extra Flashcards
what antibodies are formed in celiac disease
igA against glutin peptides and tTg
anti ttg
anti gliadin
anti endomysial
igA against skin
dermatitis herpetaformis
igA directed against epithelial ttgase III
what causes celiac
gentic most common
90 pecent have HLA DQ2 and some HLA DQ8
also enviromental hypothesis with cytokines IFN a, il15, 21 and CD4+ against gliadin - activate inhflamation or inhibit Treg
skin epithelial cells
keritinocytes- live at lowest layers and replace top layers
what immune cell in lung
alveolar macrophage
mTg
explanation why CD is more prevalent
has no sequence similarity to human but same function
helps commensal microbes survive
disease that affects phagocyte
leukocyte adjesion deficiency- affects extravasation
CID
older people
leaky hypomorphic mutations causing SCID
RAG/1/2 mutation
omenn sybdrome
what does HIV affect
CXCR4 chemokine receptor onT cells
reduction in CD4+ t cells and lost of pyers patches
isolated lymphoid follicle
secondary lymphoid tissue
transcytose Ag and igA
what cytokines important in class swithcing to igA
BAFF and APRIL
intraepithelial lymphocytes
lymphocytes resident in the MALT
what do commental organisms do in the GIT
promote tolerance w thier SCFA and PSA that skews to a T reg response
what happens to the gut when you are stressed
produce noradrenaline leading to altered gut microbiome- mycrobial dysbiosis- incerase in inflamation- increase in depression
what cell degrandulates in Th2 response
eosinophils by having the ag bound to the igE antibodies
what causes tH1 shift in celiac
if there is viral infection or tissue damage we produce INF Y that shifts to TH1 respones and damage to epithelimu by CTL that recognize self
which hypersensitivities are ab mediated and which are cell
1-3 ab
4 is cell
what cells are in the type 1 activation phse
mast cells and basophils
what causes cross linking of igE and mast cell
anti igE
anti FcERi
chemical
lectins
what increases during the activation phase
cAMP
where are mast cells found
tissue
where are basophils found
circulation
how long does igE remain on cell surface
weeks
mast cells release things
in two phases
1- primary- histamine and herapin
2- secondary- prostaglandins, interleukins, il3 and 4
second/ late phase reaction time
4-6 hours and persists for 1-2 days
third phase reaction time
3-4 days
second phase reaction mediated by
infilatration of immune cells eosinophils and neutrophils
third phase reactino mediate dby
basophils from blood recruiting more neutrophils and eosinophils
atopic march
The atopic march refers to the natural history of allergic diseases as they develop over the course of infancy and childhood
starts with excema
what genes are associated w type I hypersensitivity
il4
igE receptor b chain
MHC
hygeine hypothesis
not exposed to microbes, dont shift from th2 to th1 resposne
old friends hypothesis
not enough helminth infection to diversivy the microbiome
what do we know about what causes allergies
an initiating evnet that damages a barriers in the immune system
along w danger signals that lead to activation of innate and adaptive immune systems
dual allergen hypothesis
need to be exposed orally and cutaneously to skew to T reg response
