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1. GI 3 > mucosal immunity > Flashcards

mucosal immunity Flashcards

1
Q

mucosal immunity normal vs abnormal

A

normally- physiologic inflammation- usually tolerated and innate barriers limit immune responses to bacteria, viruses, fungi, parasites and ingested Ags

abnormal- pathophysiologic inflammation disease
Acute- infection
Chronic/recurring- ibd, celiac, food allergy

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2
Q

Host defense 3 phases

A

Immediate- an existing physical, chemical, and ecoogical barrier

Early: Existing innate, immune cells and inflammatory messengers

late- activation of adaptive immune cells (T cells and or b cells ) and messengers

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3
Q

Immediate host defenses in the epithelium

A

Epithelium- Tight junctions maintain integrity between external and internal compartments

Pattern Recognition receptors- activate immune response

Anti microbial peptide secretion

Epithelial shedding and repair

Epithelial ion transpoert and muscle contractions- diarrhea

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4
Q

immediate host defenses- microbiota

A

Compete for resources with virulent organisms, produce their own anitmicrobial peptides (AMPs)- bacteriocidins

Keep innate immune cells in a n attentive state

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5
Q

Peyers patches

A

Specialized immune tissue located in the gut

Follicle associated epithelium covers it, in the follicle epithelium contains M cells- attraction of bacteria, acts as an APC to present the gut bacteria to a Dendrtitic cell- and take it to the follicle to potentially activate T cells

Under neath the single layer of epithelium is a follicle

Parafollicular cortex (on the edge)- contains lots of T cells

In the germinal center (center)- contains lots of B cells

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6
Q

Early host defense- recognition of pathogens

A

innate receptors for bacterial PAMPs (recognized by PRRs) expressed in cytoplasm and on basolateral membrane, but not on lumenal surface

Dendritic cells in the lamina propria express low levels of TLRs

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7
Q

Cell associated pattern recognition receptors

A

TLRs on the plasma membranes of epithelial cells, Dcs, Macrophages, PMNs, they recognize PAMPs- bacterial, virla and fungal structures

Nod-like receptors- in the cytoplasm of epithelial cells, macrophages, and PMNs, they recognize- Bacterial wall components (peptidoglyans), and viral RNA

Mannose receptors on the membrane receptors on phagocytes- recognize bacterial cell wall carbohydrates and fungal wall glycans

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8
Q

Secreted pattern recognition receptors

A

CRP - in the plasma- recognizes Microbial cell wall components

Mannose binding lectin (MBL)- in plasma) recognizes bacterial cell wall carbohydrates

Complement C3- in plasma recognizes cell wall

IGM- in the plasma and gut lumen- recognizes BActerial cell walls

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9
Q

intestinal bacterial infections categories

A

Minimally invasive- Campylobacter, clostridium, candida, cryptococcus

Invasive- Listeria, enteroinvasive E coli, (opportunistic)-clostridium and shigella

Toxigenic- Enterotoxigenic E coli, vibrio cholerae, clostridium, shigella

PRRs that recognize bacteria: TLRs 2 4 5, Nod 1 2, Complement

Prrs that recognize fungi- TLRs 3 4 5, C3b, IgM

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10
Q

Early innate response phase

A

Bacteria gain entrance to interior, taken up by DCs, DC makes IL2 to activate macrophages, DC leaves the epithelium and goes to the lymphatics – goes to peyers patches, makes ILs and activate inflammaotry cells in endothelium (IL6 TFB

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11
Q

How the adaptice response phase is acitvated

A

DC enters presnts pathogen via MHC 2
CD4 cells get activated make TGFB and IL6–> make Th17 or Th1 cells

The Th 17 and Th1 cells either go back to the gut mucosa or they secrete IFNg to differentiate a Naiive B cell to a plasma cell to secrete IgG or IgA

in the gut mucosa IL 17 andIL 22 strengthen the defense mechanisms and clear the bacterial infection-> increased immune cell trafficking leads to an inflammed gut

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12
Q

anti viral host defense

A

Viral PRRs- TLRs 3 7 9, RIG 1 and IgM

Enteric viruses- rotavirus, norwalk virus, enteroviruses

DC cells phagocytoze the virus, activation, MHC 1 –> effector cytoxic cells, NK cells (making IFNg)– or IgA/IgG Plasma cell

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13
Q

Anti parasite host defense

A

not phagocytosed, Trematodes (schistisoma, nematodes (strongyloides), Cestodes (taenia saginata)

Granulocytes defend against parasites- granulocyes (eosinophils, basophils, mast cells defend the host by releasing their granule contents)- enzymatically digest tegument- stimulate propulsive muscle

Granulocytes are acitvated by Ag- bound IgE binding cell surface FceRI- require prior Ag exposure (sensitization)

Produce chemokines and cytokines to recruit and activate macrophages and lymphocytes to site of infection

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14
Q

Why do we not mount an immune response against food or microbiome bacteria

A

Immunogen- a molecule that induces an immune response
Anitgen- a molecule that is recognized and binds to antibody on B cells or T cell receptors on T cells

Tolerogen a molecule that induces immune unresponsiveness to subsequent doses of the molecule

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15
Q

tolerance

A

Self or Non self
Self?–> suppress immune response (tolerance)
Non- self?–> activate the immune response (Immunity)

Immunologic tolerance= Specific unresponsiveness to an individuals SELF antigen

Both T cells and B cells can immunologically tolerate antigenic molecules

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16
Q

in mucosa- the decision is a little complicated

A

Respond or not respond to self, food, microbiota

Respond= immunity

Not respond= tolerance

What makes something an immunogen?

