Sphingosine 1-phosphate receptor 5 (S1PR5) regulates the peripheral retention of tissue-resident lymphocytes

Evrard, Maximilien; Wynne-Jones, Erica; Peng, Changwei; Kato, Yu; Christo, Susan N; Fonseca, Raíssa; Park, Simone L.; Burn, Thomas N.; Osman, Maleika; Devi, Sapna; Chun, Jerold; Mueller, Scott N.; Kannourakis, George; Berzins, Stuart P.; Pellicci, Daniel G.; Heath, William R.; Jameson, Stephen C.; Mackay, Laura K.

doi:10.1084/jem.20210116

Cited by 70 publications

(62 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the immunosuppressive effect of the functional S1P receptor antagonists fingolimod and siponimod were attributed to the internalization and degradation of S1P 1 [ 13 , 54 , 55 , 56 , 57 ]. These findings agree with our data showing no difference in immune cell infiltration caused by S1P 5 deficiency although, potentially, subsets such as tissue-resident memory T cells were not specifically assessed [ 58 ]. Nevertheless, both of these drugs, which are approved for the treatment of multiple sclerosis, also have a high affinity for S1P 5 [ 13 , 59 , 60 ].…”

Section: Discussionsupporting

confidence: 92%

Sphingosine 1-Phosphate Receptor 5 (S1P5) Knockout Ameliorates Adenine-Induced Nephropathy

Eckes

Patyna

Koch

et al. 2022

IJMS

Self Cite

View full text Add to dashboard Cite

S1P and its receptors have been reported to play important roles in the development of renal fibrosis. Although S1P5 has barely been investigated so far, there are indications that it can influence inflammatory and fibrotic processes. Here, we report the role of S1P5 in renal inflammation and fibrosis. Male S1P5 knockout mice and wild-type mice on a C57BL/6J background were fed with an adenine-rich diet for 7 days or 14 days to induce tubulointerstitial fibrosis. The kidneys of untreated mice served as respective controls. Kidney damage, fibrosis, and inflammation in kidney tissues were analyzed by real-time PCR, Western blot, and histological staining. Renal function was assessed by plasma creatinine ELISA. The S1P5 knockout mice had better renal function and showed less kidney damage, less proinflammatory cytokine release, and less fibrosis after 7 days and 14 days of an adenine-rich diet compared to wild-type mice. S1P5 knockout ameliorates tubular damage and tubulointerstitial fibrosis in a model of adenine-induced nephropathy in mice. Thus, targeting S1P5 might be a promising goal for the pharmacological treatment of kidney diseases.

show abstract

Section: Discussionsupporting

confidence: 92%

Sphingosine 1-Phosphate Receptor 5 (S1P5) Knockout Ameliorates Adenine-Induced Nephropathy

Eckes

Patyna

Koch

et al. 2022

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…Indeed, several transcription factors that may participate in the control of ABCs have been implicated as potential upstream regulators of ABC transcriptional programs in genome‐wide analyses although their role has not yet been fully dissected at the mechanistic level. Among them are ZEB2, a well‐known target and transcriptional partner of T‐bet, 113,230,231 EGR proteins and ATF3 that appear to be broad regulators of the transcriptional networks of ABCs in SLE patients, 22,70 and Maf proteins whose downregulation may be associated with decreased expression of some of the myeloid features in autoimmune ABCs 27 . Genetic manipulations in murine models have furthermore highlighted the involvement of Bcl6 84 and c‐Myb 232 although their precise mechanistic contributions to ABC formation and differentiation have not been fully defined.…”

Section: Other Regulatorsmentioning

confidence: 99%

Molecular mechanisms controlling age‐associated B cells in autoimmunity*

Phalke

Rivera-Correa

Jenkins

et al. 2022

Immunological Reviews

View full text Add to dashboard Cite

Age-associated B cells (ABCs) have emerged as critical components of immune responses. Their inappropriate expansion and differentiation have increasingly been linked to the pathogenesis of autoimmune disorders, aging-associated diseases, and infections. ABCs exhibit a distinctive phenotype and, in addition to classical B cell markers, often express the transcription factor T-bet and myeloid markers like CD11c; hence, these cells are also commonly known as CD11c + T-bet + B cells. Formation of ABCs is promoted by distinctive combinations of innate and adaptive signals. In addition to producing antibodies, these cells display antigen-presenting and proinflammatory capabilities. It is becoming increasingly appreciated that the ABC compartment exhibits a high degree of heterogeneity, plasticity, and sex-specific regulation and that ABCs can differentiate into effector progeny via several routes particularly in autoimmune settings. In this review, we will discuss the initial insights that have been obtained on the molecular machinery that controls ABCs and we will highlight some of the unique aspects of this control system that may enable ABCs to fulfill their distinctive role in immune responses. Given the expanding array of autoimmune disorders and pathophysiological settings in which ABCs are being implicated, a deeper understanding of this machinery could have important and broad therapeutic implications for the successful, albeit daunting, task of targeting these cells.

show abstract

“…[47] The requirement for S1PR5 down regulation in mediating T cell residency was recently recognized in skin T RM cells through the T-bet-Zeb2-S1PR5 axis. [48] Interestingly, Zeb2 expression is strongly induced during NK cell maturation in a T-bet-dependent manner. [49] Collectively, Zeb2 might also act downstream of T-bet in promoting S1PR5 in NK cells, thereby contributing to NK cell migration and function.…”

Section: Control Of Tissue Residency Versus Traffickingmentioning

confidence: 99%

Eomes and T‐bet, a dynamic duo regulating NK cell differentiation

2022

View full text Add to dashboard Cite

T-bet and Eomes are two related transcription factors (TFs) that regulate the differentiation of cytotoxic lymphocytes such as Natural Killer (NK) cells and CD8 T cells.Recent genome-wide analyses suggest they have complementary roles in instructing the transcriptional program of NK cells, although their DNA binding sites appear to be very similar. In this essay, we discuss the mechanisms that could specify their action, addressing their expression profile, the cofactors they interact with, as well as their roles in the epigenetic regulation of chromatin accessibility. Based on the recent literature on these TFs, we propose different models to describe how they regulate gene expression in NK cells at steady state, or in the context of activation or exhaustion.We also discuss recent findings in the field of CD8 T cell differentiation and residency, where Eomes and T-bet appear to be major regulators, and the parallels that can be drawn between mechanisms of NK and CD8 T cell differentiation and trafficking. K E Y W O R D S cytotoxicity, development, IFN-γ, natural Killer cells, T-box transcription factors NK CELL DIFFERENTIATION, PARALLELS WITH T CELLSNK cells develop mainly in the bone marrow (BM). At early developmental stages, they actively proliferate in this anatomical site before maturation. We previously reported that immature NK cells could be dissected into two different subsets expressing or not CD27. [10] However, mathematical modeling led us to refine this model and propose that most immature NK cells were in fact CD11b − CD27 + . [11]

show abstract

Sphingosine 1-phosphate receptor 5 (S1PR5) regulates the peripheral retention of tissue-resident lymphocytes

Cited by 70 publications

References 61 publications

Sphingosine 1-Phosphate Receptor 5 (S1P5) Knockout Ameliorates Adenine-Induced Nephropathy

Sphingosine 1-Phosphate Receptor 5 (S1P5) Knockout Ameliorates Adenine-Induced Nephropathy

Molecular mechanisms controlling age‐associated B cells in autoimmunity*

Eomes and T‐bet, a dynamic duo regulating NK cell differentiation

Contact Info

Product

Resources

About