Immunology

Production: bone marrow
Maturation: Follicles of lymph nodes

Production: bone marrow
Maturation: thymus
Housing: paracortex of lymph node
Spleen site: PALS (periarterial lymphatic sheath)

axillary nodes

celiac nodeas

superior mesenteric nodes

colonic to inferior mesenteric nodes

internal iliac

superficial inguinal to PARA-AORTIC nodes

superficial inguinal

superficial inguinal

popliteal nodes

right arm and right half of head

Everything else and then goes to IVC

DiGeorge Syndrome

less IgM so less complement activation so less C3b opsonization so susceptibility for ENCAPSULATED organisms

S SHiN (salmonella, s. pneumonia, Haemophila influenza, neisseria meningitidis)

1) howell-jolly bodies
2) target cells
3) thrombocytosis

Corticomedullary junction of the thymus

Fast, non-specific, no memory; macrophages, dendritic cells, NK cells (only lymphoid cells), neutrophils and complement

Slow, specific, memory response is faster and more robust; B-cells, T-cells, circulating antibody

Almost all nucleated cells (not RBCs); presents to Cytotoxic T cells binding TCR and CD8; mediates viral immunity

All antigen presenting cells; presents to T Helper cells by binding TCR to CD4

1) Macrophages
2) Dendritic cells
3) B cells

A3

PAIR: Psoriasis, Ankylosing Spondylitis, Inflammatory bowel dz, and reiter's syndrome

DR3 and DR4

B8

DR2

DR2

DR2

DR2

DR4

DR5

DR5

Steroid responsive nephrotic sydrome

1) make antibody--opsonize bacteria, neutralize viruses
2) activate complement (IgG and IgM)
3) Sensitize mast cells (IgE)

Hyperacute: antibody (B-cell) mediated
Acute and Chronic Organ rejection: T-cell mediated

Thymic Cortex: T cells capable of binding surface self MHC survive

Corticomedullary junction: T cells with high affinity for self undergo apoptosis; want some recognition, but without attack

1) phagocytosis of foreign body by APC
2) presentation on MHC II to Th (signal 1)
3) CD7 costimulation by linking with CD28 (signal 2)
4) Release of cytokines

1) Endogenously synthesized viral or self proteins are presented on an MHC I cell to a CTL via CD8 (signal 1)
2) IL-2 from a Th cell signals T-cell to kill (signal 2)

1) Helper T activation
2) Receptor mediated endocytosis
3) IL-4, 5, 6 from Th2 (signal 1)
4) CD 40 receptor on B-cell binds CD40 ligand on Th2 (signal 2)
5) costimulation from B7 and CD28

1) Cell-mediated response
2) IFN-gamma and IL-2
3) macrophages and Cytotoxic T-cell
4) IL-10 from Th2

1) Humoral Response
2) IL-4,5 and 10
3) B-cells to make antibody
4) IFN-gamma from Th1

Virus-infected cells, neoplastic cells and donor graft cells via apoptosis (granzyme and perforin)

2 heavy and 2 light chains, binds antigen

Constant, carboxyl terminal, complement binding, Determines Isoptype

1) Recombination of V, J light chain and V D, J heavy chain genes
2) random combination of heavy chains with light chains
3) somatic hypermutation

1) Main antibody in 2ndary (delayed) response
2) Fixes complement, opsonizes bacteria, neutralizes bact toxins and viruses
3) can cross the placenta
4) most prevalent antibody in blood

1) Found in secretions
2) monomer in circulation
3) dimer when secrested

1) IMMEDIATE response to antigen
2) Fixes complement, but doesn't cross placenta
3) monomer on b-cell
4) pentamer (helps trap free antigens)

1) binds mast cells, basophils which release histmine
2) hypersensitivity type 1
3) least amount of any immunoglobulin

C1, C2, C3, C4

C3b

C3a, C5a

C5a

C5b-C9

1) Decay-accelerating factor (DAF)
2) C1 Esterase inhibitor

IgG and IgM (antibody-antigen complexes)

Microbe Surface molecules (endotoxin, etc)

hereditary angioedema (ACE inhibitors are contraindicated since more bradykinin)

Severe recurrent pyogenic sinus and respiratory tract infections

Recurrent neisseria bacteremia

complement-mediated lysis of RBCs and PNH

IL-1: Fever
IL-2: T-Cell stimulator
IL-3: Stimulates Bone Marrow
IL-4: Stimulates IgE production
IL-5: Stimulates IgA production

