Macrophages are the most important immune effector cells during the earliest stage of trauma and are activated by recognizing pathogen-associated molecular patterns (PAMPs) during the immune-defense reaction against infection.
4 The latter may be activated by P. acnes and recognize altered lipid content in sebum, followed by the production of proinflammatory cytokines.
Interestingly, the addition of the stem-loop RNA sequence to in vitro splicing reactions enhanced IDX inclusion [8], suggesting that the reaction can be activated by titrating out inhibitory factors that recognize this structure.
FII is connected to the core domains through two flexible linkers, which likely is important for the ability of PARP-1 to recognize and be activated by a large number of DNA structures, including nicked DNA, double-strand breaks, overhangs, cruciforms, and promoter regions.
These cells play a role in the transition between innate and adaptive immune [ 17]. γδ T lymphocytes can recognize and be activated by pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) in absence of other stimuli [ 18, 19], supporting the notion of an innate immune function of these cells.
It should be recognized that TRPCs can also be activated by non-lipid factors, including extracellular acid or redox protein [10,61], and can exhibit significant constitutive activity [8 10].
Conversely, the adaptive immune system (AIS) can recognize virtually everything, although it must be activated by Ag-presenting cells (APCs) that pertain to the IIS.
They can be activated by the binding of specific antibodies to receptors on their surface, and can also recognize pathogens and inflammatory proteins directly.
Earthlink's software, however, must be activated by users.
Two types of cellular immune responses appear to be clinically relevant: antigen specific immunity mediated by T cells that recognize tumor-associated peptide antigen expressed on surface HLA class I or class II molecules, and antigen nonspecific immune responses mediated by natural killer (NK) cells that are activated by the failure to recognize cognate "self" HLA class I molecules.
