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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 are the autoantibodies for graves?
Anti TSh receptor
Liver! (they are proteins circulating in the blood)
Anti U1 RNP (ribonucleoprotein)
RNA segment reassortment

2. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Local infection/inflammation; infection of the ln itself; metastasis
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

3. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Fab portion
...
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
Remove encapsulated bacateria

4. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
2 heavy chains and two light chains
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
CD56

5. other than eat and bite RBCs what else do Macrophages of spleen do>
Anti U1 RNP (ribonucleoprotein)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Remove encapsulated bacateria
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

6. What is muromonab - CD3 (OKT3)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Steroid responsive nephrotic syndrome
Para aortic
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

7. What is the presentation of Brutons agammaglobulinemia?
...
IL 5
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

8. Which diseases are associated with DR5?
DM type I
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
Antibody mediated cytotoxicity; either complement dependent or complement independent
Pernicious Anemia and Hashimotos

9. 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?
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
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
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
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
Cross link
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Th2; Th1

11. To what portion of the Antibody do the complements bind?
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Fc
Immunosuppression after kidney transplantation
Anti smooth muscle

12. What is a type I hypersensitivity reaction? What is atopic?
When you select for which MHC it will have; take out the lymphs that self react
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Activates Th1 helper cells; Macrophages
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

13. what cytokine does basophils secrete?
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
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
The igA found in breast milk
IL 4

14. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
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
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

15. What is the marginal zone of the spleen? what happens there?
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
Humoral
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
CRP - C3b - IgM

16. What are the autoantibodies for pernicious anemia?
isotype
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Anti IF
Liver! (they are proteins circulating in the blood)

17. 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
lowest concentration
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
DM type I

18. What is the defect in hyper IgM syndrome? What are the lab results?
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Its main effect is a defect in Ab opsonization for killing
Daclizumab; prevent ACUTE rejection of renal transplant

19. What are the autoantibodies for autoimmune hepatitis?
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
T cell activation; no with CD 4 or CD 8
Anti smooth muscle
Pernicious Anemia and Hashimotos

20. T/F B cells do not require a second signal
IgE; by activating eosinophils
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
False! B cell class switching requires a second signal

21. From where do cytokines come from?
Anti Jo -1
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
Lymphocytes
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

22. What are the autoantibodies for hashimotos?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Antimicrosomal and antithyroglobulin
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

23. What is oprelevkin? and What is it used for?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IL 1 and IL 6
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Recom IL 11; thrombocytopenia

24. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
IL 5
T cell dysfunction
Wiskott Aldrich syndrome
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 :(

25. can igG cross the placenta?
isotype
Yes
acute phase reactants
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

26. Which is the main antibody in the delayed or secondary response to an antigen?
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
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
IgG
If there is class switching and plasma cell production (that is when memory cells are produced)

27. Leukocyte adhesion defect presents with...
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
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
neutrophilia!
lowest concentration

28. What is recomb beta interferon used for?
DM type I
IL 1 and IL 6
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
MS

29. What does IL 5 do?
Yes
A recomb cytokine of IL 2; RCC and metastatic melanoma
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

30. What does CD16 on NK cells do?
Bind FcG for antibody dependent cellular cytotoxicity
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

31. What is hereditary angioedema? What are the C3 levels?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Glycoproteins; HLA
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
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

32. Describe complement dependent Type II hypersensitivity. Give an example.
Its main effect is a defect in Ab opsonization for killing
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
Axillary
The patient could become cyanotic in the OR!

33. What do multimeric antibodies require for assembly?
heavy chains
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)
A j chain
Local infection/inflammation; infection of the ln itself; metastasis

34. What is a factor that is a predictor for a bad transplantation?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

35. What is the late phase reaction of anaphylaxis allergy? what mediates it?
IgE
TLR ad nuclear receptors
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)
MHC class molecules bind to KIRS or CD94 to prevent killing

36. What are the autoantibodies for Mixed connective tissue disease?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Anti U1 RNP (ribonucleoprotein)
Lymphocytes
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

37. The idiotype; the Fc portion determines the...
Anti Ach receptor
Increases expression of MHC I and MHC II and also activates NK cells
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
isotype

38. other than C3a - what other complement acts as an anaphyloxin?
CRP - C3b - IgM
Stimulate the liver to release acute phase reactants
pentamer
C5a

39. What are the symptoms of serum sickness?
TLR ad nuclear receptors
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Acts as second signal on B cells to induce class switching to IgE and IgG
Negative!

40. What happens in a secondary follicle?
IL 15; IL 12 - interferon Beta and interferon alpha
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Superficial inguinal

41. when can graft versus host disease? What is the result?
Anti alpha subunit 3 of collagen on type IV bm
mesenchymal
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

42. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
All MHC 1/CD8
...
Anti mitochondrial
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

43. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
Anti topoisomerase
Secretory component
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

44. What are C1 - C2 - C3 - C4 important for?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IgM and IgA
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Viral neutralization of igM and IgG!

45. How fast does it occur?
IgG
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
The patient could become cyanotic in the OR!
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

46. What are the autoantibodies for goodpastures syndrome?
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
Receiving preformed Antibodies
isotype
Anti alpha subunit 3 of collagen on type IV bm

47. ________ regulate the cell mediated response.
Anti smooth muscle
Humoral
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

48. What is the clinical use of Muromonab?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
encapsulated
Immunosuppression after kidney transplantation

49. What are the main symptoms of B cell immunodeficiencies?
Delayed type hypersensitivity
A chemotactic factor for neutrophils
IgG
SP infections

50. What cytokines are released by Th1 cells?
Interferon gamma and IL 2
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
mesenchymal