0000000000019024

AUTHOR

Sven Hendrix

0000-0003-2344-7369

Regeneration After CNS Lesion: Help from the Immune System?

Traumatic injury to the central nervous system (CNS) is followed by an inflammatory response, which is characterized by at least two very distinct phases: First, a short highly controlled burst of acute inflammatory defense and second, a long-term remodeling phase. Similarly, at least one or two phases of T-cell infiltration have been described in CNS trauma models suggesting differential functions of T cells in the acute and remodeling phase. Thus, the role of T cells in CNS trauma is still controversial. Interestingly, vaccine strategies and injections of autoimmune T cells led to both exacerbation of CNS damage after trauma in some models and improvement in others. Here, we suggest that …

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Mast cells as protectors of health.

Mast cells (MCs), which are well known for their effector functions in T(H)2-skewed allergic and also autoimmune inflammation, have become increasingly acknowledged for their role in protection of health. It is now clear that they are also key modulators of immune responses at interface organs, such as the skin or gut. MCs can prime tissues for adequate inflammatory responses and cooperate with dendritic cells in T-cell activation. They also regulate harmful immune responses in trauma and help to successfully orchestrate pregnancy. This review focuses on the beneficial effects of MCs on tissue homeostasis and elimination of toxins or venoms. MCs can enhance pathogen clearance in many bacter…

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MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4

A body of experimental evidence suggests that T cells mediate neuroprotection following CNS injury; however, the antigen specificity of these T cells and how they mediate neuroprotection are unknown. Here, we have provided evidence that T cell-mediated neuroprotection after CNS injury can occur independently of major histocompatibility class II (MHCII) signaling to T cell receptors (TCRs). Using two murine models of CNS injury, we determined that damage-associated molecular mediators that originate from injured CNS tissue induce a population of neuroprotective, IL-4-producing T cells in an antigen-independent fashion. Compared with wild-type mice, IL-4-deficient animals had decreased functi…

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