Immuno Flashcards
1
Q
Parts of a LN
- follicle
- medulla
- paracortex
A
- where B cells reside and proliferate, primary: are dormant secondary and proliferating
- where medullary cords are, houses plasma cells
- house T cells, contain endothelial venules where B and T cells can get into blood
2
Q
Spleen
- significance with lymph
- infections
A
- T cells in the PALS, B cells in white pulp and macrophages between red cells and white pulp
- splenic macrophages remove encapsulated bacteria
3
Q
Thymus
- importance
- parts
- Digeorge
A
- where t cells go to mature
- cortex: immature cells, medulla: mature cells, and epithelial reticular cells
- thymic aplasia
4
Q
Difference between MHCI and II
A
all cells have MHCI and present self antigens -> used with CD8+ cells when looking for tumor cells or those with viruses; MHCII only APCs have it and are used to present foreigh antigen to T and B cells
5
Q
HLAs and Dx
- B8
- C
- DR2
- DR3
- DR4
- DR5
A
- Addisons, graves
- psoriasis
- MS, SLE, goodpastures
- SLE, graves hashimotos
- RA, DM1
- Hashimoto
6
Q
Differentiation of T cells
- pathway
- positive selection
- negative selection
A
precursor-> double positive (+ selection) -> single positive (- selection) -> activation (LN)
- cortex -> they are able to detect and bind MHCI
- medulla -> they do not bind to tightly to self antigen on MHCI
7
Q
Cytokines and CD4+ T cell differentiation
- Th1
- Th2
- Th17
- Treg
A
- IL 12, INF gamma
- IL 2 and 4
- TGF beta and IL 6
- TGF beta
8
Q
T helper cells secrete and function
- Th1
- Th2
- Th17
- Treg
A
- 1:INF gamma and IL2; macrophages, neutrophils and cytotoxic t cells; bacteria
- 2: IL 4, 5, 6, 10, 13 ; eosinophils and B cells -> viruses and IgE
- 17: IL 17, 21, 22; neutrophils -> extracellular microbes
- Helper: TGF beta, IL 10 and 35;
9
Q
T cell activation pathway
- pathway
A
- TCR on T cell binds MHCII (CD4+) or MHCI (CD8+) on APC, CD28 on t cell binds B7 on APC as co stimulatory effect
10
Q
B cell activation and class switch pathway
A
- Th cell activated and differentiates -> TCR on t cell binds MHC II on B cell -> CD 40 on b cell binds CD40L on T cell and T cell releases cytokines telling B cell which Ig to class switch to
11
Q
Antibody structure
- heavy chain
- light chain
A
- 2 heavy chains linked together with s hinge, have fab and Fc regions
- 2 light chains, 1 bound to each heavy chain, have variable regions that allow for class switch
12
Q
Ig Types
- G
- A
- M
- D
- E
A
- most common in blood, fixes complement, opsonizes bacteria, can cross placenta
- most common, but on mucosal surfaces, 2 Ig with j chain in between, released into secretion (in breast milk)
- in serum there are 5 connected, but they also act as BCR in monomer form attached to the cell membrane
- Used when B cell is mature and ready to leave the bone marrow to go to the LN and await activation
- On mast cells and basophils, cross links when exposed to allergen; also binds to eosinophils and and activates them in parasite infection
13
Q
Complement cascade
A
- ## --
14
Q
C1 esterase inhibitor deficiency
- what does it do?
- what med is contraindicated
A
- unregulated activation of kallikrinen -> increased bradykinin -> angioedema
- ACE i -> increase bradykinin
15
Q
Paroxsymal nocturnal hemoglobinuria
- pathogenesis
- sequlae
A
- defect in PIGA gene -> prevents formation of GPI -> complement inhibitors such as DAF/CD55 and MIRL/CD59
- complement mediated hemolysis -> decrease in haptoglobin
16
Q
Important cytokines
- IL 1
- IL 6
- TNF alpha
- IL 8
- IL 12
- INF gamma
A
- fever, endo express adhesion molecules, chemo for WBC recruitment
- fever
- activates endo and recruits more WBC
- chemotactic for PMN
- activates NK cells and differentiates T cells into Th1
- secreted by NK and Th1 cells to stimulate macrophages so they can kill phago pathogen
17
Q
Interferons
- types
- function
A
- alpha, beta, gamma
- secreted by virally invaded cell to prime neighboring cells for viral attack -> down reg protein synthesis and up reg MHC expression
18
Q
Passive vs Active immunity
- what are they
- onset
- duration
A
- P: receiving pre-formed antibodies, A: exposure to foreign antigen
- P: fact, A: slow
- P: short, A: long
19
Q
Vaccines
- Live: how does it work, kind of immuno response, benefits and disadvantages, examples
- Killed: how does it work, kind of immuno response, benefits and disadvantages, examples
- Subunit: how does it work, benefits and disadvantages, examples
- Toxoid: how does it work, benefits and disadvantages, examples
A
- micro org loses pathogenecity but retains capacity for transient growth; induces cellular and humoral response; life long response but can revert to virulent form so contraindicated in immuno deficient; adenovirus, polio, varicella, small pox, yellow fever, influenza, MMR, Rotavirus
- pathogen is inactivated by heat/ chems, maintains spitope strx on surface antigens, mainly humoral response; safer than live but not as strong of an effect; Rabies, influenza, polio, Hep A
- include only antigens that best stimulate the immune response; less chance of adverse effect but less of an immune response and much more expensive; HiB, Hep B, HPV, N menin, Strep pneumo
