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(Stroke. 2007;38:768.)
© 2007 American Heart Association, Inc.

Adaptive Immunity: Introduction

Adaptive Immunity

Introduction

John Hallenbeck, MD

From the Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md.

Correspondence to John Hallenbeck, Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 49 Convent Dr, MSC 4476, Bethesda, MD 20892-4476. E-mail hallenbj@ninds.nih.gov

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The 3 talks in this session all deal with aspects of immune response regulation and dysregulation that can be either protective or harmful in brain ischemia. As an introduction to this session, I will review several models of immune response regulation and relate these models to the upcoming talks.¹ Under normal circumstances, antigen presenting cells (APCs) such as microglia, macrophages and dendritic cells are in a resting state. In this state, they tend to produce immunomodulatory cytokines such as transforming growth factor-ß (TGF-ß) and interleukin (IL)-10. TGF-ß from the APCs and also from existing regulatory T cells (T_reg) can induce naïve T cells to differentiate into TGF-ß secreting T_reg cells. IL-10 secreting APCs can induce naïve T cells to differentiate into T-regulatory type 1 (Tr1) cells that secrete IL-10 and do not express the transcription factor FoxP3.

The APCs can be provoked by a number of stimuli that include infectious agents, inflammatory mediators, and endogenous ligands. Once activated, the antigen presenting cells are poised to elicit an immune response.

The model for immune response regulation has undergone considerable evolutionary change over the past 40 to 50 years.² In 1959 Burnet and Medawar proposed a "Self-Non-self Model" for regulation of the immune response in which each lymphocyte was viewed as having a single receptor that would react with a specific antigen or specific antigens. Because of the enormous number of lymphocytes, the vast array of potential antigens was considered to be covered and, when an antigen bound to its cognate . . . [Full Text of this Article]