IEL

TCR+

TCR-(2subset)

resident to the intestinal epithelium

express

express a homodimer of CD8α

the integrin αEβ7

90% - have TCR

induced

natural

expression

CD44,69,16,122,161

resemling ILC

iCD3

iCD8α

expression

CD2, CD5,
CD28, LFA-1 and Thy1

subsets

CD4

derived from antigen-experienced conventional TCRαβ+ T cells

CD8

largest T cell subset in peripheral lymphoid organs, are also found in the IEL compartment.

SOME

migrate into the intestinal epithelium where they can respond to subsequent antigenic challenges as bona fide effector or tissue-resident memory T cells

TCRαβ+CD4+CD8αα+ IEL

human intestinal epithelium

regulation by microbiota

cytolytic activity-granzyme expression

regulatory function

IL10 production

TCRαβ
+CD4+CD8αα+Foxp3− phenotype

by FOXP3 T reg

TCRαβ+CD8αβ+

70-80% of the total IEL

effector or memory cells

granzyme B, CD69, CD103 and β7 integrin.

lower amounts of TNF-α and IFN-γ.

some express CD8αα

express inhibitory and co-activating NK cell receptors

implicated in ciliac

TCRαβ+ or TCRγδ+ T cells

lack expression of
CD2, CD5, CD28, LFA-1 and Thy1

expression of cytotoxic mediators such as granzyme B, and display a variety of NK cell receptors

TCRαβ+ IEL

TCRαβ+CD8αα+ IEL

heterogeneous population of
cells with diverse MHC class I restriction


develop in cryptopatches

TGF-B play arole in CD8aa expression

influenced homeostasis by microbiota

NOD2

Vit D

enriched with LAG3,TGF-B3,FgL-2

immunity against colitis by IL10

TCRγδ+ IEL

10–15% of all IEL are TCRγδ+ cells

MOST Vγ7 and some express Vγ1 or Vγ4

extrathymic origin

development dependent on BTLN rather food or microbiota

expression

IFN-γ, TNF-α,

TGF-β, IL-10, and IL-13, prothymosin β4, keratinocyte growth factor (KGF), and antimicrobial proteins

migration

homotypic
interactions mediated by the tight-junction protein occludin

express antimicrobial effectors

MYD88 mediated

inhibit activation of other immune cells

resemble ILC1

express NKP44

lineage relationship with NK and ILC1

memory-activated phenotype, produce IFN-γ
in response to IL-12 and IL-15, amplified in IBD

a subset intraepithelial
NKp46−Ly49E+ cells

producing IFN-γ in response to IL-12, IL-15, or IL-18

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requires IL-15,

the transcription factor Notch1, the Cd8α enhancer E8I

the thymus leukemia (TL)antigen,

a non-classical MHC class I molecule expressed by IEC that serves as a highaffinity ligand for CD8 (Box 1). T-bet and other transcription factors such as Id2, Ahr and

RORγt are dispensable for their development

function

production of the cytokines monocyte chemotactic protein-1
(MCP-1), IFN-γ and osteopontin, and cytotoxic and phagocytic activities

Alfa4 beta 7, CCR9

Rapid response phenotype

CD4 + T cells receive such cues for re-differentiation from external stimuli within the intestinal epithelium, such as TGF-β, retinoic acid, IFN-γ and IL-27