1-Mucosal Immunity

Purpose of the GI tract's immune system

To eliminate pathogens without triggering an immune response or inflammation.

Role of Goblet Cells in the GI tract

They secrete mucins that help protect the mucosal surface.

Mucins

O-linked oligosaccharides that form a protective barrier in the GI tract.

Function of Paneth Cells

They secrete antimicrobial peptides to help protect against pathogens.

Defensins

Antimicrobial peptides that have antimicrobial properties and help activate immune cells.

Stratification strategy in mucosal immunity

It decreases direct contact between bacteria and epithelium using mucins, antibacterial proteins, and IgA.

Role of compartmentalization in mucosal immunity

It confines bacteria to intestinal sites, limiting exposure to epithelium by utilizing phagocytic cells and activated lymphocytes.

Peyer's Patches

They are found only in the small intestine and contain B cell follicles and germinal centers.

Isolated Lymphoid Follicles

Single B cell follicles found in both the small and large intestines.

Function of the Appendix in immunity

The appendix plays a role in immune surveillance and contributes to GALT.

M Cells

Specialized epithelial cells that sample and transport microbes and antigens to Peyer's Patches.

Unique characteristic of M Cells

M Cells lack microvilli and do not secrete mucus.

Cells found inside M Cells

Dendritic cells (DCs) help take in and present antigens.

Function of Intra-Epithelial Lymphocytes (IELs)

They are CD8+ T cells with a limited antigen response, important for immune surveillance in the epithelium.

Role of dendritic cells in the lamina propria

They capture pathogens and are less likely to activate a Th1 response on their own.

Contribution of Peyer's Patches to lymphocyte activation

They activate lymphocytes, turning them into effector cells that travel through lymph and blood to access mucosal tissues.

Role of Tregs in mucosal immunity

FoxP3+ Tregs suppress cell-mediated immunity, regulated by TGF-beta and IL-10.

IgE-mediated allergies

Cause acute reactions and anaphylaxis.

Non-IgE-mediated allergies

Involve chronic skin/GI symptoms and eosinophilic disorders.

Food allergens entry

Typically enter the body through ingestion, inhalation, or other routes, activating mast cells.

Immediate hypersensitivity

Occurs when IgE binds to FceR1 on mast cells, activating them and releasing mediators that cause symptoms from a runny nose to asphyxiation.

Th2 cell activation process

Allergens attach to DCs, which activate naïve T cells, inducing IL-4 to turn them into Th2 cells.

Role of IL-4 in allergic response

Induces IgE production via activation of B cells, and Th2 cells produce basophils, eosinophils, and mast cells.

Repeated exposure to allergens

Leads to an increase in the amount of IgE, resulting in stronger allergic responses.

Difference between Crohn's Disease and Ulcerative Colitis

Crohn's Disease affects the entire thickness of the bowel wall, often localized to the terminal ileum, while Ulcerative Colitis is confined to the colonic mucosa.

Immune dysfunction in IBD

Overactive Th17 cells, defective defensins, and dysregulated Tregs (FoxP3 and IL-2 or IL-2R deficiencies) contribute to inflammation.

Cause of Celiac Disease

An autoimmune disorder where CD4 T cells cause damage to the intestinal villi after exposure to gluten.

Common symptoms of Celiac Disease

Include abdominal pain, diarrhea, growth failure, anemia, and osteoporosis.

Role of Tissue Transglutaminase (TTG) in Celiac Disease

IgA antibodies to TTG are sensitive and specific for diagnosing Celiac Disease, while IgG tests are used if IgA is deficient.

Genetic risk factors for Celiac Disease

Involves the presence of HLA-DQ2 or HLA-DQ8 alleles.

Gluten processing in Celiac Disease

Gluten is transformed into gliadin via tissue transglutaminase (TTG), which then becomes deamidated and fits better into DQ pockets to trigger immune responses.

Selective IgA Deficiency

The most common immunodeficiency, often compensated by IgM and IgG, causing a higher susceptibility to infections, particularly in mucosal areas.

Novel treatments for Celiac Disease

Include enzyme therapy to digest gliadin, zonulin antagonists to increase intestinal permeability, and inhibition of DQ2/8 antigen presentation to prevent gluten peptide binding and immune activation.