Expression of Mouse Interleukin-4 by a Recombinant Ectromelia Virus Suppresses Cytolytic Lymphocyte Responses and Overcomes Genetic Resistance to Mousepox

Jackson, Ron; Ramsay, Alistair J.; Christensen, Carina D.; Beaton, Sandra; Hall, Diana; Ramshaw, Ian A.

doi:10.1128/jvi.75.3.1205-1210.2001

Cited by 491 publications

(293 citation statements)

References 46 publications

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“…Indeed, infection of C57BL͞6 mice with recombinant ECTV encoding IL-4 was shown to enhance virus replication and transformed an inapparent infection to full-blown mousepox (33). This report is consistent with our findings, which has established that the susceptible phenotype of BALB͞c and A͞J mice is associated with a type 2 cytokine response, with little or no IFN-␥.…”

Section: Discussionsupporting

confidence: 92%

Polarized type 1 cytokine response and cell-mediated immunity determine genetic resistance to mousepox

Chaudhri

Panchanathan

Buller

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

168

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Section: Discussionsupporting

confidence: 92%

Polarized type 1 cytokine response and cell-mediated immunity determine genetic resistance to mousepox

Chaudhri

Panchanathan

Buller

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

168

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“…Previous studies reported that IFN-γ production from murine NK cells cultured in the presence of IL-4 was not detected (9). IL-4 exposure also suppressed the cytotoxic capacity of NK cells in both in vitro and in vivo models (10,11). However, in contrast to those findings, IL-4 was suggested to induce IFN-γ production by NK cells.…”

mentioning

confidence: 62%

NK cells activated by Interleukin-4 in cooperation with Interleukin-15 exhibit distinctive characteristics

Kiniwa

Enomoto

Terazawa

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Natural killer (NK) cells are known to be activated by Th1-type cytokines, such as IL-2, -12, or -18, and they secrete a large amount of IFN-γ that accelerates Th1-type responses. However, the roles of NK cells in Th2-type responses have remained unclear. Because IL-4 acts as an initiator of Th2-type responses, we examined the characteristics of NK cells in mice overexpressing IL-4. In this study, we report that IL-4 overexpression induces distinctive characteristics of NK cells (B220 high /CD11b low /IL-18Rα low ), which are different from mature conventional NK (cNK) cells (B220 low /CD11b high /IL-18Rα high ). IL-4 overexpression induces proliferation of tissue-resident macrophages, which contributes to NK cell proliferation via production of IL-15. These IL-4-induced NK cells (IL4-NK cells) produce higher levels of IFN-γ, IL-10, and GM-CSF, and exhibit high cytotoxicity compared with cNK cells.

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“…For instance, IL-4 has been shown to be essential for the development of a protective anti-malaria CD8 T cell response (22), whereas other studies show that the CD8-mediated protection against viruses or tumors was impaired by IL-4 (23,24). However, the nature of the genes and underlying effector functions regulated by IL-4 in CD8 T cells remain unknown.…”

mentioning

confidence: 99%

Negative Regulation of NKG2D Expression by IL-4 in Memory CD8 T Cells

Ventre

Brinza

Schicklin

et al. 2012

The Journal of Immunology

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IL-4 is one of the main cytokines produced during Th2-inducing pathologies. This cytokine has been shown to affect a number of immune processes such as Th differentiation and innate immune responses. However, the impact of IL-4 on CD8 T cell responses remains unclear. In this study, we analyzed the effects of IL-4 on global gene expression profiles of Ag-induced memory CD8 T cells in the mouse. Gene ontology analysis of this signature revealed that IL-4 regulated most importantly genes associated with immune responses. Moreover, this IL-4 signature overlapped with the set of genes preferentially expressed by memory CD8 T cells over naive CD8 T cells. In particular, IL-4 downregulated in vitro and in vivo in a STAT6-dependent manner the memory-specific expression of NKG2D, thereby increasing the activation threshold of memory CD8 T cells. Furthermore, IL-4 impaired activation of memory cells as well as their differentiation into effector cells. This phenomenon could have an important clinical relevance as patients affected by Th2 pathologies such as parasitic infections or atopic dermatitis often suffer from viral-induced complications possibly linked to inefficient CD8 T cell responses.

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Expression of Mouse Interleukin-4 by a Recombinant Ectromelia Virus Suppresses Cytolytic Lymphocyte Responses and Overcomes Genetic Resistance to Mousepox

Abstract: Genetic resistance to clinical mousepox (ectromelia virus) varies among inbred laboratory mice and is

Cited by 491 publications

References 46 publications

Polarized type 1 cytokine response and cell-mediated immunity determine genetic resistance to mousepox

Polarized type 1 cytokine response and cell-mediated immunity determine genetic resistance to mousepox

NK cells activated by Interleukin-4 in cooperation with Interleukin-15 exhibit distinctive characteristics

Negative Regulation of NKG2D Expression by IL-4 in Memory CD8 T Cells

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