TY - JOUR
T1 - Polarization of immune responses in fish
T2 - The ‘macrophages first’ point of view
AU - Wiegertjes, Geert F.
AU - Wentzel, Annelieke S.
AU - Spaink, Herman P.
AU - Elks, Philip M.
AU - Fink, Inge R.
N1 - Publisher Copyright:
© 2015 Elsevier Ltd
PY - 2016/1/1
Y1 - 2016/1/1
N2 - In this review, we support taking polarized immune responses in teleost fish from a ‘macrophage first’ point of view, a hypothesis that reverts the dichotomous T helper (TH)1 and TH2 driving forces by building on the idea of conservation of innate immune responses in lower vertebrates. It is plausible that the initial trigger for macrophage polarization into M1 (inflammation) or M2 (healing) could rely only on sensing microbial/parasite infection or other innate danger signals, without the influence of adaptive immunity. Given the long and ongoing debate on the presence/absence of a typical TH1 cytokine environment and, in particular, TH2 cytokine environment in fish immune responses, it stands out that the presence of macrophages with polarized phenotypes, alike M1 and M2, have been relatively easy to demonstrate for fish. We summarize in short present knowledge in teleost fish on those cytokines considered most critical to the dichotomous development of TH1/M1 and TH2/M2 polarization, in particular, but not exclusively, interferon-γ and interleukin (IL)-4/IL-13. We review, in more detail, polarization of fish immune responses taken from the macrophage point of view for which we adopted the simple nomenclature of M1 and M2. We discuss inducible nitric oxide synthase, or NOS-2, as a reliable M1 marker and arginase-2 as a reliable M2 marker for teleost fish and discuss the value of these macrophage markers for the generation of zebrafish reporter lines to study M1/M2 polarization in vivo.
AB - In this review, we support taking polarized immune responses in teleost fish from a ‘macrophage first’ point of view, a hypothesis that reverts the dichotomous T helper (TH)1 and TH2 driving forces by building on the idea of conservation of innate immune responses in lower vertebrates. It is plausible that the initial trigger for macrophage polarization into M1 (inflammation) or M2 (healing) could rely only on sensing microbial/parasite infection or other innate danger signals, without the influence of adaptive immunity. Given the long and ongoing debate on the presence/absence of a typical TH1 cytokine environment and, in particular, TH2 cytokine environment in fish immune responses, it stands out that the presence of macrophages with polarized phenotypes, alike M1 and M2, have been relatively easy to demonstrate for fish. We summarize in short present knowledge in teleost fish on those cytokines considered most critical to the dichotomous development of TH1/M1 and TH2/M2 polarization, in particular, but not exclusively, interferon-γ and interleukin (IL)-4/IL-13. We review, in more detail, polarization of fish immune responses taken from the macrophage point of view for which we adopted the simple nomenclature of M1 and M2. We discuss inducible nitric oxide synthase, or NOS-2, as a reliable M1 marker and arginase-2 as a reliable M2 marker for teleost fish and discuss the value of these macrophage markers for the generation of zebrafish reporter lines to study M1/M2 polarization in vivo.
KW - Arginase
KW - Fish
KW - iNOS
KW - LPS
KW - Macrophage polarization
KW - Zebrafish
UR - http://www.scopus.com/inward/record.url?scp=84966429465&partnerID=8YFLogxK
U2 - 10.1016/j.molimm.2015.09.026
DO - 10.1016/j.molimm.2015.09.026
M3 - Article
C2 - 26471699
AN - SCOPUS:84966429465
SN - 0161-5890
VL - 69
SP - 146
EP - 156
JO - Molecular Immunology
JF - Molecular Immunology
ER -