Browsing by Subject "Myeloid cells"
Now showing 1 - 2 of 2
Results Per Page
Sort Options
- PublicationOpen AccessBruton’s Tyrosine Kinase is involved in innate and adaptive immunity(Murcia : F. Hernández, 2005) Brunner, C.; Müller, B.; Wirth, T.Btk is a cytoplasmic tyrosine kinase, which is mainly involved in B cell receptor signalling. Gene targeting experiments revealed that Btk is important for B cell development and function. However, Btk is not only expressed in B cells, but also in most other haematopoietic lineages except for T cells and plasma cells. Recently we found that Btk is involved in Toll-like receptor signalling. Toll-like receptors play an important role in innate immunity. They are highly expressed on mast cells, macrophages and dendritic cells, which are essential for the recognition and consequently for the elimination of microbial pathogens. Therefore Btk might play an important role for the function of immunocompetent cells of innate as well as adaptive immunity.
- PublicationOpen AccessMMP2 Modulates Inflammatory Response during Axonal Regeneration in the Murine Visual System(MDPI, 2021-07-02) Andries, Lien; Masin, Luca; Salinas Navarro, Manuel Ángel; Zaunz, Samantha; Claes, Marie; Bergmans, Steven; Brouwers, Véronique; Lefevere, Evy; Verfaillie, Catherine; Movahedi, Kiavash; De Groef, Lies ; Moons, Lieve; Anatomía Humana y Psicobiología; Facultades de la UMU::Facultad de MedicinaNeuroinflammation has been put forward as a mechanism triggering axonal regrowth in the mammalian central nervous system (CNS), yet little is known about the underlying cellular and molecular players connecting these two processes. In this study, we provide evidence that MMP2 is an essential factor linking inflammation to axonal regeneration by using an in vivo mouse model of inflammation-induced axonal regeneration in the optic nerve. We show that infiltrating myeloid cells abundantly express MMP2 and that MMP2 deficiency results in reduced long-distance axonal regeneration. However, this phenotype can be rescued by restoring MMP2 expression in myeloid cells via a heterologous bone marrow transplantation. Furthermore, while MMP2 deficiency does not affect the number of infiltrating myeloid cells, it does determine the coordinated expression of pro- and anti-inflammatory molecules. Altogether, in addition to its role in axonal regeneration via resolution of the glial scar, here, we reveal a new mechanism via which MMP2 facilitates axonal regeneration, namely orchestrating the expression of pro- and anti-inflammatory molecules by infiltrating innate immune cells.