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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 the main cytokine that activates eosinophils?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
IL 5
Immunosuppression after kidney transplantation
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

2. 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?
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
...
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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

3. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
Type IV
Anti glutamate carboxylase and anti insulin
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

4. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
IgM and IgD
Basophils! THey want IG E class switch!
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

5. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IgE
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
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

6. What is the general structure of an Ab?
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 :(
2 heavy chains and two light chains
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
IL 15; IL 12 - interferon Beta and interferon alpha

7. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
Active; passive - fast but short half life (3 weeks!)
Activate macrophages
Paracortex; viral infection

8. What are the main symptoms of T cell immunodeficiencies?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti Jo -1
Anti SS- A (anti RO) and Anti SS- B

9. What is serum sickness? give an example.
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
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
IgA
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

10. What is the marginal zone of the spleen? what happens there?
Anti U1 RNP (ribonucleoprotein)
carboxy terminal
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
Antidote for digoxin intoxication

11. What happens in a deficiency of C3?
Immunosuppression after kidney transplantation
Anemias (esp due to renal failure)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

12. How does complement link innate and adaptive?
Kill them because they have CD16 on them that recognize the FcG portion
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

13. What is the presentation of scid? treatment?
Local infection/inflammation; infection of the ln itself; metastasis
Daclizumab; prevent ACUTE rejection of renal transplant
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
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

14. What is hereditary angioedema? What are the C3 levels?
Anti Jo -1
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
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
NK cells

15. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Antimicrosomal and antithyroglobulin
Activates Th1 helper cells; Macrophages
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Daclizumab; prevent ACUTE rejection of renal transplant

16. The MALT/GALT are not...
Daclizumab; prevent ACUTE rejection of renal transplant
dimer
encapsulated
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

17. IgM can fix complement but...
All MHC 1/CD8
TNF alpha and IL1
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
cannot cross placenta

18. Name two endogenous pyrogens
MHC I - CD16 - CD56
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 1 and IL 6

19. What are the main symptoms of B cell immunodeficiencies?
SP infections
Previous transfusion; pregnant woman whose fetus had paternal antigens
Paracortex; viral infection
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

20. Describe complement dependent Type II hypersensitivity. Give an example.
Negative selection
Influenza; antigenic shift; antigenic drift
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
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

21. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
pale central germinal centers
Anti alpha subunit 3 of collagen on type IV bm
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
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

22. Give an example of someone who could get hyperacute transplant rejection.
type four
Previous transfusion; pregnant woman whose fetus had paternal antigens
IgM
Superficial inguinal

23. What is the treatment of acute transplant rejection?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cyclosporine - OKT3
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

24. Which are the only two antiinflammatory cytokines?
TGF beta and IL 10
Axillary
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Edema and necrosis in that region

25. How do you test for type III hypersensitivity?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Immunoflourescent staining of tissue biopsies
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

26. What is Aldesleukin? What is it used for
Cytokine IL 10 secreted by Th2
A recomb cytokine of IL 2; RCC and metastatic melanoma
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

27. What are some sinopulmonary infections?
TNF alpha and IL1
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
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)

28. What is the presentation of common variable immunodef? and What are the labs?
Tetanus - Botulinum - HBV - Rabies
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
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
except hyperacute

29. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
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!
Complement activation (active in both)
Axillary

30. What are the three types of lymphocytes?
B - T - and NK cells
IgG
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

31. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
If there is class switching and plasma cell production (that is when memory cells are produced)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

32. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Superficial inguinal
except hyperacute
dimer
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

33. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Chronic granulomatous disease
Humoral
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

34. What are the PALS?
Active; passive - fast but short half life (3 weeks!)
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IL 4 - 5 - 10 - 6
Anti topoisomerase

35. What is the toxicity of azathioprine?
Daclizumab; prevent ACUTE rejection of renal transplant
...
Internal iliac
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

36. What is the defect in hyper IgM syndrome? What are the lab results?
If there is class switching and plasma cell production (that is when memory cells are produced)
IL 5
Hereditary angioedema; PNH
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

37. Which diseases are associated with DR2?
DM type I
Steroid responsive nephrotic syndrome
MS - hay fever - SLE - goodpastures
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

38. How is i Th1 helper cell inhibited?
MHC I; from RER with help of the B2 microglobulin
Cytokine IL 10 secreted by Th2
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

39. What are superantigens? give two examples.
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
Fc
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
Anti topoisomerase

40. What are the autoantibodies for goodpastures syndrome?
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
Anti alpha subunit 3 of collagen on type IV bm
Cyclosporine - OKT3
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

41. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
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
Humoral
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

42. when can graft versus host disease? What is the result?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
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
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
Its a serine protease that activates apoptosis; NK and CD8

43. What is recomb gamma interferon used for?
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
IgG
IgAs in mothers breast milk!
Chronic granulomatous disease

44. What is filgrastim and sargramostim? and What is it used for?
IgG
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
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

45. Complements are...
acute phase reactants
No because no peptide fragment!
Rheumatic arthritis
Chronic granulomatous disease

46. ________ regulate the cell mediated response.
IgAs in mothers breast milk!
Antimicrosomal and antithyroglobulin
Steroid responsive nephrotic syndrome
Humoral

47. What does IL 10 do? who is secreted by?
MHC II - B7
isotype
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!
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

48. What are the two signals to kill for NK cells?
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
Antimicrosomal and antithyroglobulin
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Chronic granulomatous disease

49. In thymic development - What is the positive selection? negative selections?
secondary
When you select for which MHC it will have; take out the lymphs that self react
CRP - C3b - IgM
Superficial inguinal

50. What are the autoantibodies for pemphigus bulgaris?
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
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Antidesmoglein
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells