Who needs adaptive immunity?

Abstract

Several recent papers on Toll-like receptors (TLRs) suggest that the so-called innate immune response, which here-to-fore no self-respecting card-carrying immunologist would own up to having an interest in, have levels of sophistication, specificity and diversity that were previously unsuspected. TLRs represent immunology at its simplest: a host defence response is triggered by TLRs, which are there to recognize foreign molecules or, as is emerging, molecules derived from the host during tissue injury. Recent information indicates that there are 14 TLRs in the human genome. TLRs form either hetero- or homodimers, and possibly require co-receptors for their function, thus providing a diverse repertoire of receptors for a potentially large number of microbial products. Signals that are specific to particular TLRs might be activated: the use of microarrays is already indicating that TLR-4 and TLR-2 induce different blends of genes in macrophages. Certain host-derived factors, released only during tissue injury, appear to activate cells via TLRs, and triggering of TLR on B cells could form the basis for B-cell activation by T-cell-independent type 2 antigens. This last observation abrogates the need for T cells in the process of B-cell activation and overall, data on TLRs is questioning the primacy of adaptive immune responses to microbes.