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Updated: Jun 25, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

The protein tyrosine phosphatase CD45 promotes PMN transepithelial migration, antimicrobial function, and colonic

Jael Miranda, Dylan J Fink, Zachary S Wilson

    JCI Insight
    |June 23, 2026
    PubMed

    Insights

    The protein tyrosine phosphatase CD45 regulates polymorphonuclear neutrophil (PMN) migration and function in the gut. Inhibiting CD45 impaired PMN antimicrobial activity and delayed mucosal healing in inflammatory conditions.

    Area of Science:

    • Immunology
    • Gastroenterology
    • Cell Biology

    Background:

    • Polymorphonuclear neutrophils (PMNs) are crucial for host defense and tissue repair.
    • Excessive PMN transepithelial migration (TEpM) exacerbates chronic mucosal inflammation, such as inflammatory bowel disease.
    • Signaling pathways governing PMN functions remain incompletely understood.

    Purpose of the Study:

    • To investigate the role of protein tyrosine phosphatase CD45 (also known as PTPRC) in regulating PMN trafficking and effector functions within the gastrointestinal tract.
    • To elucidate the molecular mechanisms by which CD45 influences PMN behavior in the context of mucosal inflammation and repair.

    Main Methods:

    • Pharmacological inhibition of CD45 in vitro and in vivo.
    • Utilized transgenic mice with PMN-specific deletion of CD45 (MRP8-Cre;Cd45fl/fl).
    • Assessed PMN transepithelial migration, degranulation, phagocytosis, and mucosal healing in models of colitis and colonic wounding.
    • Analyzed surface expression of CD11b/CD18 and activity of the Src family kinase Lyn.

    Main Results:

    • Pharmacological CD45 inhibition and genetic deletion significantly reduced PMN colonic TEpM and intestinal trafficking.
    • CD45 depletion impaired critical PMN antimicrobial functions, including degranulation and phagocytosis.
    • PMN-specific CD45-deficient mice exhibited delayed recovery from dextran sodium sulfate (DSS)-induced colitis and biopsy-induced colonic wounding.
    • CD45 depletion led to reduced surface expression of β2 integrin CD11b/CD18 and inactivation of Lyn kinase.

    Conclusions:

    • CD45 plays a critical role in regulating PMN trafficking and effector functions in the intestine.
    • A CD45-CD11b-Lyn signaling axis is identified as crucial for PMN function in the gut.
    • CD45 represents a potential therapeutic target for modulating PMN activity to enhance mucosal tissue repair.
    Keywords:
    ImmunologyInflammationNeutrophils

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