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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. IgG...
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
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
opsonizes
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

2. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Rheumatic arthritis
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
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

3. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Superficial inguinal
Antimicrosomal and antithyroglobulin
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

4. Which disease is associated with B8?
Graves
Popliteal
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

5. What is oprelevkin? and What is it used for?
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Recom IL 11; thrombocytopenia
Anti smooth muscle

6. What is the pathogenesis of a candida skin test?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Delayed type hypersensitivity
Axillary

7. What do mature naive B lymphocytes express?
Thrombocytopenia
Local infection/inflammation; infection of the ln itself; metastasis
IgM and IgD
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

8. What lymph node drains the rectum (above the pectinate line)?
Anemias (esp due to renal failure)
No because no peptide fragment!
Internal iliac
pale central germinal centers

9. What are the main symptoms of B cell immunodeficiencies?
SP infections
...
Influenza; antigenic shift; antigenic drift
Superficial inguinal

10. which antibody is involved in the primary response or immediate response to an antigen?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Negative selection
Superficial inguinal
IgM

11. What is the main cytokine released by T cells? What does it do
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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
IL 3; supports growth and differentiation of bone marrow stem cells

12. Which diseases are associated with DR2?
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
Humoral
MS - hay fever - SLE - goodpastures
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

13. which interleukin receptor is required for NK development? activation?
IL 15; IL 12 - interferon Beta and interferon alpha
RNA segment reassortment
S. aureus - E. Coli - aspergillus
Edema and necrosis in that region

14. Which type of selection of thymic development provides central tolerance?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Negative selection
T cell precursor
Paracortex; viral infection

15. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Alternative splicing of mRNA
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Steroid responsive nephrotic syndrome
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis

16. What is the receptor for EBV? On what cells is that located?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (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
Severe pyogenic infections early in life
CD21 on B cells (although there is T cell lymphocytosis in EBV)

17. The alternative pathway is the only constutively...
Remove encapsulated bacateria
active complement pathway
TGF beta and IL 10
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

18. What is an example of a parasite showing antigenic variation?
Negative!
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Anti mitochondrial
Anti viral and anti tumor

19. What is thrombopoietin used for?
Thrombocytopenia
secondary
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
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

20. Which is the most abundant antibody in blood?
Anti Ach receptor
Increases expression of MHC I and MHC II and also activates NK cells
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IgG

21. What is filgrastim and sargramostim? and What is it used for?
False! B cell class switching requires a second signal
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
pentamer
Immunosuppression after kidney transplantation

22. How is i Th1 helper cell inhibited?
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Activates cytotoxic CD 8 T cells as second signal
Cytokine IL 10 secreted by Th2
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

23. What is the general structure of an Ab?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Graves
Th cells fail to produce interferon gamma; a lot of IgE
2 heavy chains and two light chains

24. What are the autoantibodies for polymyositis and dermatomyositis?
Complement activation (active in both)
IgM
Anti Jo -1
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

25. What are the cell surface proteins for Macrophages? which two are for opsonins?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
MHC II - B7

26. What does interferon gamma do to be antiviral?
IgAs in mothers breast milk!
Anti Ach receptor
IgG
Increases expression of MHC I and MHC II and also activates NK cells

27. What cytokines do macrophages release? who else can secrete IL 6? IL 12?
Hemochromatosis
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
type four
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

28. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Anti glutamate carboxylase and anti insulin

29. What is the autoantibody for SLE that is nonspecific? Specific?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

30. What is the common variable immunodeficiency ? How is it different from Brutons?
except hyperacute
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

31. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgM and IgG
lowest concentration
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

32. What are the autoantibodies for other vasculitides?
encapsulated
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Anti viral and anti tumor

33. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
All MHC 1/CD8
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
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

34. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Activates cytotoxic CD 8 T cells as second signal
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

35. which of the transplant rejections is antibody mediated? why does it occur?
T cell activation; no with CD 4 or CD 8
Superficial inguinal
Anti alpha subunit 3 of collagen on type IV bm
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

36. what bacteria are a splenectomy patient most susceptible to? why?
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
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
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

37. What is immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Immunosuppression after kidney transplantation
...
Cells that stil have weird parts of their membrane that macrophages usually bite off

38. If the alternative pathway is constitively active - how come normal cells don't get attacked with MAC?
Receiving preformed Antibodies
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Interferon gamma and IL 2

39. What is the main function of IL 12? other than macrophages who else can release IL 12?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
MHC II - B7
Interferon gamma and IL 2
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

40. Complements are...
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
Pernicious Anemia and Hashimotos
acute phase reactants
heavy chains

41. Give an example of someone who could get hyperacute transplant rejection.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
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
Previous transfusion; pregnant woman whose fetus had paternal antigens
DM type I and RA

42. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
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
Local infection/inflammation; infection of the ln itself; metastasis

43. are Th cells involved in trapping of antigens of endotoxin/LPS?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
No because no peptide fragment!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

44. What lymph node drains the sigmoid colon?
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
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
Inferior mesenteric
C5a

45. Which is the main antibody that provides passive immunity to infants?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
IgG
lowest concentration
Immunoflourescent staining of tissue biopsies

46. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
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
T cell activation; no with CD 4 or CD 8

47. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Thrombocytopenia
Its main effect is a defect in Ab opsonization for killing
IgG
except hyperacute

48. which type of immunity is slow but long lasting? as opposed to...
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
IL 4 - 5 - 10 - 6
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
Active; passive - fast but short half life (3 weeks!)

49. What is the presentation of Brutons agammaglobulinemia?
Inferior mesenteric
Anti IF
Wiskott Aldrich syndrome
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

50. IgM can exist as a _______ also
pentamer
Anti SS- A (anti RO) and Anti SS- B
Immunosuppression after kidney transplantation
Steroid responsive nephrotic syndrome