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  1. AU="Geraldine M. O’Connor"
  2. AU="Jim E. Banta"
  3. AU="Marti-Bonmati, Luis"
  4. AU="Doris Kampner"
  5. AU="Luca Soraci"

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  1. Artikel ; Online: Structural plasticity of KIR2DL2 and KIR2DL3 enables altered docking geometries atop HLA-C

    Shoeib Moradi / Sanda Stankovic / Geraldine M. O’Connor / Phillip Pymm / Bruce J. MacLachlan / Camilla Faoro / Christelle Retière / Lucy C. Sullivan / Philippa M. Saunders / Jacqueline Widjaja / Shea Cox-Livingstone / Jamie Rossjohn / Andrew G. Brooks / Julian P. Vivian

    Nature Communications, Vol 12, Iss 1, Pp 1-

    2021  Band 11

    Abstract: KIR2DL2 and KIR2DL3 are two inhibitory members of the killer-cell immunoglobulin-like receptors (KIR) family that share a common HLA-I preference in binding HLA from the C1 group. However, it is still unclear to what extent binding and function is ... ...

    Abstract KIR2DL2 and KIR2DL3 are two inhibitory members of the killer-cell immunoglobulin-like receptors (KIR) family that share a common HLA-I preference in binding HLA from the C1 group. However, it is still unclear to what extent binding and function is equivalent between KIR2DL2 and 2DL3. Here, the authors present the crystal structures of KIR2DL2 and 2DL3 in complex with HLA-C*07:02 and observe differences in HLA-C recognition between KIR2DL2 and 2DL3, which correlates with differences in HLA-C binding preference as they show with mutagenesis and binding studies.
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2021-04-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: LAB/NTAL facilitates fungal/PAMP-induced IL-12 and IFN-γ production by repressing β-catenin activation in dendritic cells.

    Selinda J Orr / Ashley R Burg / Tim Chan / Laura Quigley / Gareth W Jones / Jill W Ford / Deborah Hodge / Catherine Razzook / Joseph Sarhan / Yava L Jones / Gillian C Whittaker / Kimberly C Boelte / Lyudmila Lyakh / Marco Cardone / Geraldine M O'Connor / Cuiyan Tan / Hongchuan Li / Stephen K Anderson / Simon A Jones /
    Weiguo Zhang / Philip R Taylor / Giorgio Trinchieri / Daniel W McVicar

    PLoS Pathogens, Vol 9, Iss 5, p e

    2013  Band 1003357

    Abstract: Fungal pathogens elicit cytokine responses downstream of immunoreceptor tyrosine-based activation motif (ITAM)-coupled or hemiITAM-containing receptors and TLRs. The Linker for Activation of B cells/Non-T cell Activating Linker (LAB/NTAL) encoded by Lat2, ...

    Abstract Fungal pathogens elicit cytokine responses downstream of immunoreceptor tyrosine-based activation motif (ITAM)-coupled or hemiITAM-containing receptors and TLRs. The Linker for Activation of B cells/Non-T cell Activating Linker (LAB/NTAL) encoded by Lat2, is a known regulator of ITAM-coupled receptors and TLR-associated cytokine responses. Here we demonstrate that LAB is involved in anti-fungal immunity. We show that Lat2-/- mice are more susceptible to C. albicans infection than wild type (WT) mice. Dendritic cells (DCs) express LAB and we show that it is basally phosphorylated by the growth factor M-CSF or following engagement of Dectin-2, but not Dectin-1. Our data revealed a unique mechanism whereby LAB controls basal and fungal/pathogen-associated molecular patterns (PAMP)-induced nuclear β-catenin levels. This in turn is important for controlling fungal/PAMP-induced cytokine production in DCs. C. albicans- and LPS-induced IL-12 and IL-23 production was blunted in Lat2-/- DCs. Accordingly, Lat2-/- DCs directed reduced Th1 polarization in vitro and Lat2-/- mice displayed reduced Natural Killer (NK) and T cell-mediated IFN-γ production in vivo/ex vivo. Thus our data define a novel link between LAB and β-catenin nuclear accumulation in DCs that facilitates IFN-γ responses during anti-fungal immunity. In addition, these findings are likely to be relevant to other infectious diseases that require IL-12 family cytokines and an IFN-γ response for pathogen clearance.
    Schlagwörter Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Thema/Rubrik (Code) 572 ; 616
    Sprache Englisch
    Erscheinungsdatum 2013-05-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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