Things that will increase immune response: large molecule, intermediate does, Sub G (vs intragastric), complex composition, comes with bacteria, interaction with MHC is effective

17
Q

mucosal tolerance

A

Oral tolerance- the state of local and systemic immune unresponsiveness that is induced by oral administration of innocuous Ags such as food proteins

Mucosal tolerance: state of local and systemic unresponsiveness induced by the commensal microbiota

Mucosal induced tolerance helps prevent intestinal disorders (Celiac, IBS, food allergy)

Humoral NEUTRALIZING IGA is the most prevalent form of adaptive immunity in the gut

Th17 cytokine response is the most predominant cell-mediated immune response

Non responsiveness to food and microbiota is mediated by tolerogenic DCs and regulatory T cells

18
Q

Mucosal Trafficking and retinoic acid

A

Gut homing traffic signals- Immune cells a4B7 integrin an dCCR9, Endothelium- mucosal addressin MadCam, Epithelium- mucosal trafficking signal CCL25

Mucosal DCs produce REtinoic acid from dietary Vitamin A through expression of REtinal Dehydrogenases

Intestinal epithelial cells also express retinal dehydrogenase–> elevated Retinoic acid in gut tissues

19
Q

Retinoic Acid, TGFB etc establish these as tolerogenic mucosal DCs

A

Gut dendrtitic cells Take up Ags from the gut (food microbiota), travel to MLN present Ag to naive T cells

These cells produce retinoic acid and TGF B–> drive differentiation of CD4 naive T cells to become regulatory T cells (FoxP3+)- absent proinflammatory signals

20
Q

IgA Class switching

A

T dependent: Soluble Ag, Activate B cell, Phagocytosed presented to T cells, DCs in peyers patch present Ag and activate naive T cells to Th1 cells, CD40 on Th1 cells and TGFB from DCs activates naive B cells

T- independent- soluble Ag recognized by B cell, TLR on DC stimulate release of TGF B, with IL6 and Retinoic Acid

21
Q

Th17 T cells promote mucosal protection

A

MHC 2 restricted, Naive CD4 t cells differentiate into effector CD4 Th17 Cells in response to CD40L, IL6, IL 23, and TGFB

Effector CD4+ Th17 cells secrete IL 17 and Il22-> increased barrier function, anti microbial peptide secretion, Production of inflammatory cytokines, for macrophages and neutrophils

22
Q

autoimmunity- loss of immunologic tolerance

A

the principle factors in autoimmunity are:
Over activation of immune system to typically innocuous Ags (hypersensitivity)
Inheritance of susceptibility genes
environmental triggers may activate self reactive or tolerized lymphocytes

23
Q

Hypersensitivity

A

Excessive or aberrent immune responses following challenge wiht ag

Caused by- dysregulated or uncontrolled response to foreign Ags resulting in tissue damage and injury. OR failure of self tolerance followed by immune responses directed at self Ags (Autoimmunity)

Heterogenous group of disorders (type of immune response B cells vs Tcell)- nature and location

24
Q

Hypersensitivity types

A

Type 1: Allergy immediate- IgE mediated, mast cells and eosinophils, vasoactive amines, and cytokines

Type 2: antiBody mediated, IgM and IgG, surface Ags–opsonization/phagocytosis, complement, Fc recruitment of leukocytes

Type 3- immune Complex mediated- IgM and IgG soluble Ag- complement and FC recruiment of leukocytes

Type 4- Delayed cell mediated- T cells- CD4 macrophages activation and inflammation

25
Q

Autoimmunity Genetics

A

Multiple genes predispose to autoimmune diseases

HLA genes are linked

Non HLA genes- additional non-MHC genes (Nod 2 (a PRR) and ATG16 (autophagy gene in inflammation)

Mutations in MHC may contribute to autoimmune disease through- inefficient in displaying self ags or poorly stimulate regulatory T cells

26
Q

celiac disease

A

Loss of tolerance to wheat- glutn) increased levels of deamidated gliaden peptide- loaded in MHC molecule

Autoimmune disorder- associated with HLA DQ 2 and DQ8 presence of auto antibodies to tissue transglutaminase (diagnostic), endomysium and gliadin peptide

Type 4 hypersensitivty- Th1 t cells and inflammatory damage to gut tissues

27
Q

IBDs

A

loss of tolerance to microbiota- mutations in Nod PRR gene, mutations in ATG autophagy (cellular homeostasis) genes

Autoimmune disorders (Associated with HLA Dr adn HLA B27

type 4 Hs- th1 (crohns) or th2 (ulcerative colitis)–> inflammatory damage

28
Q

food allergy

A

loss of tolerance, not autoimmunity,

type 1 HS0 sensitized to food Ag, immediate response, eosinophilic esophagitis, food protein induced enterocolitis syndrom (rare cell mediated

29
Q

treating AI diisease

A

eliminating symptoms by suppressing the Immune response

1. GI 3 (13 decks)

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