Evolving Bacterial Envelopes and Plasticity of TLR2-dependent Responses: Basic Research and Translational Opportunities

Frontiers in Immunology

Dennis Sang Won Lee¹  Joaquin eMadrenas¹  Junbin (Ben) eLi¹ 

[1] McGill University;

关键词: Gram-Positive Bacteria;    microbiota;    immune response;    commensal bacteria;    Toll-like Receptors (TLR);   

DOI  :  10.3389/fimmu.2013.00347

来源: DOAJ

【 摘 要 】

Innate immune mechanisms that follow early recognition of microbes influence the nature and magnitude of subsequent adaptive immune responses. Early detection of microbes depends on pattern recognition receptors (PRRs) that sense pathogen- or microbial-associated molecular patterns (PAMPs or MAMPs, respectively). The bacterial envelope contains MAMPs that include membrane proteins, lipopeptides, glycopolymers and other pro-inflammatory molecules. Bacteria are selected by environmental pressures resulting in quantitative or qualitative changes in their envelope structures that often promote evasion of host immune responses and therefore, infection. However, recent studies have shown that slight, adaptive changes in MAMPs on the bacterial cell wall may result in their ability to induce the secretion not only of pro-inflammatory cytokines but also of anti-inflammatory cytokines. This effect can fine-tune the subsequent response to microbes expressing these MAMPs and lead to the establishment of a commensal state within the host rather than infectious disease. In this review, we will examine the plasticity of Toll-like receptor (TLR) 2 signalling as evidence of evolving MAMPs, using the better-characterized TLR4 as a template. We will review the role of differential dimerization of TLR2 and the arrangement of signalling complexes and co-receptors in determining the capacity of the host to recognize an array of TLR2 ligands and generate different immune responses to these ligands. Last, we will assess briefly how this plasticity may expand the array of interactions between microbes and immune systems beyond the traditional disease-causing paradigm.

【 授权许可】

Unknown