LMP299Y1 Lecture Notes - Lamina Propria, Muscularis Mucosae, Inflammatory Bowel Disease
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Published on 3 Jun 2013
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March 27, 2013
Multiple organs considered part of GI tract
- Divide into luminal GI – liver and pancreas – upper tract and lower tract
- Upper tract = stomach and small intestine
- Liver and pancreas are the two solid organs
Lymphoid cells of the GI – GALT
Lymphoid immune system – called GALT
Amount of T cells in gut >>> number in spleen – most abundant
Mostly t cells with gamma delta receptors – mostly CD8 positive
Plasma cells secreting IgA2
Stomach/small bowel histology
Small intestine – surface epitheium – villi considered mucosa; then muscularis mucosa; submucosa;
muscularis externa;
Ileum – most prominent lymphoid tissue is peyer’s patch – they are lymphoid follicles in lymphoid
propria – important for GI immunity
Colon – epithelium –
Appendix – more lymphoid tissue in appendix than lymphoid tissue – most common area to find
lymphoid tissues/follicles
Closer look at the appendix – crypts are glands;
Components of the GIT – area between villi – lamina propria – muscularis mucosae –
Lamina propria lymphoid cells are cells in between the villin and intraepithelial lymphocytes are
between the epithium in the villi themselves
Special GALT sites
Peyer’s patches –
FAE – intraepithelial lymphocytes are FAE – epithelium on top of lymphoid follicle – these are M cells
M cells ultrastructure – see infoldings, not vili – function has antigen presenting inside – can transport
bacteria/viral molecules into the lamina propria and as the number of the luminal bacteria increases,
the number of M cells also increase – darker looking under microscope –
FAE – M cells – usually associated with alpha beta memory T cells – instead of gamma/delta
IgG and IgA cells rarely found – most of Ig secreted by these cells are IgM and IgG
HLA receptors on the basal lateral aspects of these cells – HLA involved in immune system as well
Discontin ous – different from terminal ilium, lots of peyers’s patches
Special GALT sites
In stomach, get lymphoid tissue but do not get lymphoid follicle – lymphoid tissue has mixture of mostly
T cells but lymphoid follicle has certain structure – lighter middle, darker outline are lymphoid follicle,
should not be seen in stomach
When infection in stomach or gastritis, see lymphoid follicles – they are acquired! Not there to begin
with
Function of gut epithelium – digestion and absorption – make tight junctions so works ars barrier of
antigen and bacteria to lumen
Process the antigen and transport to lamina propria – express class 2 antigen but do not have
costimulatory molecules –
Components of GIT –
IEL vs LPC
IEL at tips of villi; LPC between villi
IEL – mostly CD3 POSITIVE; majority are CD8 positive, so cytotoxic;
GIT immune response
Will not go through lymphomas and small bowel transplantation
Can get celiac disease other parts of GI tract – mostly in lower GI tract (small intestine)
GASTRITIS
Acute – alchol induced, NSAIDS incudec, H pylori induced – also autoimmune disease
Autoimmune gastritis for the most part present as chronic disease
Eosinophilic – increase in number of eosinophils
Collagenous –
Graft vs host disease – in transplantation when the antibodies invade native organs
H pylorid present as chronic disease as well –
Autoimmune gastritis – get autoantibodies into cells – most – for intrinsic factos – two types of
antibodies there – blocking antibodies and binding antibodies – mostly blocking antibodieng – how
pernicious anemia results
B12 deficiency – pernicious anemia involve din adsorption of B12
Clinical effects of autoimmune gastritis – destroys crypts and glands – antibodies against these glands,
so get destruction and thus atrophy – atrophy of glands can result from other things as well like
prolonged h ylorid infection
Decreased in intrinsic factor – does not bind, so B12 not absorbed
Divisions of the stomach
Autoimmune gastritis mostly involved body
Normal gastric folds – when there is atrophy, these folds are gone in an advanced stage of gastritis
Autoimmune gastritis with hyperplasia of endocrine cells – glands - little dark areas are lymphocytes
increased in numbrs – endocrine cells – not enough stimulation to proeduce acid, so cells that stimulate
acidsecrection increase to compensate for eduction in acid – so get hyperplasia of endocrine cells
IF picture – highlights autoantibodies in parietal cells – see all the bright areas – have antibody against
parietal cells
Gastritis – eosinophilic gastritis and lymphocytic gastritis not discussed
H pylorid gastritis