- denatured bacterial toxin w/ intact receptor binding -> stimulates immune response w/o causing dx; protects against toxin but anti-toxin levels decrease over time and may need booster; Tetanus, diptheriae
20
Q
Type I Hypersensitivity
- what is it
- immediate
- late
A
- IgE reaction to allergens
- immediate: antigen cross links IgE on mast cell causing degraulation and release of histamine
- the chemokines bring other cells into the area to mediate an inflammatory response
21
Q
Type II Hypersensitivity
- what is it
- cell fate: destruction: what happens, examples
- cell fate: inflammation: what happens, examples
- cell fate: dysfunction: what happens, examples
A
- antibodies bind to cell surface antigens and induce apoptosis or dysfunction of the cell leading to decreased tissue function
- cell opsonized by antibodies and either phago or NK destroys it, AI hemo anemia, immune thrombocytopenia, transfusion reactions
- antibodies bind to cell and complement system is activated causing MAC complex and destruction; goodpasture, hyperacute transplant rejection
- antibody will bind to receptor -> abnormal blockade or activation of downstream process
22
Q
Type III Hypersensitivity
- what is it
- usual presentation
- serum sickness
A
- immune complexes (antigen and antibody) free floating in serum end up implanting in vacular beds, complement attaches and attract PMNS, causes damage to surrounding tissue
- fever, urticaria, arthralgia, proteinuriaoccur 1-2 weeks after antigen exposure
- antibodies to foreign proteins are produced and 1-2 wks later deposit and cause tissue destruction
23
Q
Type IV Hypersensitivity
- what is it
- Mechanisms
- examples
A
- T cells induce tissue destruction due to foreign antigen
- CD8+ T cells kill targeted cells and CD4+ release inflammation-inducing cytokines
- PPD for TB, contact dermatitis
24
Q
Blood Transfusion reactions
- allergic reaction: how does it happen, time frame
- acute hemolytic transfusion reaction: how does it happen, time frame
- febrile nonhemolytic transfusion reaction: how does it happen, time frame
- transfusion related lung injury: how does it happen, time frame
A
- Type I hypersensitivity against plasma proteins in blood; minutes to 3 hours
- Type II hypersensitivity, ABO incompatitibilty (intravasc) or reaction against foreign antigen on RBC (extravasc); within 1 hr
- cytokines build up during storage of blood products or type II hypersensitivity to donor HLA and WBC; 1-6 hrs
- donor has antibodies that attack host PMNs and pulm endo cells; 6 hrs
25
Q
Auto antibodies
- Anti Ach
- Antinuclear
- IgM against IgG Fc region
- Anti hemidesmosome
- Anti-desmoglein
- Anti- thyroglobulin or thyroid peroxidase
- Ant-TSH receptor
- Anti-glutatmic decarboxylase, islet cell cytoplasmic antibodies
- Anti-glomerular basement membrane
A
- Myasthenia gravis
- SLE
- Rheumatoid Arth
- Bullous pemphigoid
- Pemphigus vulgaris
- Hashimotos
- Graves
- DMI
- Goodpastures
26
Q
Immunodeficiencies
- selective IgA deficiency: sxs, labs
- thymic aplasia: cause, labs
- auto dom hyper IgE: cause, labs
- SCID: causes, sxs, tx
- Hyper IgM : cause, sxs, labs
- Wiskott Aldrich: cause, sxs
- Chronic granulomatous dx: cause, sxs
A
- airway and GI infections, anaphlaxis with IgA containing products; decrease in IgA w/ normal IgG and M
- 22q11 microdeletion -> do not develop 3rd and 4th pharyngeal pouches -> absent thymus and parathyroid; decreased T cell, PTH, Ca
- STAT3 mutation -> deficiency of Th17 helper cells -> cant effectively call PMN when needed; lots of IgE and eosinophils
- defective IL2 (x-linked recessive) and adenosine deaminase deficiency (auto recessive); constant infections; bone marrow transplant
- defective CD40L -> B cells cant class switch (x-linked), severe fevers with infection, lots of IgM
- mutation in WAS -> WBC and platelets cant reorganize cytoskeleton -> defective antigen presentation; thrombocytopenia, eczema, recurrent infections
- defect in NADPH oxidase -> decrease in reactive oxygen -> decrease in respiratory burst in PMNs; increase susceptibility to catalase + org
27
Q
Transplant rejections
- Hyper acute: time frame, how does it occur, consequences
- Acute: time frame, how does it occur, consequences, prevention
- Chronic: time frame, how does it occur, consequences
- Graft vs host dx: time frame, how does it occur, consequences, location of occurence
A
- w/i min, pre-existing recipient antibodies attack donor antigens and activate complement (type II hyper); widespread thrombosis in graft vessels
- weeks to months; CD8+ and CD4+ t cells activated agains donor MHC; vasculitis of graft vessels w/ lots of WBC; prevented/reversed w/ immunosuppresion
- months to years; CD4+ T cells respond to APC presenting donor peptides -> react and secrete cytokines -> proliferation of vascular SM, interstitial fibrosis, parenchyma atrophy
- years; T cells from the graft proliferate in immunocompromised host and reject host cells -> activate host CD4+ and CD8+ cells; most often happens in liver and bone marrow transplants;
