Preservation of the delayed-type hypersensitivity response to alloantigen by xyloglucans or oligogalacturonide does not correlate with the capacity to reject ultraviolet-induced skin tumors in mice

Citation
Fm. Strickland et al., Preservation of the delayed-type hypersensitivity response to alloantigen by xyloglucans or oligogalacturonide does not correlate with the capacity to reject ultraviolet-induced skin tumors in mice, J INVES DER, 116(1), 2001, pp. 62-68
Citations number
40
Categorie Soggetti
Dermatology,"da verificare
Journal title
JOURNAL OF INVESTIGATIVE DERMATOLOGY
ISSN journal
0022202X → ACNP
Volume
116
Issue
1
Year of publication
2001
Pages
62 - 68
Database
ISI
SICI code
0022-202X(200101)116:1<62:POTDHR>2.0.ZU;2-P
Abstract
Chronic exposure to ultraviolet radiation suppresses T cell-mediated immune responses and induces the formation of suppressor T lymphocytes that preve nt the rejection of highly antigenic ultraviolet-induced skin cancers in mi ce. Tamarind seed xyloglucans and pectinic oligogalacturonides prevent supp ression of delayed-type hypersensitivity immune responses in mice to Candid a albicans and alloantigen caused by a single exposure of ultraviolet radia tion. We therefore investigated the ability of these poly/oligosaccharides to prevent suppression of T cell-mediated immune responses and suppressor c ell induction during chronic ultraviolet irradiation and to preserve the ca pacity of ultraviolet-irradiated mice to reject a transplanted, highly anti genic, ultraviolet-induced tumor. C3H/HeN mice were treated 3X per week for 12 wk with 15 kJ per m(2) ultraviolet B radiation followed by application of the polysaccharides/oligosaccharides. The delayed-type hypersensitivity responses to C. albicans and alloantigen were measured after 1, 6, and 12 w k of treatment. Following the 12th wk of treatment the remaining mice were injected with the highly antigenic ultraviolet-induced, syngeneic tumor cel l line UV5497-5. The polysaccharides/oligosaccharides protected delayed-typ e hypersensitivity responses to C, albicans but not contact hypersensitivit y responses to dinitrofluorobenzene for up to 6 wk of ultraviolet radiation after which protection declined and suppressor cells were observed. In con trast, the delayed-type hypersensitivity response to alloantigen was preser ved for the entire 12 wk of ultraviolet irradiation. Despite protection of immunity to alloantigen, the transplanted tumor cells grew equally well, in all ultraviolet-irradiated animals. These results indicate that delayed-ty pe hypersensitivity responses are heterogeneous and that delayed-type hyper sensitivity to alloantigen is not a surrogate marker for rejection of ultra violet-induced skin tumors.