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Protection from vaccinia virus‐induced severe skin lesions by natural killer cells in a mouse model of eczema vaccinatum
Author(s) -
Kawakami Yuko,
Hasegawa Shunji,
Yumoto Kenji,
Yao Libo,
Tomimori Yoshiaki,
Tagaya Yutaka,
Crotty Shane,
Kawakami Toshiaki
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.670.17
Subject(s) - vaccinia , immunology , virus , smallpox vaccine , adoptive cell transfer , orthopoxvirus , atopic dermatitis , immune system , virology , cytotoxic t cell , medicine , vaccination , smallpox , disease , natural killer cell , biology , t cell , pathology , biochemistry , gene , in vitro , recombinant dna
Threats of bioterrorism have recently renewed efforts to better understand the disease mechanism of smallpox and to develop a safer vaccine against this dreadful disease. Individuals with atopic dermatitis (AD) are excluded from smallpox vaccination due to their propensity to develop eczema vaccinatum, a disseminated vaccinia virus infection. To study the underlying mechanism of the vulnerability of atopic patients to vaccinia virus infection, we developed a mouse model of eczema vaccinatum by infecting eczematous skin with virus. Virus infection induced severe erosive skin lesions in mice with preexisting dermatitis, but not in mice with healthy skin. The former mice exhibited lower natural killer (NK) cell activity, but similar cytotoxic T lymphocyte activity and humoral immune responses, as compared to the latter mice. The role for NK cells in suppressing vaccinia virus‐induced development of erosive and satellite skin lesions was demonstrated by depletion and adoptive transfer of NK cells. Consistent with low NK cell activities in AD patients, these results can at least partly explain the increased susceptibility of AD patients to eczema vaccinatum. Funded by the NIH through the ADVN consortium.