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Abstract
Toll-like receptors (TLRs) were shown to play a critical role in the recognition and activation of pathogens by the innate immune system. Pathogen engagement of the TLR–myeloid differentiation protein 88 (MyD88) pathway favours the development of a protective T-helper (TH)1-biased T cell response. Interruption of TLR recognition or signalling has profound effects on protective immunity and enhances a TH2-biased immune response. Agonists or antagonists of specific TLRs have effects beyond infectious control and may represent a novel therapeutic for immunostimulation in vaccines, cancer, inflammatory disorders and allergy.