IL-1, Il-6, IL-8, IL-12, TNF-alpha

Causes fever and acute inflammation; induces chemokine secretion to recruit leukocytes

Fever and production of acute-phase proteins

Major chemotactic factor for neutrophils

1)Induces differentiation into Th1 cells
2) activates NK cells
3) deficiency leads to recurrent mycobacterium infection

1) Mediates septic shock
2) Leukocyte recruitment/vascular leak
3) secrete by macrophages

All: IL-3
Th1: IFN-gamma, IL-2
Th2: IL-4, IL-5, IL-10

Growth and differentiation of Bone Marrow stem cells (like GM-CSF)

Stimulates T-cell production (both kinds)

1) activates macrophages and Th1 cells
2) suppresses Th2 cells
3) Anti-viral and anti-tumor properties

1) Induces differentiation to Th2 cells
2) class switching to IgE and IgG

1) differentiation of B-cells
2) Class switching to IgA
3) Eosinophil production

1) Inhibits Th1
2) Activates Th2
3) TGF-B is similar since they both INHIBIT INFLAMMATION

Induce the production of a ribonuclease that inhibits viral but not host protein synthesis by degrading viral mRNA

All: CD3, TCR, CD28
T-helper: CD4
Cytotoxic: CD8

Ig, CD19. CD20, CD21 (EBV receptor), CD40, B7, MHC II

CD14, CD40, MHC II, B7, Fc, C3b

CD16, CD56

MHC I

Self-reactive T-cells become non-reactive w/o costimulatory molecule

Cross-link TCR to MHC II on APCs releasing IFN-gamma from Th1 and subsequent cytokines from macrophages

directly stimulate macrophages by binding to endotoxin receptor CD14

1) receiving preformed antibodies
2) Rapid
3) Short span (3-weeks)
4) IgA in breast milk, antitoxin, humanized monoclonal antibody

tetanus toxin, botulinum toxin, HBV, Rabies (RSV for premies)

1) Exposure to foreign antigens
2) slow
3) long
4) natural infections, vaccines, toxoid

Pros: strong life-long immunity
Cons: may revert to virulent
Examples: Sabin, MMR, VSV, Yellow Fever
Type of rxn: Cellular response (t cells)

Pros: stable and safer
Cons: Need booster
Examples: Salk, Rabies, Cholera, HepA, influenza

1) Anaphylatic and atopic
2) IgE on mast cells and basophils; release of histamine
3) Scratch test (wheel and flare)
4) hives/asthma

1) Antibody mediated: IgM, IgG bind to fixed antigen on enemy cell leading to lysis by complement (MAC) or phagocytosis
2) Test: direct and indirect coomb's
3) disease often specific to site where antigen is found

1) Immune-complex (antibody-antigen-complement stuck together...3 things) activate complement which attracts neutrophils
2) Serum sickness (now caused by drugs)
3) Arthus reaction
4) Test: immunofluorescent staining
5) often vasculitis and systemic involvement

A type III hypersensitivity rxn now caused by drugs resulting in fever, lymphadenopathy, urticaria, arthralgias and proteinuria 5-10 days after exposure; immune complexes are deposited in membranes where they fix complement

A type III hypersensitivity where intradermal injection of antigens induces antibodies which form complexes in skin.
Characterized by edema, necrosis and activation of complement

1) Delayed (T-cell mediated) type
2) T-lymphocytes encounter antigen and release lymphokines leading to macrophage activation (no antibody involved)
3) 4T's: T-lymphocytes, Touching (contact dermatitis), TB testing, Transplant rejection
4) Test: path test
3)

ACID:
Anaphylatic and atopic
Cytotoxic
Immune Complex
Delayed (cell mediated)

Type I reaction against plasma proteins;
Urticaria, pruritis, wheezing, fever

SEVERE, IgA deficient people MUST receive blood that lacks IgA
Dyspnea, bronchospasm, hypotension, resp arrest, shock

Type II hypersenstivity; host antibodies again HLA antigens
Fever, flushing, headaches, chills

Type II; Intravascular (ABO incompatability) or Extravascular (foreign antigen) hemolysis
Fever, jaundice, flank pain, tachypnea, tachycardia, hemoglobinemia