Cytotoxic T-cells: Difference between revisions

From The School of Biomedical Sciences Wiki
Jump to navigation Jump to search
Nnjm2 (talk | contribs)
No edit summary
No edit summary
Line 3: Line 3:
The cytotoxic T-cells can trigger an endogenous pathway within the target cell leading to [[Apoptosis|apoptosis]]. This is due to the cytotoxic T-cells releasing "preformed effector molecules"<ref>Janeway CA Jr, et al.;2001</ref><ref>Janeway C. Immunobiology. 5th ed. Paris: De Boeck; 2003.</ref>.  
The cytotoxic T-cells can trigger an endogenous pathway within the target cell leading to [[Apoptosis|apoptosis]]. This is due to the cytotoxic T-cells releasing "preformed effector molecules"<ref>Janeway CA Jr, et al.;2001</ref><ref>Janeway C. Immunobiology. 5th ed. Paris: De Boeck; 2003.</ref>.  


=== References  ===
Cytotoxic T-cells contain the CD8+ receptor. They are responsible for binding [[MHC_Molecules|MHC class I]] present in most cells, which presents the foreign antigen of the endogenous origin. <ref>https://www.ncbi.nlm.nih.gov/books/NBK27101/</ref><br>


<references />
=== References&nbsp; ===
 
<references />
 
 
 
<br>

Revision as of 13:32, 20 October 2018

Cytotoxic T cells are able to search the intracellular compartments to remove or destroy any foreign objects such as bacteria and pathogens which have the potential to cause harm. Also known as a killer T-cell. These cells kill host cells that have become infected by some sort of intracellular pathogen[1].

The cytotoxic T-cells can trigger an endogenous pathway within the target cell leading to apoptosis. This is due to the cytotoxic T-cells releasing "preformed effector molecules"[2][3].

Cytotoxic T-cells contain the CD8+ receptor. They are responsible for binding MHC class I present in most cells, which presents the foreign antigen of the endogenous origin. [4]

References 

  1. alberts, B (2008). molecular biology of the cell. USA: garland science. glossary
  2. Janeway CA Jr, et al.;2001
  3. Janeway C. Immunobiology. 5th ed. Paris: De Boeck; 2003.
  4. https://www.ncbi.nlm.nih.gov/books/NBK27101/