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==[[Innate Immunity Cellular Responses]]==
 
==[[Innate Immunity Cellular Responses]]==
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=Innate Immunity to Viruses=
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=[[Innate Immunity to Viruses]]=
[[Image:Innate viral response.jpg|thumb|right|150px|Innate response to dsRNA - B. Catchpole, RVC 2008]]
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Because viruses invade host cells to take over a host's cellular machinery, the innate system has a more difficult time detecting viruses as foreign agents.  However, there is a give-away element of the viral attack that the innate system can recognize: the '''double-stranded RNA''' (dsRNA) produced by a virus in its replication phase.  Because mammalian cells only ever produce single-stranded RNA, the presence of dsRNA signals a foreign intruder.  dsRNA can be detected by TLR-3R on the cell surface or intracellularly by the presence of dsRNA-dependent protein kinase. 
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The innate response to viral attack also depends on the presence of '''Type-1 Interferons''', which are produced by all cells on recognition of a viral attack.  Interferons serve to increase degradation of mRNA, inhibit protein synthesis, and increase the effectiveness of the adaptive response by increasing antigen presentation to antibody. 
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Lastly, the final line of defense for the innate response to viruses lies in the actions of [[Lymphocytes#Natural Killer (NK) Cells|'''Natural Killer (NK) cells''']].  These warriors monitor the production of [[MHC - WikiBlood|MHC]] (Major Histocompatibility Complex) on the surface of cells, which is produced as part of the adaptive response.  A cell whose cellular machinery is compromised by viral infection will experience a drop in the amount of MHC it produces.  When a cell's MHC production drops, NK cells are triggered to phagocytose these cells.  As such, this is a non-specific targeting based simply on the ability of a cell to function normally, which also lends them to playing a role in targeting malignant cells.  NK cells are incapable of directly targeting viral infection.
      
=Innate Immunity to Bacteria=
 
=Innate Immunity to Bacteria=
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