Today I came across an interesting concept that I may have missed during my degree in Immunology. This concept is the bystander effect in the context of CD8 T cells in response to intracellular pathogens such as Listeria monocytogenes (L. monocytogenes). L. monocytogenes is a gram-positive bacteria that can create an inflammatory environment that can “license” dendritic cells, through toll-like receptors, to express co-stimulatory molecules such as B7, CD40 and 4-1BBL. This, in turn , allows “licensed” DCs presenting L. monocytogenes peptides to directly activate CD8 T cells without CD4 T cell help.

The bystander effect: if you are around, you are in

So what I’ve found was that, in addition to the above pathway, naive antigen-nonspecific CD8 T cells can be activated to produce proinflammatory cytokines when they receive IL-12 and IL-18 made by activated DCs in response to L. monocytogenes or Burkholderia pseudomallei. This allows mice to fight against the infection before the generation and expansion of specific CD4 and CD8 T cells. Thus, it seems like this mechanism acts in an innate-kinda way, helping contain the pathogens at bay before the more effective cell types arrive.

Baby Immunologist

Disclaimer: this article has not been peer reviewed and the knowledge was gained from Janeway’s Immmunobiology 7th edition.