Th17 Differentiation Pathway

Click on one of the boxes below to see the processes that promote Th17 differentiation and the transcription factors, secreted molecules, and some of the cell surface markers that distinguish a differentiated Th17 cell from the other T helper cell subtypes.

TLR
TLR
IL-23
IL-23
IL-6
IL-6
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TGF-beta
TGF-beta
IL-1 beta
IL-1 beta
MHC II
MHC II
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TCR-CD3
TCR-CD3
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CD4
CD4
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CD28
CD28
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B7
B7
TGF-beta
TGF-beta
TGF-beta RI
TGF-beta RI
TGF-beta RII
TGF-beta RII
Smad
Smad
IL-6
IL-6
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IL-6 R alpha
IL-6 R alpha
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gp130
gp130
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gp130
gp130
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Jak1
Jak1
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Jak2
Jak2
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Tyk2
Tyk2
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Jak1
Jak1
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Jak2
Jak2
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Tyk2
Tyk2
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STAT3
STAT3
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STAT3 Dimer
STAT3 Dimer
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STAT3 Dimer
STAT3 Dimer
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IL-21
IL-21
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IL-21
IL-21
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Pathogen
Pathogen
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Dendritic Cell
Dendritic Cell
Naive CD4+ T Cell
Naive CD4+ T Cell
TGF-beta
TGF-beta
TGF-beta RI
TGF-beta RI
TGF-beta RII
TGF-beta RII
Smad
Smad
IL-6 R alpha
IL-6 R alpha
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gp130
gp130
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gp130
gp130
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IL-6
IL-6
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Jak1
Jak1
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Jak2
Jak2
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Tyk2
Tyk2
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Jak1
Jak1
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Jak2
Jak2
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Tyk2
Tyk2
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STAT3
STAT3
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STAT3 Dimer
STAT3 Dimer
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Common gamma
chain
Common gamma
chain
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IL-21 R
IL-21 R
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IL-21
IL-21
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Jak1
Jak1
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Jak3
Jak3
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STAT3
STAT3
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STAT3 Dimer
STAT3 Dimer
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IL-1 beta
IL-1 beta
IL-1 RAcP
IL-1 RAcP
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IL-1 RI
IL-1 RI
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ROR gamma t
ROR gamma t
IL-23 R
IL-23 R
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IL-17A
IL-17A
IL-21
IL-21
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Th17 Cell
Th17 Cell
IL-23
IL-23
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IL-23 R
IL-23 R
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IL-12 R beta 1
IL-12 R beta 1
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Jak2
Jak2
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Tyk2
Tyk2
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STAT3
STAT3
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STAT4
STAT4
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STAT5
STAT5
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STAT1
STAT1
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STAT3 Dimer
STAT3 Dimer
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TGF-beta
TGF-beta
TGF-beta RI
TGF-beta RI
TGF-beta RII
TGF-beta RII
IL-6 R alpha
IL-6 R alpha
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gp130
gp130
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gp130
gp130
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IL-6
IL-6
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IL-1 beta
IL-1 beta
IL-1 RAcP
IL-1 RAcP
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IL-1 RI
IL-1 RI
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Common gamma chain
Common gamma chain
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IL-21 R
IL-21 R
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IL-21
IL-21
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STAT3Dimer
STAT3Dimer
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ROR gamma t
ROR gamma t
IL-23 R
IL-23 R
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IL-17A
IL-17A
ROR gamma t
ROR gamma t
IL-17A
IL-17A
IL-17F
IL-17F
IL-22
IL-22
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IL-21
IL-21
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IL-22
IL-22
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IL-17F
IL-17F
IL-17A
IL-17A
IL-26
(human)
IL-26
(human)
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Th17 Cell
Th17 Cell

Overview of Th17 Differentiation

Upon TCR activation, naive CD4+ T cells differentiate into one of several T helper cell lineages depending primarily on cytokines present in the surrounding environment. Each T helper cell subset expresses a unique set of cell surface markers and transcription factors, and secretes a defined array of cytokines that determines its functional properties. Th17 cells are required for immune responses to specific extracellular bacteria and fungi. In mice, naïve CD4+ T cells differentiate into T helper type 17 (Th17) cells in the presence of TGF-beta and IL-6. These cytokines establish early commitment to the Th17 lineage by activating STAT3, which induces the expression of IL-21. Autocrine signaling by IL-21 promotes STAT3-dependent expression of IL-23 R, IL-17A, and the transcription factor, ROR gamma t. IL-23 R heterodimerizes with IL-12 R beta 1 to form a functional IL-23 receptor, which in the presence of IL-23, maintains STAT3-dependent expression of IL-23 R, ROR gamma t, and IL-17A to stabilize the Th17 phenotype. ROR gamma t is considered to be the master transcriptional regulator of Th17 cells due to its ability to drive the expression of IL-17A, IL-17F, and IL-22, three hallmark cytokines secreted by Th17 cells. These cytokines stimulate the expression of secondary pro-inflammatory mediators and anti-microbial peptides. Additional transcription factors that have been suggested to be involved in Th17 differentiation include ROR alpha, Batf, and IRF4, which along with ROR gamma t, may also control IL-17 gene expression. In contrast to mouse Th17 differentiation, differentiation of human Th17 cells requires IL-6, IL-21, IL-23, and IL-1 beta, but may be less dependent on TGF-beta. One other notable difference is that in addition to IL-17A, IL-17F, and IL-22, human Th17 cells secrete IL-26, an IL-10 family cytokine without a murine homologue. Although cytokines secreted by Th17 cells play an important role in eliminating harmful microbes, unregulated expression of these cytokines may also contribute to the pathogenesis of a number of autoimmune diseases, including rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disorders.

To learn more, please visit our Th17 Cells Research Area.