Tolllike receptor, recognise bacterial products and stimulate immune response by
Ref Robbins 9/e 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 proteins(proteins 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 kinases(IKKi, 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.
Perforin and granzyme mediated apoptosis
FADD ligand apoptosis
Transcription of nuclear factor mediated by N-FkBwhich recruits cytokine
Cyclin
General anatomy