IFN-α8 enhances the proliferation of human
B cells, as well as being able to activate
NK cells. The subtypes α10 and α2, along with α8, are the most efficient and powerful NK cell activators. Subtypes α21 and α2 enhance the expression of
IFN-gamma-inducible protein-10 (IP-10) in
dendritic cells. Activated dendritic cells initiate
immune responses and induce the
expression of IP-10, a
chemokine which promotes a
Th1 inflammatory response. IFN-α1 causes increased
HLA-II expression, and can directly inhibit
tumor cell growth
in vitro. However, it is a poor activator of NK cells, has relatively little
antiviral activity, does not induce B cell proliferation, and does not enhance
HLA-I or
tumor antigen expression. Despite its apparent inactivity, it is still used clinically in the treatment of
metastatic renal cell carcinoma, with a reported lower
toxicity than the
recombinant IFN-α2. Overall, IFN-α has a general inflammatory action which skews the immune response towards a Th1 profile. Subtype α2 increases the expression of HLA-I molecules, which correlates with IFN-α-mediated activation of
memory CD8 cells and increased
cytolytic action against
virally infected cells and tumor cells (via
cytotoxic CD8 cells). == References ==