Neurological consequences of immune dysfunction: lessons from HIV infection and multiple sclerosis

J Neuroimmunol. 1992 Sep;40(1):115-9. doi: 10.1016/0165-5728(92)90219-b.

Abstract

In a recent workshop held on Sanibel Island, Florida (18-21 January 1992), the two most common neuroimmunologic diseases of young adults, multiple sclerosis (MS) and HIV encephalopathy, were jointly discussed. The logic of assembling investigators from these two fields was based not on an assumed etiologic connection between MS and retroviral infection of the central nervous system (CNS), but rather in the hope of uncovering potential common pathogenic mechanisms, particularly as might relate to trafficking of mononuclear cells into the central nervous system, the distribution and function of macrophages and microglia, the structure and function of the blood-brain barrier, and the role of cytokines released by activated cells. Multiple sclerosis is a disease without a known etiologic agent or pathogenesis. While the causative agent for HIV leukoencephalopathy is known, the pathogenesis of the disease remains entirely enigmatic (a topic covered by R. Johnson). This meeting brought together two different groups of investigators to compare and contrast the diseases and to share perspectives, paradigms, and data with the aim of cross-fertilizing the disciplines and generating healthy hybrids.

Publication types

  • Congress
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Acquired Immunodeficiency Syndrome / pathology
  • Acquired Immunodeficiency Syndrome / physiopathology*
  • Central Nervous System / immunology
  • Central Nervous System / pathology
  • Cerebrospinal Fluid / immunology
  • Culture Techniques
  • Disease Models, Animal
  • Humans
  • Immune System Diseases / physiopathology*
  • Multiple Sclerosis / pathology
  • Multiple Sclerosis / physiopathology*
  • Nervous System / physiopathology*