CNS Autoimmune Inflammation: RICK Must NOD!

Neurodegeneration and -protection in autoimmune CNS inflammation.

Neurodegeneration in multiple sclerosis (MS) is the structural correlate of permanent neurological disability in patients. The histopathological features of neurodegeneration include destruction of axons as well as apoptotic cell death of neuronal cell bodies. Therapeutic efforts to control these clinically important aspects of MS pathology showed limited success so far. In this review article,...

NOD-like receptors and inflammation

The nucleotide-binding and oligomerization domain, leucine-rich repeat (also known as NOD-like receptors, both abbreviated to NLR) family of intracellular pathogen recognition receptors are increasingly being recognized to play a pivotal role in the pathogenesis of a number of rare monogenic diseases, as well as some more common polygenic conditions. Bacterial wall constituents and other cellul...

Hunting Autoimmune Disease Genes in NOD:

CNS Inflammation and Epileptogenesis

An association between acute CNS infections and seizures is reported in the literature. The etiology of these seizures is, in some cases, precipitated by epileptogenic pathogenesis of the infectious agent in the brain parenchyma. A different etiology of seizures as a consequence of infections, independent of the infectious agent, relates to the inflammatory reaction. Thirdly, the febrile respon...

TRPM2 Cation Channels Modulate T Cell Effector Functions and Contribute to Autoimmune CNS Inflammation

TRPM2, a highly Ca(2+)-permeable member of the transient receptor potential melastatin-related (TRPM) family of cation channels, is expressed in cells of the immune system. We demonstrate firstly that TRPM2 cation channels on T cells critically influence T cell proliferation and proinflammatory cytokine secretion following polyclonal T cell receptor stimulation. Consistently, trpm2-deficient mi...