Retinoic Acid Determines the Precise Tissue Tropism of Inflammatory Th17 Cells in the Intestine

Wang, Chuanwu; Kang, Seung Goo; HogenEsch, Harm; Love, Paul E.; Kim, Chang H.

doi:10.4049/jimmunol.0903942

Cited by 94 publications

(99 citation statements)

References 51 publications

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“…To determine whether T/F HIV also targets gut-homing CCR6 + T cells for preferential replication, FACS-sorted memory CCR6 + and CCR6 -T cells stimulated via CD3/CD28 in the presence/absence of ATRA were exposed in parallel to T/F THRO (44) and NL4.3BaL HIV ( Figure 1A). The relative frequency of CCR6 + and CCR6 -T cells in peripheral blood mononuclear cells (PBMCs) before sort is depicted in Figure 1, B and C. The dose of ATRA used (10 nM) (42) is consistent with physiological plasma levels (40) and had no influence on cell viability (data not shown). ATRA robustly increases replication of both NL4.3BaL and T/F THRO HIV in CCR6 + T cells, while the effects on CCR6 -T cells were only minor, as reflected by the quantification of early (RU5), late (Gag), and integrated (Alu/HIV) HIV reverse transcripts ( Figure 1, D and E).…”

Section: Transmitted/founder Hiv Preferentially Infects Retinoic Acidmentioning

confidence: 66%

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HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

Planas¹,

Zhang²,

Monteiro³

et al. 2017

JCI Insight

160

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Section: Transmitted/founder Hiv Preferentially Infects Retinoic Acidmentioning

confidence: 66%

“…The imprinting for gut homing is induced by all-trans retinoic acid (ATRA) (40), a vitamin A metabolite produced by GALT dendritic cells (41). Our previous studies demonstrated that ATRA increases HIV-1 permissiveness preferentially in CCR6 + T cells compared with CCR6 -T cells (42).…”

Section: Cxcr3mentioning

confidence: 99%

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

Planas¹,

Zhang²,

Monteiro³

et al. 2017

JCI Insight

160

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“…CCL25, the chemokine for CCR9, is constitutively produced in the gut (48), and thus, once CCR9 is expressed, T cell homing toward this site may become the default trafficking pathway. CCR9 is important in homing of T cells to SILP, while integrin α 4 β 7 has a broader impact, homing T cells to the mLNs, Peyer patches, and SILP (36,49). While expression of CCR6 is critical for CNS migration of T helper cells in EAE, it promotes migration of T helper cells to any sites where IL-17 is produced, related to increased CCL20 (50).…”

mentioning

confidence: 99%

Diverting T helper cell trafficking through increased plasticity attenuates autoimmune encephalomyelitis

Califano¹,

Sweeney²,

Lê³

et al. 2013

J. Clin. Invest.

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Naive T helper cells differentiate into functionally distinct effector subsets that drive specialized immune responses. Recent studies indicate that some of the effector subsets have plasticity. Here, we used an EAE model and found that Th17 cells deficient in the transcription factor BCL11B upregulated the Th2-associated proteins GATA3 and IL-4 without decreasing RAR-related orphan receptor γ (RORγt), IL-17, and GM-CSF levels. Surprisingly, abnormal IL-4 production affected Th17 cell trafficking, diverting migration from the draining lymph nodes/CNS route to the mesenteric lymph nodes/gut route, which ameliorated EAE without overt colitis. T helper cell rerouting in EAE was dependent on IL-4, which enhanced retinoic acid (RA) production by dendritic cells, which further induced expression of gut-homing receptors CCR9 and α 4 β 7 on Bcl11b-deficient CD4 + T cells. Furthermore, IL-4 treatment or Th2 immunization of wild-type mice with EAE caused no alteration in Th17 cytokines or RORγt, but diverted T helper cell trafficking to the gut, which improved EAE outcome without overt colitis. Our data demonstrate that Th17 cells are permissive to Th2 gene expression without affecting Th17 gene expression. This Th17 plasticity has an impact on trafficking, which is a critical component of the immune response and may represent a possible avenue for treating multiple sclerosis.

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“…ϩ , Th17, and CD4 ϩ T-regulatory cells [16,20,21,[23][24][25]45]). Blocking RAR can cause a significant decrease in T cell homing.…”

mentioning

confidence: 99%

Reduced Frequencies and Heightened CD103 Expression among Virus-Induced CD8⁺T Cells in the Respiratory Tract Airways of Vitamin A-Deficient Mice

Rudraraju¹,

Surman²,

Jones³

et al. 2012

Clin. Vaccine Immunol.

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ABSTRACTVitamin A deficiency (VAD) has profound effects on immune responses in the gut, but its effect on other mucosal responses is less well understood. Sendai virus (SeV) is a candidate human parainfluenza virus type 1 (hPIV-1) vaccine and a candidate vaccine vector for other respiratory viruses. A single intranasal dose of SeV elicits a protective immune response against hPIV-1 within days after vaccination. To define the effect of VAD on acute responses toward SeV, we monitored both antibodies and CD8+T cells in mice. On day 10 following SeV infection, there was a trend toward lower antibody activities in the nasal washes of VAD mice than in those of controls, while bronchoalveolar lavage (BAL) fluid and serum antibodies were not reduced. In contrast, there was a dramatic reduction of immunodominant CD8+T cell frequencies in the lower respiratory tract (LRT) airways of VAD animals. These T cells also showed unusually high CD103 (the αE subunit of αEβ7) expression patterns. In both VAD and control mice, E-cadherin (the ligand for αEβ7) was better expressed among epithelial cells lining the upper respiratory tract (URT) than in LRT airways. The results support a working hypothesis that the high CD103 expression among T cell populations in VAD mice alters mechanisms of T cell cross talk with URT and LRT epithelial cells, thereby inhibiting T cell migration and egress into the lower airway. Our data emphasize that the consequences of VAD are not limited to gut-resident cells and characterize VAD influences on an immune response to a respiratory virus vaccine.

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Retinoic Acid Determines the Precise Tissue Tropism of Inflammatory Th17 Cells in the Intestine

Abstract: Material

Cited by 94 publications

References 51 publications

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

Diverting T helper cell trafficking through increased plasticity attenuates autoimmune encephalomyelitis

Reduced Frequencies and Heightened CD103 Expression among Virus-Induced CD8⁺T Cells in the Respiratory Tract Airways of Vitamin A-Deficient Mice

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Retinoic Acid Determines the Precise Tissue Tropism of Inflammatory Th17 Cells in the Intestine

Abstract: Material

Cited by 94 publications

References 51 publications

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

Diverting T helper cell trafficking through increased plasticity attenuates autoimmune encephalomyelitis

Reduced Frequencies and Heightened CD103 Expression among Virus-Induced CD8+T Cells in the Respiratory Tract Airways of Vitamin A-Deficient Mice

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Product

Resources

About

Reduced Frequencies and Heightened CD103 Expression among Virus-Induced CD8⁺T Cells in the Respiratory Tract Airways of Vitamin A-Deficient Mice