C-type lectin-like receptor 2 (CLEC-2)-dependent DC migration is controlled by tetraspanin CD37

Winde, Charlotte M. de; Matthews, Alexandra L.; Deventer, Sjoerd van; Schaaf, Alie van der; Tomlinson, N.; Yang, Jing; Jansen, Erik; Eble, Johannes A.; Nieswandt, Bernhard; McGettrick, Helen M.; Figdor, Carl G.; Acton, Sophie E.; Tomlinson, Michael G.; Spriel, Annemiek B. van

doi:10.1101/227918

Cited by 1 publication

(2 citation statements)

References 80 publications

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“…As such, podoplanin ligand function is not dependent on CD44 or CD9 expression on FRCs. This is in agreement with published data showing that soluble recombinant podoplanin-Fc can induce DC protrusions (Acton et al, 2012;de Winde et al, 2018).…”

Section: Cd44 and Cd9 Control Podoplanin-dependent Frc Responses To Clec-2 + Dcssupporting

confidence: 93%

“…We next tested whether CD44 or CD9 expression by FRCs is required for podoplanin ligand function using 3D co-culture of FRC cell lines with bone marrow-derived CLEC-2 + DCs. Contact with podoplanin + FRCs induces DCs to extend protrusions, in a CLEC-2 (Acton et al, 2012) and tetraspanin CD37-dependent manner (de Winde et al, 2018). DCs co-cultured with PDPN KD FRCs do not spread or make protrusions (Fig.…”

Section: Cd44 and Cd9 Control Podoplanin-dependent Frc Responses To Clec-2 + Dcsmentioning

confidence: 91%

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Fibroblastic reticular cell response to dendritic cells requires coordinated activity of podoplanin, CD44 and CD9

Winde

Makris

Millward

et al. 2021

Journal of Cell Science

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In adaptive immunity, CLEC-2+ dendritic cells (DCs) contact fibroblastic reticular cells (FRCs) inhibiting podoplanin-dependent actomyosin contractility, permitting FRC spreading and lymph node (LN) expansion. The molecular mechanisms controlling LN remodelling are incompletely understood. We asked how podoplanin is regulated on FRCs in the early phase of LN expansion, and which other proteins are required for the FRC response to DCs. We find that podoplanin and its partner proteins CD44 and CD9 are differentially expressed by specific LN stromal populations in vivo, and their expression in FRCs is coregulated by CLEC-2. Both CD44 and CD9 suppress podoplanin-dependent contractility. We find that beyond contractility, podoplanin is required for FRC polarity and alignment. Independently of podoplanin, CD44 and CD9 affect FRC-FRC interactions. Further, our data show that remodelling of the FRC cytoskeleton in response to DCs is a two-step process requiring podoplanin partner proteins CD44 and CD9. Firstly, CLEC-2/podoplanin-binding inhibits FRC contractility, and secondly FRCs form protrusions and spread which requires both CD44 and CD9. Together, we show a multi-faceted FRC response to DCs, which requires CD44 and CD9 in addition to podoplanin.

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Section: Cd44 and Cd9 Control Podoplanin-dependent Frc Responses To Clec-2 + Dcssupporting

confidence: 93%

Section: Cd44 and Cd9 Control Podoplanin-dependent Frc Responses To Clec-2 + Dcsmentioning

confidence: 91%

Fibroblastic reticular cell response to dendritic cells requires coordinated activity of podoplanin, CD44 and CD9

Winde

Makris

Millward

et al. 2021

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

C-type lectin-like receptor 2 (CLEC-2)-dependent DC migration is controlled by tetraspanin CD37

Cited by 1 publication

References 80 publications

Fibroblastic reticular cell response to dendritic cells requires coordinated activity of podoplanin, CD44 and CD9

Fibroblastic reticular cell response to dendritic cells requires coordinated activity of podoplanin, CD44 and CD9

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