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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 some sinopulmonary infections?
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
Antidote for digoxin intoxication
Sinusitis - otitis media - pneumonia
Carbohydrate

2. What are the autoantibodies for drug induced lupus?
MHC II - B7
Antihistone
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antidesmoglein

3. What are the autoantibodies for Mixed connective tissue disease?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Anti U1 RNP (ribonucleoprotein)
Recom IL 11; thrombocytopenia

4. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Yes
active complement pathway
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

5. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
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
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Immunoflourescent staining of tissue biopsies

6. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
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)
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
delayed!

7. what secretes IL 4?
Basophils! THey want IG E class switch!
Cytokine IL 10 secreted by Th2
Anti Ach receptor
A chemotactic factor for neutrophils

8. The idiotype; the Fc portion determines the...
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
isotype
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
CD21 on B cells (although there is T cell lymphocytosis in EBV)

9. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Glycoproteins; HLA
Anti Jo -1
Lymphocytes
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. What are the two signals required for T cells? what happens after?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Stimulate the liver to release acute phase reactants
Basophils! THey want IG E class switch!

11. What are four results of a splenectomy?
IL 15; IL 12 - interferon Beta and interferon alpha
T cell activation; no with CD 4 or CD 8
1) susceptibility to encapsulated organisms 2) Howell Jolly Bodies 3) Target cells 4) Thrombocytosis
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

12. What is a factor that is a predictor for a bad transplantation?
Antihistone
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
carboxy terminal

13. which cytokine inhibits TH2 cells? secreted by who?
Interferon gamma; Th1
cannot cross placenta
B - T - and NK cells
MHC I - CD16 - CD56

14. What are the autoantibodies for pernicious anemia?
T cell dysfunction
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Anti IF

15. 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?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Graves
MHC I - CD16 - CD56
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies

16. which type of immunity is slow but long lasting? as opposed to...
Active; passive - fast but short half life (3 weeks!)
A j chain
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
A - B - C; all the D's

17. What are the autoantibodies for wegeners granulomatosis?
Cyclosporine - OKT3
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic

18. What do multimeric antibodies require for assembly?
IgG
IgM and IgA
Antidesmoglein
A j chain

19. What lymph node drains the thigh?
Superficial inguinal
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
The igA found in breast milk

20. which antibody is involved in the primary response or immediate response to an antigen?
IgM
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
Hereditary angioedema; PNH
In the germinal center of secondary follicles (In the paler center)

21. What are the main cell surface proteins on B cells?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Previous transfusion; pregnant woman whose fetus had paternal antigens
The igA found in breast milk

22. What is the general structure of an Ab?
2 heavy chains and two light chains
Th cells fail to produce interferon gamma; a lot of IgE
Cytokine IL 10 secreted by Th2
Superior mesenteric

23. other than mediating shock - what else does TNF alpha do? who releases it mainly?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Secretory component
Activates Th1 helper cells; Macrophages
Sinusitis - otitis media - pneumonia

24. What is the white pulp of the spleen?
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
Axillary
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

25. 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)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
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
except hyperacute

26. What is the pathogenesis of acute transplant rejection? When does it occur?
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
DM type I
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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

27. give an example of how influenza does a major antigenic shift.
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
RNA segment reassortment
Recom IL 11; thrombocytopenia

28. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
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
Pernicious Anemia and Hashimotos
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

29. The MALT/GALT are not...
Delayed type hypersensitivity
2 heavy chains and two light chains
encapsulated
Daclizumab; prevent ACUTE rejection of renal transplant

30. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
Interferon gamma and IL 2
Antihistone
IL 4

31. What are the PALS?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Anti SS- A (anti RO) and Anti SS- B
Anti Ach receptor
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

32. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Paracortex
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

33. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Activates Th1 helper cells; Macrophages
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

34. What are C1 - C2 - C3 - C4 important for?
Viral neutralization of igM and IgG!
DM type I and RA
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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

35. What lymph node drains the lateral side of the dorsum of the foot?
DM type I
Delayed type hypersensitivity
Popliteal
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

36. 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?
Interferon gamma; Th1
DM type I and RA
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
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

37. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Axillary

38. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Paracortex; viral infection
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

39. What does granzyme do? who secretes it?
Rheumatic arthritis
Complement activation (active in both)
Its a serine protease that activates apoptosis; NK and CD8
Kill them because they have CD16 on them that recognize the FcG portion

40. What does IL 5 do?
heavy chains
Cells that stil have weird parts of their membrane that macrophages usually bite off
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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

41. What are the autoantibodies for goodpastures syndrome?
Anti alpha subunit 3 of collagen on type IV bm
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
except hyperacute
Negative selection

42. What is the common variable immunodeficiency ? How is it different from Brutons?
Anti glutamate carboxylase and anti insulin
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Immunosuppression after kidney transplantation
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

43. Type IV hypersensitivity is i...
not Ab mediated
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Anti topoisomerase
lowest concentration

44. What is the presentation of Brutons agammaglobulinemia?
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Increases expression of MHC I and MHC II and also activates NK cells
Secretory component
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

45. what cytokine does basophils secrete?
2 heavy chains and two light chains
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!
IL 4
not Ab mediated

46. What is recomb gamma interferon used for?
A - B - C; all the D's
If there is class switching and plasma cell production (that is when memory cells are produced)
Superior mesenteric
Chronic granulomatous disease

47. IgM can exist as a _______ also
Popliteal
...
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
pentamer

48. What do mature naive B lymphocytes express?
MHC I; from RER with help of the B2 microglobulin
IgM and IgD
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

49. What is the toxicity of muromonab?
Complement activation (active in both)
Its main effect is a defect in Ab opsonization for killing
IgE; by activating eosinophils
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

50. What is oprelevkin? and What is it used for?
Recom IL 11; thrombocytopenia
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
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
CD56