Immuno Flashcards
Parts of a LN
- follicle
- medulla
- paracortex
- 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
Spleen
- significance with lymph
- infections
- T cells in the PALS, B cells in white pulp and macrophages between red cells and white pulp
- splenic macrophages remove encapsulated bacteria
Thymus
- importance
- parts
- Digeorge
- where t cells go to mature
- cortex: immature cells, medulla: mature cells, and epithelial reticular cells
- thymic aplasia
Difference between MHCI and II
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
HLAs and Dx
- B8
- C
- DR2
- DR3
- DR4
- DR5
- Addisons, graves
- psoriasis
- MS, SLE, goodpastures
- SLE, graves hashimotos
- RA, DM1
- Hashimoto
Differentiation of T cells
- pathway
- positive selection
- negative selection
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
Cytokines and CD4+ T cell differentiation
- Th1
- Th2
- Th17
- Treg
- IL 12, INF gamma
- IL 2 and 4
- TGF beta and IL 6
- TGF beta
T helper cells secrete and function
- Th1
- Th2
- Th17
- Treg
- 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;
T cell activation pathway
- pathway
- TCR on T cell binds MHCII (CD4+) or MHCI (CD8+) on APC, CD28 on t cell binds B7 on APC as co stimulatory effect
B cell activation and class switch pathway
- 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
Antibody structure
- heavy chain
- light chain
- 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
Ig Types
- G
- A
- M
- D
- E
- 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
Complement cascade
- ## --
C1 esterase inhibitor deficiency
- what does it do?
- what med is contraindicated
- unregulated activation of kallikrinen -> increased bradykinin -> angioedema
- ACE i -> increase bradykinin
Paroxsymal nocturnal hemoglobinuria
- pathogenesis
- sequlae
- defect in PIGA gene -> prevents formation of GPI -> complement inhibitors such as DAF/CD55 and MIRL/CD59
- complement mediated hemolysis -> decrease in haptoglobin
Important cytokines
- IL 1
- IL 6
- TNF alpha
- IL 8
- IL 12
- INF gamma
- 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
Interferons
- types
- function
- alpha, beta, gamma
- secreted by virally invaded cell to prime neighboring cells for viral attack -> down reg protein synthesis and up reg MHC expression
Passive vs Active immunity
- what are they
- onset
- duration
- P: receiving pre-formed antibodies, A: exposure to foreign antigen
- P: fact, A: slow
- P: short, A: long
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
- 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
Type I Hypersensitivity
- what is it
- immediate
- late
- 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
Type II Hypersensitivity
- what is it
- cell fate: destruction: what happens, examples
- cell fate: inflammation: what happens, examples
- cell fate: dysfunction: what happens, examples
- 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
Type III Hypersensitivity
- what is it
- usual presentation
- serum sickness
- 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
Type IV Hypersensitivity
- what is it
- Mechanisms
- examples
- 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
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
- 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