TY - JOUR
T1 - A protective role of interleukin-15 in a mouse model for systemic infection with herpes simplex virus
AU - Tsunobuchi, Hironaka
AU - Nishimura, Hitoshi
AU - Goshima, Fumi
AU - Daikoku, Tohru
AU - Suzuki, Haruhiko
AU - Nakashima, Izumi
AU - Nishiyama, Yukihiro
AU - Yoshikai, Yasunobu
N1 - Funding Information:
We sincerely thank K. Itano for excellent technical assistance. This work was supported by a grant from the Ministry of Education, Science, and Culture of the Japanese Government, JSPS-RFTF97L00703, the Center of Excellence.
PY - 2000/9/15
Y1 - 2000/9/15
N2 - To define the role of cytokine binding to the IL-2/IL-15Rβ chain in protective immunity against systemic infection with herpes simplex virus type 2 (HSV-2), IL-2/IL-15 receptor(R)β knock-out mice were inoculated intraperitoneally with HSV-2 strain 186. IL-2/IL-15Rβ-deficient mice were susceptible to systemic HSV-2 infection compared with their heterozygous littermates. The emergence of natural killer (NK) cells was impaired in IL-2/IL-15Rβ knock-out mice, but CD4+ T cell receptor (TOR) αβ+ T cells were normally detected in the peritoneal cavity after infection with HSV-2. However, the generation of HSV-2-specific CD4+ T helper (Th) 1 cells producing interferon-γ was impaired in IL-2/IL-15Rβ knock-out mice following HSV-2 infection. The serum IL-15 level in control mice was increased in the early stage after HSV-2 infection but was not detectable in IL-2/IL-15Rβ knock-out mice. In vivo administration of recombinant IL-15 protected normal mice from HSV-2-induced lethality, accompanied by increases in numbers of NK cells and HSV-2-specific Th1 cells. Taken together, these results suggest that IL-15, using the IL-2/IL15Rβ chain, plays an important role in mounting protective immunity during the course of systemic HSV-2 infection. (C) 2000 Academic Press.
AB - To define the role of cytokine binding to the IL-2/IL-15Rβ chain in protective immunity against systemic infection with herpes simplex virus type 2 (HSV-2), IL-2/IL-15 receptor(R)β knock-out mice were inoculated intraperitoneally with HSV-2 strain 186. IL-2/IL-15Rβ-deficient mice were susceptible to systemic HSV-2 infection compared with their heterozygous littermates. The emergence of natural killer (NK) cells was impaired in IL-2/IL-15Rβ knock-out mice, but CD4+ T cell receptor (TOR) αβ+ T cells were normally detected in the peritoneal cavity after infection with HSV-2. However, the generation of HSV-2-specific CD4+ T helper (Th) 1 cells producing interferon-γ was impaired in IL-2/IL-15Rβ knock-out mice following HSV-2 infection. The serum IL-15 level in control mice was increased in the early stage after HSV-2 infection but was not detectable in IL-2/IL-15Rβ knock-out mice. In vivo administration of recombinant IL-15 protected normal mice from HSV-2-induced lethality, accompanied by increases in numbers of NK cells and HSV-2-specific Th1 cells. Taken together, these results suggest that IL-15, using the IL-2/IL15Rβ chain, plays an important role in mounting protective immunity during the course of systemic HSV-2 infection. (C) 2000 Academic Press.
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U2 - 10.1006/viro.2000.0455
DO - 10.1006/viro.2000.0455
M3 - Article
C2 - 11017787
AN - SCOPUS:0034665018
SN - 0042-6822
VL - 275
SP - 57
EP - 66
JO - Virology
JF - Virology
IS - 1
ER -