Batf3 deficiency is not critical for the generation of CD8α⁺ dendritic cells

Immunobiology. 2015 Apr;220(4):518-24. doi: 10.1016/j.imbio.2014.10.019. Epub 2014 Oct 30.


Recently, we have reported that CD8α(+) DCs, rather than CD8(+) T cells, are involved in the establishment and maintenance of HSV-1 latency in the trigeminal ganglia (TG) of ocularly infected mice. In the current study, we investigated whether similar results can be obtained using Batf3(-/-) mice that previously were reported to lack CD8α(+) DCs. However, our results demonstrate that Batf3(-/-) mice, without any known infection, express CD8α(+) DCs. Consequently, due to the presence of CD8α(+) DCs, no differences were detected in the level of HSV-1 latency between Batf3(-/-) mice compared with wild type control mice.

Keywords: Compensation; Dendritic cells; HSV-1; Knockout; Latency.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Basic-Leucine Zipper Transcription Factors / deficiency*
  • CD8 Antigens / genetics
  • CD8 Antigens / metabolism*
  • Dendritic Cells / immunology*
  • Dendritic Cells / metabolism*
  • Disease Models, Animal
  • Gene Knockout Techniques
  • Herpes Simplex / genetics
  • Herpes Simplex / immunology
  • Herpes Simplex / metabolism
  • Herpesvirus 1, Human / immunology
  • Immunohistochemistry
  • Immunophenotyping
  • Mice
  • Mice, Knockout
  • Phenotype
  • Rabbits
  • Repressor Proteins / deficiency*


  • Basic-Leucine Zipper Transcription Factors
  • CD8 Antigens
  • CD8 antigen, alpha chain
  • Repressor Proteins
  • SNFT protein, mouse