Basic Immunology

active vs passive immunity

pt produces Ab

follows immunization or infn

has memory

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Ab transferred to pt ie gamma glob injections or placenta

no memory

natural vs adaptive immunity

non-specific

no memory ie PMNs, NK, stomach acid

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specific

memory ie T cells, B cells

cellular vs humoral immunity

T cell / lymphokines

1ry defense for viral / fung infn (intracellular orgs)

delayed hypersensitivity ie transplant rejection

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B cell / Ab

1ry defense for bact infn (extracellular org)

Ab dependent cellular cytotox (ADCC)

diagram of Ig

classes of Ig are based on

heavy chains

IgG

highest conc in serum (75% of total Ab conc)

4 subclasses which activate comp (except IgG4)

x-placenta

IgG 2 and 4 assoc w autoimmune d/o

IgG 1 and 3 “ “ dominant in infns

IgM

largest Ab (pentamer)

fixes comp the best!

prominent in early immune response (= acute infn)

5-10% of total Ab conc

IgA

predom Ab in secretions

serum (monomer) & secretory form (dimer)

1ry defense against some local infns at mucosal surface

2 subclasses

IgD

unknown fxn

present on B cell surface

IgE

allergEE

triggers release of histamines from mast cells

immune response curve

IgM followed by IgG → 2nd exposure to Ag → higher IgG response (anamnestic response)

Rosette test for T and B cells

a. incubate srbc w known # of purified lymph (srbc bind to E-rosette receptor CD2 on T cells

b. count rosetted lymphs; % of T cell is calculated

c. estimate B cells = 100% - calc % of T cells

d. estim of absolute counts: pt total lymph ct * % T or B cells

T cells

80% of circulating lymp cell

has TCR-1/2

CD2, 3+ (forms rosette w srbc)

• CD4+ = T helper cell → release cytokines

• CD8+ = T cytotoxic/suppressor cell

• CD4 to CD8 ratio normal = 2:1

• in AIDS pt → flipped 1:2

for viral infn & tumors, delayed hypersens rxn

B cells

5-15% of circulating lymph

has IgD or IgM & comp receptors (C3b) on surface

CD19, 20, 21+

Ab neutralize toxins, activate copm, act as opsonins

Null cells (NK, K)

large lymph, 5-15%

no TCR or Ig on surface

CD16, 56+

kills virus infd cells & tumor cells

can distinguish healthy cells w MHC class I

NK cells: cytotoxic w/o MHC restriction

killer cells: Ab dependent cellular cytotoxicity

_ is mediator of immune complex at a tissue injury

neutrophils recruited by cytokines > release lysosomal enzymes > inflammation

C3b and Fc rcp are present on

B cells and monocytes

normal T to B cell ratio

8:1 ; B cells produce a lot of Ab, they do the job

or 80% T cell, 20% B cell (from ascp boc)

complement fxn

control inflammation

• activates phagocytes (chemotaxis)

• lyses target cells (foreign org)

• opsonization - enhances phagocytic binding by coating foreign org & attaching to complement receptors on neutrophils & monocytes

classical complement pathway

bind in order except at beginning C1, 4, 2, 3

a fragments = go into plasma

b = attach to cell (except C2a and C2b)

alternative complement pathway

starts w C3 → involves C3 again → C5 → MAC complex

activated by LPS, polysacc

involves factors B & D and control factors H&I

both complement cascades require

Ca and Mg++

complement ctrl proteins

classical

C1 esterase inhibitor

C4 binding protein

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alternative

factor I - degrades C3b

factor H - completes w factor B

hypersensitivity rxn types I & II

I = immediate, anaphylactic

IgE-sens mast cells → histamine ie bee sting, hay fever, asthma

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II = Ab-dep

Ab attaches to Ag → cell death

ie tx rxn, AIHA, hashimotos, Goodpasture’s dz

hypersensitivity rxns III & IV

III = large formation of immune complex, not cleared by lymphs

ie Rhematoid arthritis, SLE, serum sickness

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IV = delayed sens-T cells release IL; monocyte & lymp infiltration

takes >12 hr to develop

ie contact dermatitis, TB, leprosy, GVHD

tests for allergy (or for cellular immunity)

skin tests, RIST, RAST

eosinophils in nasal secretions

allergic rxns

phagocytic wbc

neutro, eos, mono

lymph & baso are NOT phagocytic