CD8+ type-2 T cells enhance the severity of acute herpes virus infection in mice.
The role of CD8+ suppressor T cells in acute herpes simplex virus type 1 (HSV) infection was investigated in mice. CD8+ CD11b+ TCR-gamma/delta + suppressor T cells (HSV-STC) were demonstrated in spleens of mice infected intraperitoneally (i.p.) with HSV. When HSV-STC from mice infected with a 10 LD50 of HSV (donors) were adoptively transferred to mice 3 days after being infected with a 1 LD50 dose of HSV (recipients), the morbidity and mortality of recipients were greatly increased (mean survival time in days (MSD): 9.4 days; mortality, 100%) as compared with controls that received CD4+ T cells or a whole T-cell lysate from donors (MSD, > 19.6 days or > 19.1 days; mortality, 38% or 50%). The morbidity and mortality of mice exposed to a 1 LD50 of HSV were also increased when they were continuously treated with recombinant murine IL-4. However, the survival rate of mice exposed to a 10 LD50 of HSV increased after multiple treatments of these mice with anti-IL-4 monoclonal antibody. IL-4-producing cells were detected in a population of HSV-STC, and IL-4 was produced when these cells were cultured in the presence of UV-inactivated HSV in vitro. These results indicate that IL-4 plays an important role in the progression of acute HSV infection and, through the production of IL-4, HSV-STC may increase the severity of the acute-phase infection of HSV in mice.
Ikemoto
K
K
Department of Neurology, Yamaguchi University School of Medicine, Japan.
Pollard
R B
RB
Fukumoto
T
T
Morimatsu
M
M
Suzuki
F
F
D000208:Acute Disease; D000818:Animals; D006561:Herpes Simplex / Q000209:etiology* / Q000276:immunology* / Q000401:mortality; D006801:Humans; D016130:Immunophenotyping; D016219:Immunotherapy, Adoptive / Q000009:adverse effects*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018139:Simplexvirus / Q000472:pathogenicity; D013154:Spleen / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000145:classification / Q000276:immunology / Q000637:transplantation*