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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. The MALT/GALT are not...
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
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
SP infections
encapsulated

2. What are the two signals required for Th1 cells? what happens after then activated?
Pernicious Anemia and Hashimotos
Acts as second signal on B cells to induce class switching to IgE and IgG
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 4

3. 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
Anti topoisomerase
Secretory component
Acts as second signal on B cells to induce class switching to IgE and IgG

4. Describe the complement independent Type II hypersenstivity reaction. Give an example.
MS
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels

5. what secretes IL 4?
Local infection/inflammation; infection of the ln itself; metastasis
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
Activates Th1 helper cells; Macrophages
Basophils! THey want IG E class switch!

6. What are some sinopulmonary infections?
Popliteal
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Sinusitis - otitis media - pneumonia

7. What is the main function of interferons?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
T cell activation; no with CD 4 or CD 8
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
Anti viral and anti tumor

8. 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?
carboxy terminal
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
Bind FcG for antibody dependent cellular cytotoxicity
Macrophages - Dendritic cells - B cells

9. What are the autoantibodies for pemphigus bulgaris?
Daclizumab; prevent ACUTE rejection of renal transplant
Antidesmoglein
Paracortex; viral infection
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

10. What are the autoantibodies for other vasculitides?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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
Anti topoisomerase
Para aortic

11. Type Iv hypersensitivity is...
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
delayed!
Its main effect is a defect in Ab opsonization for killing
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

12. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
SP infections
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

13. Which MHC presents intracellular peptides? how so?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
MHC I; from RER with help of the B2 microglobulin
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

14. The pathogenesis of contact dermatitis is ________ hypersensitivity
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
type four
carboxy terminal
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

15. Other than stimulating fever - what else does IL 6 do?
Alternative splicing of mRNA
Stimulate the liver to release acute phase reactants
2 heavy chains and two light chains
Macrophages - Dendritic cells - B cells

16. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Type IV
Severe pyogenic infections early in life
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
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

17. What are the main cell surface proteins on B cells?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

18. What is the clinical use of Muromonab?
Immunosuppression after kidney transplantation
...
Paracortex
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

19. what cytokine does basophils secrete?
Severe pyogenic infections early in life
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
IL 4
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

20. The secondary follicles have __________; primary follicles are dense
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
pale central germinal centers
Activates cytotoxic CD 8 T cells as second signal

21. What links the adaptive and innate immunity?
Complement activation (active in both)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Remove encapsulated bacateria
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

22. Which is the most abundant antibody in blood?
Anemias (esp due to renal failure)
B - T - and NK cells
MS - hay fever - SLE - goodpastures
IgG

23. what prevents NK cells from killing normal cells if their default is to kill?
S. aureus - E. Coli - aspergillus
Macrophages - Dendritic cells - B cells
Graves
MHC class molecules bind to KIRS or CD94 to prevent killing

24. What are the mediators that mast cells release?
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 :(
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Superficial inguinal
Remove encapsulated bacateria

25. How do you test for type III hypersensitivity?
Its main effect is a defect in Ab opsonization for killing
Immunoflourescent staining of tissue biopsies
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
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

26. What lymph node drains the scrotum?
Remove encapsulated bacateria
Superficial inguinal
Interferon gamma and IL 2
Internal iliac

27. So antibodies are the effectors for the humoral response. List some of their functions.
Severe pyogenic infections early in life
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
...
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

28. What is the main function of IL 12? other than macrophages who else can release IL 12?
A - B - C; all the D's
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Macrophages - Dendritic cells - B cells

29. What is the mechanism for sirolimus? what else it known as?
IgA
Activates cytotoxic CD 8 T cells as second signal
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
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

30. What is anergy? why does this occur?
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

31. which antibody is involved in the primary response or immediate response to an antigen?
IgM
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Thrombocytopenia
B - T - and NK cells

32. What are the two signals required for T cells? what happens after?
Graves
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

33. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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
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
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

34. What are the cell surface proteins on NK cells?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
MHC I - CD16 - CD56
encapsulated
Bind FcG for antibody dependent cellular cytotoxicity

35. What is the white pulp of the spleen?
No because no peptide fragment!
Edema and necrosis in that region
Basophils! THey want IG E class switch!
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

36. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Anti glutamate carboxylase and anti insulin
CD56

37. __________ are a part of the innate system.
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
NK cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
If there is class switching and plasma cell production (that is when memory cells are produced)

38. What cytokines to Th2 secrete?
Th cells fail to produce interferon gamma; a lot of IgE
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 4 - 5 - 10 - 6
Activates Th1 helper cells; Macrophages

39. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
...
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

40. Which diseases are associated with DR2?
MS - hay fever - SLE - goodpastures
IL 5
acute phase reactants
DM type I and RA

41. Which disease is associated with HLA A3?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Increases expression of MHC I and MHC II and also activates NK cells
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Hemochromatosis

42. To what portion of the Antibody do the complements bind?
Fc
Antibody mediated cytotoxicity; either complement dependent or complement independent
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
IL 4

43. What is serum sickness? give an example.
IgG
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
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

44. What is the main cytokine that activates eosinophils?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
lowest concentration
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
IL 5

45. What is the treatment of acute transplant rejection?
Activate macrophages
Cyclosporine - OKT3
False! B cell class switching requires a second signal
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

46. Describe complement dependent Type II hypersensitivity. Give an example.
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
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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 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

47. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
acute phase reactants
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
active complement pathway
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

48. What portion of the lymph node is not well developed in DiGeorge Syndrome?
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Paracortex
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

49. What does interferon gamma do to be antiviral?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Increases expression of MHC I and MHC II and also activates NK cells
Hereditary angioedema; PNH

50. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
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
Influenza; antigenic shift; antigenic drift
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive