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Interleukin‐4 and listeriosis
Author(s) -
Kaufman Stefan H. E.,
Emoto Masashi,
Szalay Gudrun,
Barsig Johannes,
Flesch Inge E. A.
Publication year - 1997
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/j.1600-065x.1997.tb00995.x
Subject(s) - listeria monocytogenes , immune system , immunology , biology , chemokine , listeria , immunity , exacerbation , listeria infection , microbiology and biotechnology , bacteria , genetics
Summary: Experimental infection of mice with Listeria monocytogenes (L. monocytogenes) has served as an appropriate model for analyzing Thl nil driven immune responses. Generally, Th2 responses are absent and IL‐4 is not detectable. Here, we describe experimental settings under which IL‐4 is detectable in listeriosis. Our data suggest that IL‐4 is rapidly produced after infection. This prompt IL‐4 burst seems to stimulate chemokine responses and, therefore, may participate in the regulation of the early antilisterial host response. Soon thereafter, lL‐4 production wanes. At least partially this seems to be caused by downregulation of IL‐4–producing CD4+ NK1+ TCRαβ int lymphocytes by IL‐12. In the absence of IFN‐γ responsiveness, IL‐4 production is demonstrable during acquired immunity against L. monocytogenes, and this elevated IL‐4 production apparently contributes to disease exacerbation. In conclusion, the data are consistent with a detrimental role of IL‐4 in listeriosis and active control of IL‐4 synthesis by the antilisterial immune response. The rapid, but transient, IL‐4 burst in listeriosis probably contributes to host defense without impairing development of the acquired T‐cell response because of its shortness.