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  1. Article ; Online: Conversion of CD73hiFR4hi anergic T cells to IFN-γ-producing effector cells disrupts established immune tolerance.

    Dangi, Anil / Husain, Irma / Jordan, Collin Z / Yu, Shuangjin / Luo, Xunrong

    The Journal of clinical investigation

    2023  Volume 133, Issue 5

    MeSH term(s) T-Lymphocytes ; Clonal Anergy ; Immune Tolerance ; Lymphocytes
    Language English
    Publishing date 2023-03-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI163872
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: AXL inhibition suppresses early allograft monocyte-to-macrophage differentiation and prolongs allograft survival.

    Jordan, Collin Z / Tunbridge, Matthew / Husain, Irma / Kitai, Hiroki / Dilts, Miriam E / Fay, Olivia K / Abe, Koki / Xiang, Catherine / Kwun, Jean / Souma, Tomokazu / Thorp, Edward B / Luo, Xunrong

    JCI insight

    2024  Volume 9, Issue 5

    Abstract: Innate immune cells are important in the initiation and potentiation of alloimmunity in transplantation. Immediately upon organ anastomosis and reperfusion, recipient monocytes enter the graft from circulation and differentiate to inflammatory ... ...

    Abstract Innate immune cells are important in the initiation and potentiation of alloimmunity in transplantation. Immediately upon organ anastomosis and reperfusion, recipient monocytes enter the graft from circulation and differentiate to inflammatory macrophages to promote allograft inflammation. However, factors that drive their differentiation to inflammatory macrophages are not understood. Here, we show that the receptor tyrosine kinase AXL was a key driver of early intragraft differentiation of recipient infiltrating monocytes to inflammatory macrophages in the presence of allogeneic stimulation and cell-to-cell contact. In this context, the differentiated inflammatory macrophages were capable of efficient alloantigen presentation and allostimulation of T cells of the indirect pathway. Consequently, early and transient AXL inhibition with the pharmacological inhibitor bemcentinib resulted in a profound reduction of initial allograft inflammation and a significant prolongation of allograft survival in a murine heart transplant model. Our results support further investigation of AXL inhibition as part of an induction regimen for transplantation.
    MeSH term(s) Mice ; Animals ; Monocytes ; Macrophages ; Transplantation, Homologous ; Allografts ; Inflammation
    Language English
    Publishing date 2024-03-08
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.178502
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Blocking CCL8-CCR8-Mediated Early Allograft Inflammation Improves Kidney Transplant Function.

    Dangi, Anil / Husain, Irma / Jordan, Collin Z / Yu, Shuangjin / Natesh, Naveen / Shen, Xiling / Kwun, Jean / Luo, Xunrong

    Journal of the American Society of Nephrology : JASN

    2022  Volume 33, Issue 10, Page(s) 1876–1890

    Abstract: Background: In kidney transplantation, early allograft inflammation impairs long-term allograft function. However, precise mediators of early kidney allograft inflammation are unclear, making it challenging to design therapeutic interventions.: ... ...

    Abstract Background: In kidney transplantation, early allograft inflammation impairs long-term allograft function. However, precise mediators of early kidney allograft inflammation are unclear, making it challenging to design therapeutic interventions.
    Methods: We used an allogeneic murine kidney transplant model in which CD45.2 BALB/c kidneys were transplanted to CD45.1 C57BL/6 recipients.
    Results: Donor kidney resident macrophages within the allograft expanded rapidly in the first 3 days. During this period, they were also induced to express a high level of
    Conclusions: Targeting the CCL8-CCR8 axis is a promising measure to reduce early kidney allograft inflammation.
    MeSH term(s) Mice ; Animals ; Kidney Transplantation ; Mice, Inbred C57BL ; Transplantation, Homologous ; Inflammation ; Allografts ; Graft Rejection ; Graft Survival ; Mice, Inbred BALB C ; Receptors, CCR8
    Chemical Substances Ccr8 protein, mouse ; Receptors, CCR8
    Language English
    Publishing date 2022-08-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2022020139
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3344: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Heightened TLR7 signaling primes BCR-activated B cells in chronic graft-versus-host disease for effector functions.

    Bracken, Sonali J / Suthers, Amy N / DiCioccio, Rachel A / Su, Hsuan / Anand, Sarah / Poe, Jonathan C / Jia, Wei / Visentin, Jonathan / Basher, Fahmin / Jordan, Collin Z / McManigle, William C / Li, Zhiguo / Hakim, Frances T / Pavletic, Steven Z / Bhuiya, Nazmim S / Ho, Vincent T / Horwitz, Mitchell E / Chao, Nelson J / Sarantopoulos, Stefanie

    Blood advances

    2023  Volume 8, Issue 3, Page(s) 667–680

    Abstract: Abstract: Chronic graft-versus-host disease (cGVHD) is a debilitating, autoimmune-like syndrome that can occur after allogeneic hematopoietic stem cell transplantation. Constitutively activated B cells contribute to ongoing alloreactivity and ... ...

    Abstract Abstract: Chronic graft-versus-host disease (cGVHD) is a debilitating, autoimmune-like syndrome that can occur after allogeneic hematopoietic stem cell transplantation. Constitutively activated B cells contribute to ongoing alloreactivity and autoreactivity in patients with cGVHD. Excessive tissue damage that occurs after transplantation exposes B cells to nucleic acids in the extracellular environment. Recognition of endogenous nucleic acids within B cells can promote pathogenic B-cell activation. Therefore, we hypothesized that cGVHD B cells aberrantly signal through RNA and DNA sensors such as Toll-like receptor 7 (TLR7) and TLR9. We found that B cells from patients and mice with cGVHD had higher expression of TLR7 than non-cGVHD B cells. Using ex vivo assays, we found that B cells from patients with cGVHD also demonstrated increased interleukin-6 production after TLR7 stimulation with R848. Low-dose B-cell receptor (BCR) stimulation augmented B-cell responses to TLR7 activation. TLR7 hyperresponsiveness in cGVHD B cells correlated with increased expression and activation of the downstream transcription factor interferon regulatory factor 5. Because RNA-containing immune complexes can activate B cells through TLR7, we used a protein microarray to identify RNA-containing antigen targets of potential pathological relevance in cGVHD. We found that many of the unique targets of active cGVHD immunoglobulin G (IgG) were nucleic acid-binding proteins. This unbiased assay identified the autoantigen and known cGVHD target Ro-52, and we found that RNA was required for IgG binding to Ro-52. Herein, we find that BCR-activated B cells have aberrant TLR7 signaling responses that promote potential effector responses in cGVHD.
    MeSH term(s) Humans ; Mice ; Animals ; Toll-Like Receptor 7/metabolism ; Bronchiolitis Obliterans Syndrome ; Receptors, Antigen, B-Cell/metabolism ; Nucleic Acids ; RNA ; Immunoglobulin G
    Chemical Substances Toll-Like Receptor 7 ; Receptors, Antigen, B-Cell ; Nucleic Acids ; RNA (63231-63-0) ; Immunoglobulin G ; TLR7 protein, human
    Language English
    Publishing date 2023-12-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2023010362
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7153: Show issues Location:
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