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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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1. what prevents NK cells from killing normal cells if their default is to kill?
Alternative splicing of mRNA
except hyperacute
MHC class molecules bind to KIRS or CD94 to prevent killing
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

2. What does granulysin do?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Type IV
Influenza; antigenic shift; antigenic drift
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

3. What are the two signals required for T cells? what happens after?
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 U1 RNP (ribonucleoprotein)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

4. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Fc
Interferon gamma; Th1

5. are Th cells involved in trapping of antigens of endotoxin/LPS?
No because no peptide fragment!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Th cells fail to produce interferon gamma; a lot of IgE
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

6. Name the three opsonins
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
CRP - C3b - IgM
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
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

7. What are howell jolly bodies?
Complement activation (active in both)
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
False! B cell class switching requires a second signal
Popliteal

8. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Its main effect is a defect in Ab opsonization for killing
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
In the germinal center of secondary follicles (In the paler center)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

9. IgM can fix complement but...
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
cannot cross placenta
T cell precursor

10. What is the marginal zone of the spleen? what happens there?
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Hemochromatosis
Bind FcG for antibody dependent cellular cytotoxicity

11. 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?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
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)
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

12. What is the cause of thymic aplasia? What is its presentation? What are the labs?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
TGF beta and IL 10

13. what cytokine does basophils secrete?
IL 4
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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
Anti U1 RNP (ribonucleoprotein)

14. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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
Its a serine protease that activates apoptosis; NK and CD8
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

15. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
The patient could become cyanotic in the OR!
neutrophilia!
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

16. Which are the only two antiinflammatory cytokines?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
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
TGF beta and IL 10
NK cells

17. What are the autoantibodies for wegeners granulomatosis?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
IL 4
Influenza; antigenic shift; antigenic drift

18. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Cross link
Superior mesenteric
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

19. Which disease is associated withB B27?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

20. What are the autoantibodies for myasthenia gravis?
Celiac
Antimicrosomal and antithyroglobulin
Anti Ach receptor
Histamine; post capillary venules - vasodilation

21. What is epo used for?
CRP - C3b - IgM
IgM and IgG
Anemias (esp due to renal failure)
Celiac

22. other than mediating shock - what else does TNF alpha do? who releases it mainly?
...
Type IV
Activates Th1 helper cells; Macrophages
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

23. Describe the Mannose Lectin pathway
MS
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
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

24. what bacteria are a splenectomy patient most susceptible to? why?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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
DM type I and RA

25. How does the alternative pathway lead to MAC activation?
IgAs in mothers breast milk!
Liver! (they are proteins circulating in the blood)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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

26. which of the transplant rejections is antibody mediated? why does it occur?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Chronic granulomatous disease

27. Which is the main antibody that provides passive immunity to infants?
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
pathogenesis
IgG
Active; passive - fast but short half life (3 weeks!)

28. What is thrombopoietin used for?
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
Secretory component
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Thrombocytopenia

29. What is the pathogenesis of a hypersensitivity reaction?
Alternative splicing of mRNA
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
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
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

30. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Antimicrosomal and antithyroglobulin
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
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
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

31. From where do cytokines come from?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
carboxy terminal
Lymphocytes

32. which cells have more complete tolerance - B or T cells?
TLR ad nuclear receptors
T
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Para aortic

33. Which disease is associated with B8?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti Jo -1
Graves
Increases expression of MHC I and MHC II and also activates NK cells

34. 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
Activates cytotoxic CD 8 T cells as second signal
IL 1 and IL 6
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

35. Give an example of someone who could get hyperacute transplant rejection.
CRP - C3b - IgM
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Previous transfusion; pregnant woman whose fetus had paternal antigens
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

36. which interleukin receptor is required for NK development? activation?
RNA segment reassortment
IgM and IgD
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
IL 15; IL 12 - interferon Beta and interferon alpha

37. What is the pathology of acute transplant rejection? is it reversible?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Cells that stil have weird parts of their membrane that macrophages usually bite off

38. What are four results of a splenectomy?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
...
Carbohydrate
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

39. Give three examples of bacteria that use antigenic variation and how.
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
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Immunoflourescent staining of tissue biopsies

40. What is the most common example of passive immunity?
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
IgAs in mothers breast milk!

41. What is immune complex disease? give an example.
Activate macrophages
MS
A - B - C; all the D's
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

42. What do multimeric antibodies require for assembly?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
A j chain
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

43. what characterizes an arthus reaction?
Edema and necrosis in that region
Recom IL 11; thrombocytopenia
Antidesmoglein
S. aureus - E. Coli - aspergillus

44. What are the three types of APCs?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Macrophages - Dendritic cells - B cells

45. Which disease is associated with DR3?
Interferon gamma; Th1
Hemochromatosis
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
DM type I

46. What are the autoantibodies for primary biliary cirrhosis?
Anti mitochondrial
Anti glutamate carboxylase and anti insulin
Anti alpha subunit 3 of collagen on type IV bm
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

47. which of the hypersensitivity reactions is not Ab mediated?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Type IV
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
cannot cross placenta

48. What links the adaptive and innate immunity?
opsonizes
pathogenesis
Influenza; antigenic shift; antigenic drift
Complement activation (active in both)

49. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Graves
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

50. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Fab portion
except hyperacute