Neuroinflammation in the rat – CNS cells and their role in the regulation of immune reactions

Abstract

Recent discoveries suggest that the resident cells of the central nervous system (CNS) the nerve cells and glia, play a more immunologically active role than was previously assumed. Neuroglial communication is of central interest in virtually all types of pathological conditions that affect the brain and several features of the activation that results from nerve cell damage resemble the type of innate immune reactions that occur in other parts of the body In particular, the characteristics of the activation of these CNS cells will affect both the interaction with cells of the immune system as well as processes related to neurodegeneration and regeneration. We here review data regarding 3 different aspects of local inflammatory activation in the rat nervous system: (i) the genetic heterogeneity of glial activation across inbred strains after nerve injury, (ii) expression of MHC class I genes in the CNS and (iii) neuroprotective effects of CNS antigen autoreactive immune reactions. Apart from neuroimmune diseases such as experimental autoimmune encephalomyelitis/multiple sclerosis, these features are also of relevance for a wider range of neurological diseases which present pathological signs of inflammation, such as Alzheimer's dementia, cerebrovascular diseases and CNS trauma.

The Induction and Kinetics of Antigen-Specific CD8 T Cells Are Defined by the Stage Specificity and Compartmentalization of the Antigen in Murine Toxoplasmosis

“…This assumption is experimentally supported by the crucial protective role of CD8 T cells in the TE of retrovirus-infected immunocompromised mice (35,36). The failure of CD8 T cells to completely eliminate T. gondii from the brain may be caused by an immune evasion of tachyzoites in which CD8 T cells switch into bradyzoites, which do not induce a primary ␤-gal-specific CD8 T cell response, as well as the formation of cysts in neurons (37,38), which in general lack expression of MHC class I and II Ag (39).…”

Gene expression during the priming phase of liver regeneration after partial hepatectomy in mice

“…Inflammatory responses have been implicated in the priming of liver and other types of regeneration (51). For example, prevention of macrophage invasion impairs peripheral axonal regeneration, whereas implantation of macrophages into central nervous system nerves allows them to regenerate after axonal crush (51). Inflammation also is implicated in secondary degeneration after spinal cord injury (51).…”

“…The pioneering work by Taub and coworkers regarding the role of IL-6 in liver regeneration in mice establishes the importance of inflammatory cytokines during hepatocyte priming (8). Inflammatory responses have been implicated in the priming of liver and other types of regeneration (51). For example, prevention of macrophage invasion impairs peripheral axonal regeneration, whereas implantation of macrophages into central nervous system nerves allows them to regenerate after axonal crush (51).…”

“…For example, prevention of macrophage invasion impairs peripheral axonal regeneration, whereas implantation of macrophages into central nervous system nerves allows them to regenerate after axonal crush (51). Inflammation also is implicated in secondary degeneration after spinal cord injury (51). Inflammatory responses can be triggered by cytokines such as those of the TNF family, which activate immediate-early genes such as AP-1 (52).…”

Microglia, major player in the brain inflammation: their roles in the pathogenesis of Parkinson's disease

“…For instance, some latent viruses such as JC virus or varicella zoster produce clinical syndromes mainly in immuno-compromised individuals. MHC and co-stimulatory molecules are strongly increased in CNS infection and a number of CNS pathologic conditions, including ischemia, neoplasm, traumatic nerve injury and neurodegenerative diseases such as AD, PD, MS, HIV-dementia and Creutzfeldt-Jacob disease (Maehlen et al, 1989;McGeer et al, 1993;Graeber et al, 1998;Perry, 1998;Dorries, 2001;Piehl and Lidman, 2001;O'Keefe et al, 2002;Owens, 2002). Recent evidence has implied that the CNS equips itself with a unique defense system with its own molecular and cellular components despite sharing certain properties with the peripheral immune system.…”