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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.
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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 three types of APCs?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Macrophages - Dendritic cells - B cells
...
Severe pyogenic infections early in life

2. What are four results of a splenectomy?
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
pentamer
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

3. How is the thymus organized? what happens in each section?
Cytokine IL 10 secreted by Th2
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
Anti smooth muscle
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

4. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
Its main effect is a defect in Ab opsonization for killing
MS - hay fever - SLE - goodpastures
active complement pathway

5. What is the pathology seen in chronic transplant rejection?
When you select for which MHC it will have; take out the lymphs that self react
encapsulated
Histamine; post capillary venules - vasodilation
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

6. Which cytokines do Th2 release and For what?
IL 15; IL 12 - interferon Beta and interferon alpha
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Macrophages - Dendritic cells - B cells

7. What is the most common example of passive immunity?
IgG
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
IgAs in mothers breast milk!

8. What lymph node drains the testes?
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Para aortic
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

9. Name the three opsonins
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
TGF beta and IL 10
CRP - C3b - IgM
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage

10. What are C1 - C2 - C3 - C4 important for?
IL 4
Viral neutralization of igM and IgG!
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Anti glutamate carboxylase and anti insulin

11. What is the main function of IL 8?
opsonizes
Secretory component
A chemotactic factor for neutrophils
Graves

12. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Paracortex
not Ab mediated
Basophils! THey want IG E class switch!
Rheumatic arthritis

13. What are the three types of lymphocytes?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
B - T - and NK cells
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
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

14. What happens in a deficiency of C3?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
DM type I
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

15. what ensure that a memory response is generated?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
If there is class switching and plasma cell production (that is when memory cells are produced)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
T

16. What is three common causes of severe combined immunodef? What is the result of all three?
Negative nitroblue tetrazolium reduction test
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
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

17. What are some catalase positive organisms?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
mesenchymal
S. aureus - E. Coli - aspergillus

18. can igG cross the placenta?
Alternative splicing of mRNA
Yes
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
Rheumatic arthritis

19. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Hereditary angioedema; PNH
Superficial inguinal
TNF alpha and IL1

20. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Its a serine protease that activates apoptosis; NK and CD8
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

21. What is the presentation of Brutons agammaglobulinemia?
Th cells fail to produce interferon gamma; a lot of IgE
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
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
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect

22. 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
Edema and necrosis in that region
Activates Th1 helper cells; Macrophages

23. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Kill them because they have CD16 on them that recognize the FcG portion
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
MS - hay fever - SLE - goodpastures
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

24. What is the receptor for EBV? On what cells is that located?
Anti Jo -1
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Complement activation (active in both)

25. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Carbohydrate
Increases expression of MHC I and MHC II and also activates NK cells
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 :(

26. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
Steroid responsive nephrotic syndrome
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
Superficial inguinal
Anti Ach receptor

27. What are the two signals required for T cells? what happens after?
IgM
The patient could become cyanotic in the OR!
mesenchymal
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

28. What are the two signals to kill for NK cells?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
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

29. which cells have more complete tolerance - B or T cells?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
T
Celiac

30. In general What are T cells good for?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Negative nitroblue tetrazolium reduction test
Anti viral and anti tumor
Axillary

31. other than C3a - what other complement acts as an anaphyloxin?
C5a
DM type I
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Negative selection

32. What are the major functions of Antibodies?
...
Anti mitochondrial
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Cyclosporine - OKT3

33. What are the autoantibodies for type I diabetes mellitus?
Immunosuppression after kidney transplantation
IgM and IgA
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Anti glutamate carboxylase and anti insulin

34. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

35. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Immunoflourescent staining of tissue biopsies
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

36. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
Paracortex; viral infection
secondary
Wiskott Aldrich syndrome
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis

37. 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)
Paracortex; viral infection
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!

38. are Th cells involved in trapping of antigens of endotoxin/LPS?
All MHC 1/CD8
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
If there is class switching and plasma cell production (that is when memory cells are produced)
No because no peptide fragment!

39. What does CD16 on NK cells do?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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 :(
Bind FcG for antibody dependent cellular cytotoxicity
Superficial inguinal

40. Name two endogenous pyrogens
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
Basophils! THey want IG E class switch!
IL 1 and IL 6
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

41. What does IL 4 do?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Acts as second signal on B cells to induce class switching to IgE and IgG
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
not Ab mediated

42. What is the common variable immunodeficiency ? How is it different from Brutons?
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
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
Superficial inguinal
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal

43. which antibodies can bind complement?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
IgE; by activating eosinophils
IgM and IgG

44. which antibody is involved in the primary response or immediate response to an antigen?
IgAs in mothers breast milk!
IgM
CD56
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

45. What is serum sickness? give an example.
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
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IgG
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

46. What does IL 10 do? who is secreted by?
Para aortic
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
MHC II - B7
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

47. What do mature naive B lymphocytes express?
IgM and IgD
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Activates Th1 helper cells; Macrophages
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

48. How is the antigen loaded onto a MHC II?
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
Activates Th1 helper cells; Macrophages
IgAs in mothers breast milk!
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

49. give an example of how influenza does a major antigenic shift.
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
RNA segment reassortment
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

50. What is the defect in hyper IgM syndrome? What are the lab results?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Cyclosporine - OKT3
Negative selection
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E