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Interferons: Type II & III
CATEGORY: RECEPTORS & MOLECULES
Interferons: Type II & III
Ellen Margaret Moran, Charles Institute of
Dermatology, University College Dublin, Ireland
Two additional interferon subtypes have also been identified as being biologically significant: type II
interferon or IFN-γ and the type III interferons IFN-λ1, IFN-λ2 and IFN-λ3. IFN-γ is secreted by natural
killer (NK) cells, T cells and antigen presenting cells (monocytes, macrophages and dendritic cells)
whereas to date the only source of type III interferons identified is plasmacytoid dendritic cells (DCs).
IFN-γ was initially described as an antiviral factor, however, it has since been demonstrated to
contribute to a much wider range of biological activities. Binding of IFN-γ to its receptors promotes
cellular immune responses; activation of macrophages and NK cells; upregulation of MHC expression
and promoting leucocyte migration. IFN-γ is also considered the key cytokine in the Th1 immune
response.
Type III interferons are co-expressed with type I interferons by virally infected cells and both contribute
to the early antiviral response. In addition, type III IFNs are capable of modulating the adaptive immune
response. IFN-λ increases MHC I and II expression on DCs as well as levels of CCR7, the chemokine
receptor crucial for DC migration to lymph nodes.
The broad functions of the interferon family are evidenced by the treatments currently in use and/or in
development that modulate the various members for the treatment of diseases such as chronic
hepatitis C infection and multiple sclerosis.
.
Table 1. Members of the Type II and III Interferon Family
Members
Cellular
Functions
source
Type II
IFN-γ
NK cells,
-
Activates macrophages and NK cells
T cells,
-
Upregulation of MHC expression
antigen
-
Drives leucocyte migration
presenting
-
Mediator of Th1 immune response
-
Upregulation
cells
Type III
IFN- λ1, IFN-λ2, IFN- Plasmacytoid
λ3
DCs
of
DC
MHC
I
and
II
expression
-
Modulation
migration
of
CCR7
mediated
DC
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Interferons were first described in the late 1950s by two scientists – Isaacs and Lindenmann – who
assigned an antiviral factor the name ‘interferon’. This was due to the molecule’s ability to ‘interfere’
with the growth of the influenza virus. In the subsequent twenty years, the type I interferon family –
comprising key members such as IFN-α and IFN-β – was well characterised. The type I interferons are
considered the first line of defence against numerous viral infections in humans.