Postmortem analyses of Alzheimer's disease (AD) brain tissue reveal reactive microglia expressing high levels of major histocompatibility complex (MHC) glycoproteins, immunoglobulin receptors, and complement receptors; small but significant numbers of T-lymphocytes infiltrating tissue; enhanced cytokine and cytokine receptor expression; and profuse immunoreactivity for complement proteins of the classic pathway colocalized with senile plaques, dystrophic neurites, and some neurofibrillary tangles. Protectin, clusterin, and vitronectin, three proteins designed to defend host cells against "bystander lysis" caused by the membrane attack complex of complement, are all expressed at high levels in AD tissue but not in normal tissue. Taken together, these findings indicate that immune-mediated autodestructive processes may occur in AD. In view of the urgency to find treatments for AD and disappointing results with the many classes of pharmacologic agents that have so far been given clinical trials, exploration of the effectiveness of anti-inflammatory agents may now be warranted.