IgA
mucosal surface immunity
innate immunity of GI
goblet cells - mucous
epithelial cells - barrier
paneth cells - antibacterial
M cells - antigen sampling
adaptive immunity of GI
IgA - anti-inflammatory
Th17 - IL-17 and IL-22
suppression of cell-mediated immunity - T regs
FoxP3
T reg cell
-inhibit immune responses
CD103
dendritic cells
cytokines of adaptive immunity
TGF-beta
IL-10
IL-2
celiac disease
deficient fox-p3 cells
-no T regs to inhibit response
stratification
minimize contact between bacteria and epithelium
mucous
compartmentalization
confine bacteria to intestinal sites and limiting systemic exposure
abnormalities in inflammatory bowel disease
dysregulated innate immunity
abnormal cell mediated immunity - overactive Th17
defect T regs
defective autophagy
NLR
PAMP recognition
-in cytoplasm*
crohns disease susceptibility gene
NOD2
is an NLR
food allergies
IgE mediated
non IgE mediated
induction of tolerance in gut
CD103 dendritic cells
TGF-beta
retinoic acid
all 3 to stimulate foxp3 T reg cells
events in immediate hypersensitivity
allergen exposure
repeat exposure
-IgE activate mast cells
release of vasoactive amines and cytokines occurs**
immediate hypersensitivty rxns
vasoactive amines
lipid mediators
late phase rxn
cytokines - hours after exposure
why food allergies
inappropriate digestion hypothesis
celiac disease
T cell mediated
-with other autoimmune disease
sx-abdominal pain, growth failure, anemia, osteoporosis
Abs to tissue transglutaminase
celiac disease
Abs are IgA
useful for diagnosis
celiac genetics
HLA-DQ2 or DQ8
necessary, but not sufficient to develop disease
celiac path
tissue response is to de-aminated gluten
damage is due to the T cells
antibodies - useful for diagnosis
gliadin
breakdown of gluten
resistant to protelytic digestion by GI proteases
celiac disease antibodies
tissue transglutaminase
endomysium
gliadin
deamidated gliadin