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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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1. Leukocyte adhesion defect presents with...
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
acute phase reactants
neutrophilia!
Axillary

2. Which disease is associated withB B27?
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
Its a serine protease that activates apoptosis; NK and CD8
Type IV
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

3. are Th cells involved in trapping of antigens of endotoxin/LPS?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
No because no peptide fragment!
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
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

4. What does Interferon alpha and beta do? how?
TGF beta and IL 10
Alternative splicing of mRNA
Tetanus - Botulinum - HBV - Rabies
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

5. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
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
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

6. 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 )
Local infection/inflammation; infection of the ln itself; metastasis
Chronic granulomatous disease
mesenchymal

7. What are C1 - C2 - C3 - C4 important for?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Type IV
Viral neutralization of igM and IgG!
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

8. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
Alternative splicing of mRNA
MHC I; from RER with help of the B2 microglobulin
If there is class switching and plasma cell production (that is when memory cells are produced)
Immunosuppression after kidney transplantation

9. is IgM an opsonizer?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
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
except hyperacute
Negative!

10. What is the general structure of an Ab?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
2 heavy chains and two light chains
opsonizes
Barrel hoop basement membrane fenestrations

11. The two heavy chains of an antibody contribute to the...
Fab portion
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
Superficial inguinal
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

12. What happens in a deficiency of C3?
Yes
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Antidote for digoxin intoxication
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

13. Which HLA's are included in MHC I? MHC II?

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14. What are the cell surface proteins for Macrophages? which two are for opsonins?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
type four
MS
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

15. What does IL 5 do?
Anti U1 RNP (ribonucleoprotein)
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Increases expression of MHC I and MHC II and also activates NK cells
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

16. What is the presentation of Brutons agammaglobulinemia?
Anemias (esp due to renal failure)
No because no peptide fragment!
Increases expression of MHC I and MHC II and also activates NK cells
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

17. What do mature naive B lymphocytes express?
IL 5
Active; passive - fast but short half life (3 weeks!)
MS
IgM and IgD

18. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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
carboxy terminal
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

19. So antibodies are the effectors for the humoral response. List some of their functions.
Thrombocytopenia
IgE; by activating eosinophils
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

20. What does interferon gamma do? What two type of cells does it attack mostly?
False! B cell class switching requires a second signal
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Rheumatic arthritis

21. The MALT/GALT are not...
secondary
encapsulated
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Inferior mesenteric

22. Monomer in circulation - ___ when secreted
MS - hay fever - SLE - goodpastures
pathogenesis
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
dimer

23. What are the cell surface proteins on NK cells?
Anti alpha subunit 3 of collagen on type IV bm
Activates Th1 helper cells; Macrophages
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
MHC I - CD16 - CD56

24. What are the autoantibodies for systemic sclerosis?
isotype
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Cytokine IL 10 secreted by Th2
Anti topoisomerase

25. What are the main cell surface proteins on B cells?
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Paracortex
NK cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

26. What cytokines are released by Th1 cells?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Interferon gamma and IL 2
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
DM type I

27. what secretes IL 4?
Basophils! THey want IG E class switch!
T
Hemochromatosis
Fab portion

28. What are the autoantibodies for polymyositis and dermatomyositis?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Anti Jo -1

29. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
A - B - C; all the D's
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Anti alpha subunit 3 of collagen on type IV bm
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

30. What lymph node drains the duodenum - jejunum?
Activate macrophages
Previous transfusion; pregnant woman whose fetus had paternal antigens
Superior mesenteric
Liver! (they are proteins circulating in the blood)

31. what cell surface marker is used for NK cells as it is unique to them?
IgAs in mothers breast milk!
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
CD56
Inferior mesenteric

32. What are the two signals required for T cells? what happens after?
NK cells
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

33. What is passive immunity?
Tetanus - Botulinum - HBV - Rabies
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
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
Receiving preformed Antibodies

34. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
type four
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Activates Th1 helper cells; Macrophages
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!

35. Give an example of someone who could get hyperacute transplant rejection.
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Previous transfusion; pregnant woman whose fetus had paternal antigens
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Negative nitroblue tetrazolium reduction test

36. Name the three opsonins
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
CRP - C3b - IgM
IgM and IgG
DM type I and RA

37. In general What are T cells good for?
Anti viral and anti tumor
NK cells
pathogenesis
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

38. What do multimeric antibodies require for assembly?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
A j chain
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Influenza; antigenic shift; antigenic drift

39. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Complement activation (active in both)
Th cells fail to produce interferon gamma; a lot of IgE
Anti U1 RNP (ribonucleoprotein)

40. What are four results of a splenectomy?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Negative nitroblue tetrazolium reduction test
Axillary

41. What bugs can actually infect the lymph node itself?
Acts as second signal on B cells to induce class switching to IgE and IgG
Immunosuppression after kidney transplantation
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
S. aureus - E. Coli - aspergillus

42. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
Anti IF
Antidesmoglein
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

43. Which diseases are associated with DR4?
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
DM type I and RA
NK cells
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

44. which B and T cell disorder presents with specifically low IgM?
Active; passive - fast but short half life (3 weeks!)
A j chain
MHC I - CD16 - CD56
Wiskott Aldrich syndrome

45. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
IgM and IgA
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
C5a
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

46. Which is the main antibody in the delayed or secondary response to an antigen?
Superficial inguinal
IgG
Not thymus - BM
Bind FcG for antibody dependent cellular cytotoxicity

47. what cytokine does basophils secrete?
Lymphocytes
IL 4
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

48. What is the mechanism for sirolimus? what else it known as?
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
type four
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

49. What does interferon gamma do to be antiviral?
Increases expression of MHC I and MHC II and also activates NK cells
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

50. 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
T
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Complement activation (active in both)

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USMLE Step 1 Immunology

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