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David A. Martin^a,b and Keith B. Elkon^a,b

^a D.A.M. and K.B.E. are at the Department of Medicine, University of Washington, Seattle, WA 98195.
^b K.B.E. is at the Department of Immunology, University of Washington, Seattle, WA 98195.

CORRESPONDENCE K.B.E.: elkon{at}u.washington.edu

Abstract
Like the immune response itself, our efforts to understand the "rules" for self–nonself discrimination are constantly evolving. The discovery of pattern recognition receptors—the Toll-like receptor (TLR) family in particular—shifted the emphasis of self–nonself recognition from lymphocytes functioning in the adaptive immune system to antigen-presenting cells (APCs) functioning in the innate immune system. Two new articles, one in a recent issue (1) and one in this issue (see Vollmer et al. [2] on p. 1575), demonstrate that antigen–antibody complexes containing RNAs activate B lymphocytes and dendritic cells (DCs) through interaction with TLR7 and/or TLR8. From these and other papers, one begins to see how specific types of autoantigens—by virtue of their capacity to act as TLR ligands—favor autoantibody production. This is known as the Toll hypothesis.

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