Inflammation is a key element in the pathophysiology of Central Nervous System (CNS) diseases, irrespective of the etiology of such diseases. From inflammatory or infectious diseases to neurodegenerative, ischemic or traumatic diseases, inflammation plays a fundamental role both in controlling the ongoing pathological processes and in promoting neuroprotection or regeneration. Indeed, due to the complex architecture and activities in the brain, the side effects of brain inflammation are fundamental to the outcome of neurological diseases (for example bystander neuronal damage). The CNS differs from the other organs as it is partially isolated from the immune system by the restrictive blood-brain barrier and the presence of an immunosuppressive environment (brain immune privilege). Inappropriate immune responses are responsible for diseases such as Multiple Sclerosis (MS) or for the increased disability after brain trauma or stroke. Inflammation also plays an important role in neurodegenerative diseases such as Alzheimer (AD) or Parkinson diseases (PD). However, in certain circumstances immune responses in the brain might have a neuroprotective effect, possibly mediating the release of trophic factors by inflammatory or glial cells. Neurotrophic factors protect axons and myelin from inflammatory damage, and they have immunosuppressive properties that contribute to the maintenance of brain immune privilege. Thus, in addition to their neuroprotective activities, neurotrophic factors may offer new therapeutic perspectives by targeting inflammatory processes in brain disorders.