Immune Cells

Mast Cells

Inflammatory

target of corticosteroids

Leukocytes

Neutrophils

Phagocyte

Inflammation

makes compliment
(as does liver)

Monocytes/MDM
(phagocytes)

Eosinophils
(Parasites)

Basophil
(Inflam)

LYMPHOCYTES
(adaptive immunity)

B Cell

VDJ recomb

Rag

AID1

Immunoglobulin

M: Complement activation

G: Opsinization, complement, passive immunity

E: Mast Degranulation - hypersensitivity

A: Mucosal immunity (passive)

Plasma B Cell

IgG

IgE

T Cell
(AIRE)

CD8+

Cytotoxic T cell
+ Macrophages

CD4+ (Th0)
APC: CD4/CD3 binding

Bact/Virus phag by proAPC,
which makes IFNg and IL12,
which binds to STAT4 on Th0

Th1

Simultaneously produces IFNg while downregulating the receptor - so that IFNg only inhibits Th2

Cytokines

TNFa

IL2

GM-CSF

IFNg

Inhibits growth when bound to receptor

Subtopic

Parasite/Allergen
IL-4 / STAT6

Th2

Unknown mechanism - IL-4 is released in response to parasite that stimulates

Cytokines

IL-10

IL-5

IL-4

TGFB

IL-13

no CD28
ANERGY

NK Cells

Macrophages

IL-12
(cellular)

IL-4
(humoral)

=

Main topic

CELLULAR IMMUNITY

Integrin

ICAM/VCAM (endothelium)

Allergy (type 4 DTH)

Poison Ivy

HUMORAL

AB

Allergy

RhIgG = Hemolytic Anemia

Subtopic

Parasite

Aff Mat

After a B cell with antigen is initially activated by at Th cell Affinity Maturation happens in germinal center - B cell is activated by Th2, starts rapidly reproducing and mutating (regulated by Th2). The one with the highest affinity reproduces - some become plasma.1) IgM released by B cells to make immune complexes2) Dentric cells pick up complexes and bring to follicle to allow affinity maturation of B cells3) If B cell has high affinity to an antigen and gets costimulation by Th2 then it starts to proliferate