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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. 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?
DM type I and RA
Antidote for digoxin intoxication
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
T cell activation; no with CD 4 or CD 8

2. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
CD56
Fc
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

3. Which disease is associated with DR7?
pathogenesis
Superficial inguinal
Wiskott Aldrich syndrome
Steroid responsive nephrotic syndrome

4. What are the two signals required for T cells? what happens after?
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Remove encapsulated bacateria
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

5. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
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
RNA segment reassortment
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

6. which antibodies can bind complement?
IgM and IgG
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anti IF
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

7. What is the treatment of acute transplant rejection?
Cyclosporine - OKT3
opsonizes
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
DM type I

8. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
dimer
Daclizumab; prevent ACUTE rejection of renal transplant
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
CRP - C3b - IgM

9. In thymic development - What is the positive selection? negative selections?
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
IL 5
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
When you select for which MHC it will have; take out the lymphs that self react

10. Leukocyte adhesion defect presents with...
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!
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
neutrophilia!
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

11. So antibodies are the effectors for the humoral response. List some of their functions.
IgM and IgG
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

12. What type of side chains are found on Fc region of an antibody?
Humoral
Carbohydrate
mesenchymal
C5a

13. 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
All MHC 1/CD8
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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

14. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
By transcytosis

15. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Anemias (esp due to renal failure)

16. Name 5 ways Antibody diversity is generated?
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
Paracortex; viral infection
Lymphocytes
CD21 on B cells (although there is T cell lymphocytosis in EBV)

17. What is the mechanism for sirolimus? what else it known as?
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
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!

18. What is the toxicity of azathioprine?
...
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
A recomb cytokine of IL 2; RCC and metastatic melanoma
False! B cell class switching requires a second signal

19. The Fc region is found on the...
Increases expression of MHC I and MHC II and also activates NK cells
carboxy terminal
Superficial inguinal
A - B - C; all the D's

20. IgM can fix complement but...
Thrombocytopenia
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Active; passive - fast but short half life (3 weeks!)
cannot cross placenta

21. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Glycoproteins; HLA
Activate macrophages
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

22. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
...
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
Anti U1 RNP (ribonucleoprotein)

23. which antibodies prevent antigens from binding mucosal surfaces?
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
Th cells fail to produce interferon gamma; a lot of IgE
IgA
Anti SS- A (anti RO) and Anti SS- B

24. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Wiskott Aldrich syndrome
Axillary
Activates cytotoxic CD 8 T cells as second signal
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

25. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
lowest concentration
Graves

26. Which diseases are associated with DR5?
except hyperacute
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Pernicious Anemia and Hashimotos

27. How do you test for chronic granulomatous disease?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Negative nitroblue tetrazolium reduction test
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

28. What is Aldesleukin? What is it used for
Graves
Anti U1 RNP (ribonucleoprotein)
Negative nitroblue tetrazolium reduction test
A recomb cytokine of IL 2; RCC and metastatic melanoma

29. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
Bind FcG for antibody dependent cellular cytotoxicity
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Superficial inguinal

30. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
carboxy terminal
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

31. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
Recom IL 11; thrombocytopenia
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
neutrophilia!
Anti TSh receptor

32. What are the autoantibodies for Celiac disease?
secondary
Superficial inguinal
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Viral neutralization of igM and IgG!

33. What is the clinical use for azathioprine?
Liver! (they are proteins circulating in the blood)
...
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
T cell dysfunction

34. T/F B cells do not require a second signal
Yes
Carbohydrate
Influenza; antigenic shift; antigenic drift
False! B cell class switching requires a second signal

35. The pathogenesis of contact dermatitis is ________ hypersensitivity
Immunoflourescent staining of tissue biopsies
type four
Active; passive - fast but short half life (3 weeks!)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

36. What are the labs in brutons agammaglobulinemia?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
TNF alpha and IL1
Alternative splicing of mRNA
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

37. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
All MHC 1/CD8

38. 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?
Receiving preformed Antibodies
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
IL 15; IL 12 - interferon Beta and interferon alpha
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

39. What is the cause of thymic aplasia? What is its presentation? What are the labs?
Superior mesenteric
Antimicrosomal and antithyroglobulin
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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. other than C3a - what other complement acts as an anaphyloxin?
C5a
Th cells fail to produce interferon gamma; a lot of IgE
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Cyclosporine - OKT3

41. what prevents NK cells from killing normal cells if their default is to kill?
MHC class molecules bind to KIRS or CD94 to prevent killing
Edema and necrosis in that region
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Activate macrophages

42. What type of fenestrations are found in the red pulp of the spleen?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Activates cytotoxic CD 8 T cells as second signal
Barrel hoop basement membrane fenestrations
Immunosuppression after kidney transplantation

43. What is the late phase reaction of anaphylaxis allergy? what mediates it?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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)
pathogenesis

44. Which diseases are associated with DR4?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
DM type I and RA
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

45. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
Recom IL 11; thrombocytopenia
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
CRP - C3b - IgM

46. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Graves
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
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

47. What is immune complex disease? give an example.
SP infections
IgG
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

48. Type Iv hypersensitivity is...
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
MHC I - CD16 - CD56
delayed!
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

49. What are the autoantibodies for pernicious anemia?
heavy chains
Anti IF
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
mesenchymal

50. What are the autoantibodies for graves?
encapsulated
Bind FcG for antibody dependent cellular cytotoxicity
Anti TSh receptor
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis