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Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells.

Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Research Abstract Details 

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  • Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Abstract Text:

    heather m seitzHeather M Seitz,todd d camenischTodd D Camenisch,greg lemkeGreg Lemke,h shelton earpH Shelton Earp,glenn k matsushimaGlenn K Matsushima,

    The clearance of apoptotic cells is important for regulating tissue homeostasis, inflammation, and autoimmune responses. The absence of receptor tyrosine kinases (Axl, Mertk, and Tyro3) results in widespread accumulation of apoptotic cells and autoantibody production in mice. In this report, we examine the function of the three family members in apoptotic cell clearance by different phagocytic cell types. Mertk elimination nearly abolished macrophage apoptotic cell phagocytosis; elimination of Axl, Tyro3, or both, reduced macrophage phagocytosis by approximately half, indicating that these also play a role. In contrast, apoptotic cell clearance in splenic and bone marrow-derived dendritic cells (DCs) is prolonged compared with macrophages and relied primarily on Axl and Tyro3. The slower ingestion may be due to lower DC expression of Axl and Tyro3 or absence of GAS6 expression, a known ligand for this receptor family. In vivo, phagocytosis of apoptotic material by retinal epithelial cells required Mertk. Unlike macrophages, there did not appear to be any role for Axl or Tyro3 in retinal homeostasis. Likewise, clearance of apoptotic thymocytes in vivo was dramatically reduced in mertk(kd) mice, but was normal in axl/tyro3(-/-) mice. Thus, cell and organ type specificity is clearly delineated, with DCs relying on Axl and Tyro3, retina and thymus requiring Mertk, and macrophages exhibiting an interaction that involves all three family members. Surprisingly, in macrophages, tyrosine phosphorylation of Mertk in response to apoptotic cells is markedly diminished from axl/tyro3(-/-) mice, suggesting that the interactions of these receptors by heterodimerization may be important in some cells.

    Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Publishing Authors By Initials

    hm seitzHM Seitz,td camenischTD Camenisch,g lemkeG Lemke,hs earpHS Earp,gk matsushimaGK Matsushima,

    For similar tissues: lymphoid tissue: thymus gland research abstracts see: tissues: lymphoid tissue: thymus gland research

    PUBMED ID PMID:

    MEDLINE DATE:

    Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    VOLUME: 178

    Page Numbers: 5635-42

    Journal Abbreviation:

    ISSN: 0022-1767

    DAY: 1

    MONTH: May

    YEAR: 2007

    Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Keywords Mesh Terms:

    KEYWORDS: Thymus Gland

    MESH TERMS: immunology

    Chemical & Substance for Abstract: Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells. Information

    Substance Name: axl receptor tyrosine kinase

    Registry Number: EC 2.7.1.112

    Grant and Affiliation Information for Macrophages and dendritic cells use different Axl/Mertk/Tyro3 receptors in clearance of apoptotic cells.

    AFFILIATION: Department of Microbiology and Immunology, University of North Carolina-Chapel Hill, Chapel Hill, NC 27599, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAID

    GRANT: AI 5317 02

    ACRONYM: AI

    MEDLINETA: J Immunol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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