T cell-mediated neuroprotection involves antithrombin activity

Friedmann, Igor; Hauben, Ehud; Yoles, Eti; Kardash, Elena; Schwartz, Michal

doi:10.1016/s0165-5728(01)00397-6

Cited by 18 publications

(11 citation statements)

References 41 publications

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“…This neuroprotection is attributed to the expression of neurotrophins and antithrombin III by MBP-specific T cells (see Fig. 1D) (45). Because these protective effects are not evident in all rat or mouse strains, the application of therapeutic vaccines in humans will require a better understanding of how genetics influences autoimmunity (62;85).…”

Section: Lymphocytesmentioning

confidence: 99%

Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury

Donnelly

Popovich

2008

Experimental Neurology

838

755

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Trauma to the central nervous system (CNS) triggers intraparenchymal inflammation and activation of systemic immunity with the capacity to exacerbate neuropathology and stimulate mechanisms of tissue repair. Despite our incomplete understanding of the mechanisms that control these divergent functions, immune-based therapies are becoming a therapeutic focus. This review will address the complexities and controversies of post-traumatic neuroinflammation, particularly in spinal cord. In addition, current therapies designed to target neuroinflammatory cascades will be discussed.

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Section: Lymphocytesmentioning

confidence: 99%

Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury

Donnelly

Popovich

2008

Experimental Neurology

838

755

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“…With recent progress in gene technology, represented by various knock-out or transgenic mice, expression of the target genes can now be easily modified in mice. [13][14][15] Accordingly, with in vivo observations of leukocyte rolling and migration in mouse retina, we can accurately evaluate the genetic regulation of leukocyte behavior in inflammatory responses.…”

mentioning

confidence: 99%

In Vivo Three-Dimensional Evaluation of Leukocyte Behavior in Retinal Microcirculation of Mice

Miyahara

Kiryu

Miyamoto

et al. 2004

Invest. Ophthalmol. Vis. Sci.

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“…Most serum proteins are normally denied CNS entry (5,14). However, when the BBB integrity is compromised due to trauma, stroke, viral and bacterial infection, autoimmune diseases, or neurodegenerative processes, blood content can more or less inundate the tissue (1,5,12,13,15). Proteases, protease inhibitors or their complexes, lipid-loaded albumin, complement factors, immunoglobulins, or cytokines may then gain access to neurons and glial cells (1, 3, 5, 14, 16 -22).…”

mentioning

confidence: 99%

The Microglia-activating Potential of Thrombin

Hanisch

Rossum

Xie

et al. 2004

Journal of Biological Chemistry

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The serine protease thrombin is known as a blood coagulation factor. Through limited cleavage of proteinase-activated receptors it can also control growth and functions in various cell types, including neurons, astrocytes, and microglia (brain macrophages). A number of previous studies indicated that thrombin induces the release of proinflammatory cytokines and chemokines from microglial cells, suggesting another important role for the protease beyond hemostasis. In the present report, we provide evidence that this effect is not mediated by any proteolytic or non-proteolytic mechanism involving thrombin proper. Inhibition of the enzymatic thrombin activity did not affect the microglial release response. Instead the cyto-/chemokine-inducing activity solely resided in a high molecular weight protein fraction that could be isolated in trace amounts even from apparently homogenous ␣-and ␥-thrombin preparations. High molecular weight material contained thrombin-derived peptides as revealed by mass spectrometry but was devoid of thrombin-like enzymatic activity. Separated from the high molecular weight fraction by fast protein liquid chromatography, enzymatically intact ␣-and ␥-thrombin failed to trigger any release. Our findings may force a revision of the notion that thrombin itself is a direct proinflammatory release signal for microglia. In addition, they could be relevant for the study of other cellular activities and their assignment to this protease.

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T cell-mediated neuroprotection involves antithrombin activity

Cited by 18 publications

References 41 publications

Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury

Inflammation and its role in neuroprotection, axonal regeneration and functional recovery after spinal cord injury

In Vivo Three-Dimensional Evaluation of Leukocyte Behavior in Retinal Microcirculation of Mice

The Microglia-activating Potential of Thrombin

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