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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 autoantibodies for autoimmune hepatitis?
Th2; Th1
TNF alpha and IL1
Anti smooth muscle
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

2. What are the four steps in phagocytosis? What are the four disease that correspond to each step?
Anti glutamate carboxylase and anti insulin
Glycoproteins; HLA
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
IgM

3. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Immunoflourescent staining of tissue biopsies

4. other than eat and bite RBCs what else do Macrophages of spleen do>
MHC I - CD16 - CD56
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
Remove encapsulated bacateria
cannot cross placenta

5. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Kill them because they have CD16 on them that recognize the FcG portion
No because no peptide fragment!
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

6. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Axillary
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
DM type I

7. What are the autoantibodies for Mixed connective tissue disease?
IgM
Sinusitis - otitis media - pneumonia
Anti U1 RNP (ribonucleoprotein)
Antihistone

8. What happens in a secondary follicle?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
TGF beta and IL 10
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)
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep

9. 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 )
If there is class switching and plasma cell production (that is when memory cells are produced)
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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

10. What is the white pulp of the spleen?
Activate macrophages
MS - hay fever - SLE - goodpastures
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Anti TSh receptor

11. where do NK cells develop?
Histamine; post capillary venules - vasodilation
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Not thymus - BM
Activate macrophages

12. What is recomb beta interferon used for?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
MS
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Secretory component

13. What does IL 4 do?
MS
Acts as second signal on B cells to induce class switching to IgE and IgG
IgE
Remove encapsulated bacateria

14. Give three examples of bacteria that use antigenic variation and how.
DM type I and RA
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti SS- A (anti RO) and Anti SS- B
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

15. What is the pathology of acute transplant rejection? is it reversible?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor

16. What is the treatment of acute transplant rejection?
RNA segment reassortment
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
Cyclosporine - OKT3
Fab portion

17. What lymph node drains the anal canal (below the pectinate line)?
Activates Th1 helper cells; Macrophages
Cyclosporine - OKT3
Superficial inguinal
Hereditary angioedema; PNH

18. How does igA cross the epithelium?
By transcytosis
delayed!
Anti Jo -1
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

19. Which is the main antibody that provides passive immunity to infants?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
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

20. What does Interferon alpha and beta do? how?
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; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Barrel hoop basement membrane fenestrations
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

21. What is recomb gamma interferon used for?
Edema and necrosis in that region
Th2; Th1
Chronic granulomatous disease
Activates cytotoxic CD 8 T cells as second signal

22. To what portion of the Antibody do the complements bind?
Graves
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Antimicrosomal and antithyroglobulin
Fc

23. which cells have more complete tolerance - B or T cells?
T
neutrophilia!
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antidesmoglein

24. when can graft versus host disease? What is the result?
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Th cells fail to produce interferon gamma; a lot of IgE
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!
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

25. What are the autoantibodies for primary biliary cirrhosis?
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Anti mitochondrial
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
Fc

26. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
cannot cross placenta
Complement activation (active in both)
T cell dysfunction

27. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
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

28. what characterizes an arthus reaction?
Edema and necrosis in that region
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
SP infections

29. what bacteria are a splenectomy patient most susceptible to? why?
T cell activation; no with CD 4 or CD 8
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Interferon gamma and IL 2

30. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Viral neutralization of igM and IgG!
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Activates cytotoxic CD 8 T cells as second signal

31. What are the mediators that mast cells release?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
T cell activation; no with CD 4 or CD 8
MHC I; from RER with help of the B2 microglobulin
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

32. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
Delayed type hypersensitivity
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Anti Ach receptor
Daclizumab; prevent ACUTE rejection of renal transplant

33. What is the clinical use of Muromonab?
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Immunosuppression after kidney transplantation
pentamer
Internal iliac

34. Which helper T cells' development is induced by IL 4? IL 12?
A - B - C; all the D's
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
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Th2; Th1

35. Which MHC presents intracellular peptides? how so?
IgG
T cell dysfunction
MHC I; from RER with help of the B2 microglobulin
Anti U1 RNP (ribonucleoprotein)

36. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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 :(

37. 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?
Hereditary angioedema; PNH
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
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
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation

38. What are C1 - C2 - C3 - C4 important for?
Axillary
Th cells fail to produce interferon gamma; a lot of IgE
encapsulated
Viral neutralization of igM and IgG!

39. What is the receptor for EBV? On what cells is that located?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
C5a
cannot cross placenta

40. which B and T cell disorder presents with specifically low IgM?
MS
Wiskott Aldrich syndrome
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency

41. 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?
IgG
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
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
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 :(

42. What are the PALS?
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
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Graves
Chronic granulomatous disease

43. What is colostrum?
IgAs in mothers breast milk!
The igA found in breast milk
Inferior mesenteric
Lymphocytes

44. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
IL 4
All MHC 1/CD8
Anti Jo -1

45. IgE has the ___________ in the serum
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
type four
lowest concentration
Lymphocytes

46. What are the main Cell surface proteins on T cells?
When you select for which MHC it will have; take out the lymphs that self react
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
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

47. IgM can fix complement but...
T cell precursor
Its a serine protease that activates apoptosis; NK and CD8
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
cannot cross placenta

48. what secretes IL 4?
secondary
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Basophils! THey want IG E class switch!
DM type I and RA

49. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
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 :(
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Basophils! THey want IG E class switch!

50. What type of side chains are found on Fc region of an antibody?
A - B - C; all the D's
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 Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Carbohydrate