Anomalous Type 17 Response to Viral Infection by CD8+ T Cells Lacking T-bet and Eomesodermin

CD8+ T cells that have defective transcription factors T-bet and eomesodermin (Eomes) were shown to be unable to defend the body against lymphocytic choriomeningitis viral infection, as a study conducted by the University of Pennsylvania demonstrates.

Naïve CD8+ T cells in mammals are primed by invading pathogens and turn into cytotoxic killer cells upon contact. To fight intracellular pathogens, they can lyse the infected mammalian cells and secrete cytokines to activate intracellular microbes.

Virus-specific CD8+ T cells that lack T-bet and Eomes only differentiate into interleukin-17-secreting cells, similar to T helper cells that have been associated with autoimmunity and extracellular microbial defense. Mice with this kind of cells develop a CD8+ T cell-dependent, progressive inflammatory and wasting syndrome upon viral infection, characterised by multi-organ infiltration of neutrophils.

T-bet and Eomes are responsible for CD8+ T cells to differentiate into their designated cell fate and to turn into killer cells that are specific in intracellular instead of extracellular destruction.

Related antibodies on antibodies-online.com:

CD8+ T cells

T-bet

Eomesodermin (Eomes)

Interleukin-17 (IL-17)

Neutrophils

Lymphocytic choriomeningitis virus

Antibodies for the research area immunology: »Show antibodies

Antibodies for the research area inflammation: »Show antibodies

Antibodies for the research area virology: »Show antibodies