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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
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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
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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
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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

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5
Q

HLAs and Dx

  • B8
  • C
  • DR2
  • DR3
  • DR4
  • DR5
A
  • Addisons, graves
  • psoriasis
  • MS, SLE, goodpastures
  • SLE, graves hashimotos
  • RA, DM1
  • Hashimoto
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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
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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
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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;
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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
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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
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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
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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
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13
Q

Complement cascade

A
  • ## --
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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
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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
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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;

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