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IL‐5 dominates cytokine responses during expression of protective immunity to Onchocerca lienalis microfilariae in mice
Author(s) -
HOGARTH PHILIP J.,
BIANCO ALBERT E.
Publication year - 1999
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.1999.00204.x
Subject(s) - biology , immunology , immune system , immunity , spleen , antigen , eosinophil , splenocyte , cytokine , cellular immunity , interferon gamma , asthma
In a model of protective immunity against Onchocerca microfilariae (mf), it has been demonstrated previously that immunocompetent mice clear a primary infection and are highly resistant to re‐infection. This immunity correlates with CD4 + Th2 cells, is dependant on IL‐5 but not IL‐4, and can be transferred adoptively with spleen cells. In the current investigation, high levels of spontaneous proliferation and of IFNγ production were observed in splenocyte cultures from immune mice, compared with cells from naive controls. Antigen‐specific proliferation also occurred in immune cells, being vigorous following stimulation with adult worm antigen, but not with antigens from developing embryos or mf. Levels of IL‐4, IL‐5 and IFNγ induced by the various antigens was similar, indicating that activation of alternate T helper cell sub‐sets was unlikely to explain the lack of cellular responsiveness. After a primary inoculation with mf, spleen cells from infected mice co‐produced IFNγ and IL‐5. In contrast, IFNγ production was downregulated while IL‐5 levels remained high during active elimination of a challenge infection. Significant levels of IL‐4 production occurred only once parasite clearance had begun. These data confirm the importance of IL‐5 in protection against Onchocerca mf in mice and question the role of IFNγ in the expression of immunity. Production of high levels of IL‐5 correlated with blood and tissue eosinophil mobilization during the clearance of a challenge infection .