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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.
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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 part of the lymph node specifically expands during a cellular immune response? when would this occur?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Paracortex; viral infection
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

2. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IgE; by activating eosinophils

3. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
The patient could become cyanotic in the OR!
Anti smooth muscle

4. Complements are...
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
acute phase reactants
IL 4
Anti topoisomerase

5. ________ regulate the cell mediated response.
Humoral
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Superior mesenteric

6. What is anergy? why does this occur?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Anti viral and anti tumor

7. How is the antigen loaded onto a MHC II?
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
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
The igA found in breast milk

8. What does granulysin do?
All MHC 1/CD8
dimer
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

9. What lymph node drains the breast?
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
Axillary
Influenza; antigenic shift; antigenic drift
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

10. What is the clinical use for sirolimus? what should you combine it with?
Chronic granulomatous disease
Anti glutamate carboxylase and anti insulin
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

11. What is recomb beta interferon used for?
Anti smooth muscle
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Delayed type hypersensitivity
MS

12. What are the two signals to kill for NK cells?
Influenza; antigenic shift; antigenic drift
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Axillary

13. Which are the only two antiinflammatory cytokines?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
TGF beta and IL 10

14. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
In the germinal center of secondary follicles (In the paler center)
All MHC 1/CD8
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

15. What lymph node drains the stomach?
Celiac
MS - hay fever - SLE - goodpastures
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

16. What are the two signals required for T cells? what happens after?
cannot cross placenta
T cell precursor
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Basophils! THey want IG E class switch!

17. What is the main cytokine that activates eosinophils?
Th2; Th1
IL 5
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
delayed!

18. Which diseases are associated with DR5?
A chemotactic factor for neutrophils
IL 4
Anemias (esp due to renal failure)
Pernicious Anemia and Hashimotos

19. What is the presentation of scid? treatment?
TNF alpha and IL1
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

20. give an example of how influenza does a major antigenic shift.
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
IgM and IgG
RNA segment reassortment
Hereditary angioedema; PNH

21. what cell surface proteins are on all APCs?
MHC II - B7
Rheumatic arthritis
Wiskott Aldrich syndrome
Recom IL 11; thrombocytopenia

22. 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?
Antihistone
B - T - and NK cells
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

23. What are the autoantibodies for primary biliary cirrhosis?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
TGF beta and IL 10
Anti mitochondrial

24. 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
By transcytosis
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Macrophages - Dendritic cells - B cells

25. What is the clinical use for azathioprine?
Recom IL 11; thrombocytopenia
Thrombocytopenia
Chronic granulomatous disease
...

26. What type of side chains are found on Fc region of an antibody?
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
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Carbohydrate
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

27. The MALT/GALT are not...
Anemias (esp due to renal failure)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
A chemotactic factor for neutrophils
encapsulated

28. What is the pathology in hyperacute transplant rejection?
except hyperacute
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
...
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

29. What links the adaptive and innate immunity?
MHC I; from RER with help of the B2 microglobulin
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Complement activation (active in both)
encapsulated

30. What can cause a lymph node enlargement?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
2 heavy chains and two light chains
Local infection/inflammation; infection of the ln itself; metastasis
IL 5

31. Describe the capsular structure of a lymph node; What are the functions of the LN?
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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
IL 15; IL 12 - interferon Beta and interferon alpha
MHC I - CD16 - CD56

32. Leukocyte adhesion defect presents with...
Its a serine protease that activates apoptosis; NK and CD8
Antibody mediated cytotoxicity; either complement dependent or complement independent
neutrophilia!
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

33. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
active complement pathway
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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

34. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Interferon gamma and IL 2

35. How does igA cross the epithelium?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
When you select for which MHC it will have; take out the lymphs that self react
By transcytosis
Antimicrosomal and antithyroglobulin

36. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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
Glycoproteins; HLA
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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)

37. What are the autoantibodies for drug induced lupus?
Antihistone
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
isotype
MHC II - B7

38. Which antibodies can be multimeric?
CRP - C3b - IgM
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
IgM and IgA
Severe pyogenic infections early in life

39. What is the main function of TNF alpha? How does it do this?
Para aortic
Thrombocytopenia
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Anti U1 RNP (ribonucleoprotein)

40. How does the alternative pathway lead to MAC activation?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti glutamate carboxylase and anti insulin

41. What is the main function of IL 8?
Cyclosporine - OKT3
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
A chemotactic factor for neutrophils
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

42. What is thrombopoietin used for?
Thrombocytopenia
...
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
Interferon gamma; Th1

43. What does IL 4 do?
Acts as second signal on B cells to induce class switching to IgE and IgG
IgG
Paracortex
A chemotactic factor for neutrophils

44. To what portion of the Antibody do the complements bind?
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
IgG
Fc
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

45. What is the pathogenesis of HyperIgE syndrome? What are the labs?
type four
Severe pyogenic infections early in life
Th cells fail to produce interferon gamma; a lot of IgE
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

46. What cytokines are released by Th1 cells?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Interferon gamma and IL 2
Cross link
Para aortic

47. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
DM type I
Sinusitis - otitis media - pneumonia
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)
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

48. What are the function of B cells?
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
S. aureus - E. Coli - aspergillus
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
Receiving preformed Antibodies

49. What are the autoantibodies for hashimotos?
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
Antimicrosomal and antithyroglobulin
MHC II - B7
MHC I; from RER with help of the B2 microglobulin

50. what will NK cells do to cells covered in IgG Ab? why?
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
RNA segment reassortment
Kill them because they have CD16 on them that recognize the FcG portion