The helminth
glycan LNFPIII is an immunomodulatory molecule, driving CD4(+) Th2-type biasing as well as immune suppression.
Psoriasis is an
autoimmune disease where the immune mechanisms as well as the
antigens responsible for development of immune autoreactivity are still not known. In the absence of defined immunological mechanisms, we asked whether
LNFPIII would function as novel
therapy for
psoriasis. We tested the therapeutic efficacy of
LNFPIII using the flaky skin (fsn)/fsn mutant mouse model of
psoriasis-like lesion development. We found that treatment of mice with
LNFPIII prevented the appearance of psoriatic skin lesions on fsn/fsn mice. Examination of the skin 2 weeks
after treatment demonstrated that prevention of skin lesions was associated with maintenance of normal epidermis thickness in
LNFPIII-treated mice as compared with a significantly thickened epidermis in control treated and diseased mice. In addition, cells from skin of
LNFPIII-treated mice produced lower amounts of
interferon-gamma as compared with cells from skin of control treated diseased mice. Examination of macrophages and T cells from peripheral lymph nodes of control and
LNFPIII-treated fsn/fsn mice showed that
glycan treatment reduced the numbers of Gr1(+)F4/80(+) macrophages and the numbers of CD8(+) T cells, restoring the numbers of these two cell populations as well as the CD4 : CD8 ratio to near normal levels. Overall, the results from this study suggest that the helminth immunomodulatory
glycan LNFPIII functions to prevent development of psoriatic-like skin lesions in fsn/fsn mice.