<prompt> Tolllike receptor, recognise bacterial products and stimulate immune response byPerforin and granzyme mediated apoptosisFADD ligand apoptosisTranscription of nuclear factor mediated by N-FkBwhich recruits cytokineCyclin  <response>: Ref Robbins 9e p187 The ability of immune system to recognize moleculesthat are broadly shared by pathogens is, in pa, due to the presence of Immune receptors called toll-like receptors TLRs that are expressed on the membranes of leukocytes including dendritic cells, macrophages, natural killer cells, cells of the adaptive immunity T and B lymphocytes and non immune cells epithelial and endothelial cells, and fibroblasts. The binding of ligands - either in the form of adjuvant used in vaccinations or in the form of invasive moieties during times of natural infection - to the TLR marks the key molecular events that ultimately lead to innate immune responses and the development of antigen-specific acquired immunity. Upon activation, TLRs recruit adapter proteinsproteins that mediate other protein-protein interactions within the cytosol of the immune cell in order to propagate the antigen-induced signal transduction pathway. These recruited proteins are then responsible for the subsequent activation of other downstream proteins, including protein kinasesIKKi, IRAK1, IRAK4, and TBK1 that fuher amplify the signal and ultimately lead to the upregulation or suppression of genes that orchestrate inflammatoryresponses and other transcriptional events. Some of these events lead to cytokine production, proliferation, and survival, while others lead to greater adaptive immunity. If the ligand is a bacterial factor, the pathogen might be phagocytosed and digested, and its antigens presented to CD4 T cells. In the case of a viral factor, the infected cell may shut off its protein synthesis and may undergo programmed cell death apoptosis. Immune cells that have detected a virus may also release anti-viral factors such as interferons. 