作者: Yaping Sun , Pavan Reddy
DOI: 10.1016/B978-0-12-416004-0.00018-5
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摘要: In recent years there has been a much greater understanding of the several different types intracellular sensors that recognize both pathogen-derived (non-self) and ‘self’ substances have danger-associated molecular patterns. These trigger divergent signaling pathways activate innate immunity shape adaptive immune responses. The include those directly initiate responses indirectly modulate by sensing metabolic perturbations. Most typically various forms nucleic acids, i.e. ssDNA, dsDNA, ssRNA dsRNA irrespective their endogenous or exogenous origins. Several families these sensors, including certain TLRs, Nod-like receptors (NLRs), RIG-I-like (RLRs) AIM2-like (ALRs) identified in years. mTOR, HDAC enzymes – sirtuins inflammasomes. To date, amongst TLR role for 7/8, 9 3 demonstrated regulation allo-responses after BMT. Nod2 shown to be associated with graft-versus-host disease (GVHD). No specific impact suggested clearly experimental clinical BMT through modulation mTOR pathways. Much remains understood about cellular subsets regulating allogeneic Furthermore, is burgeoning evidence inflammation induce changes (amino acid, glucose metabolism) can further perpetuate mitigate Understanding will refine our allo-immunity could potentially lead newer therapeutic approaches mitigating GVHD.