Role of IFN-α in SLE is still disputed
In addition to abnormal B cells, IFN-α is the cytokine that induces the
differentiation of activated B cells into plasma cells, contributes to
the migration of leukocyte, and promotes the production of antibodies22, 61-63. However, the role of IFN-α is still
disputed. Most researchers believe that IFN-α is essential to inducing
SLE and promoting its progression 61, 64, 65. IFN-α
may enhance the antigen-presenting abilities of monocytes and dendritic
cells, which may result in self-antigens being presented and the
subsequent breakage of immunological self-tolerance66. However, some researchers have demonstrated that
IFN-γ, but not IFN-α, promotes the development of SLE; IFN-α has even
been shown to play a protective role in SLE 48, 51,
67. Although the frequency of plasma cells has been demonstrated to be
significantly increased in lupus mice, the majority of CD138+ plasma
cells have been revealed to be abnormal T cells and those expressing the
marker CD3 12-14. However, B cells in lupus mice have
been found not to accumulate significantly; contrarily, the frequency of
B cells has been shown to decrease dramatically, compared with that of
healthy mice 12, 68. Moreover, IFN-α has been reported
to suppress Th1 polarization by inhibiting IL-12 secretion and
preventing IFN-γ production via signal transducer and activator of
transcription 1 (STAT1) 69, 70. However, some
researches have also shown that the frequency of Th1 cells, but not that
of Th2 cells, in Fas-deficient lupus mice is significantly increasedin vivo 12, 50, 71, 72.