL 5
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
MHC II - B7
Barrel hoop basement membrane fenestrations

43. Complements are...
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Inferior mesenteric
isotype
acute phase reactants

44. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
delayed!

45. How is i Th1 helper cell inhibited?
IgE; by activating eosinophils
Barrel hoop basement membrane fenestrations
Cytokine IL 10 secreted by Th2
S. aureus - E. Coli - aspergillus

46. The two heavy chains of an antibody contribute to the...
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
Fab portion
Anti alpha subunit 3 of collagen on type IV bm

47. What links the adaptive and innate immunity?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Complement activation (active in both)
Celiac

48. which type of immunity is slow but long lasting? as opposed to...
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
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
The patient could become cyanotic in the OR!
Active; passive - fast but short half life (3 weeks!)

49. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
MHC I; from RER with help of the B2 microglobulin
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
Tetanus - Botulinum - HBV - Rabies
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

50. What cytokines to Th2 secrete?
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
TGF beta and IL 10
Wiskott Aldrich syndrome
IL 4 - 5 - 10 - 6