IL-4 mediated resistance of BALB/c mice to visceral Leishmaniasis is independent of IL-4R$α$ signaling via T cells

IL-4 mediated resistance of BALB/c mice to visceral Leishmaniasis is independent of IL-4R$α$ signaling via T cells. McFarlane, E., Mokgethi, T., Kaye, P. M, Hurdayal, R., Brombacher, F., Alexander, J., & Carter, K. C Frontiers in Immunology, 10:1957, Frontiers, aug, 2019.

Paper doi abstract bibtex

Previous studies infecting global IL-4R-/-, IL-4-/- and IL-13-/- mice on a BALB/c background with the visceralising parasite Leishmania donovani have shown that the T helper 2 cytokines, IL-4 and IL-13, play influential but not completely overlapping roles in controlling primary infection. Subsequently, using macrophage/neutrophil-specific IL-4R deficient BALB/c mice, we demonstrated that macrophage/neutrophil unresponsiveness to IL-4 and IL-13 did not have a detrimental effect during L. donovani infection. Here we expand on these findings and show that CD4+ T cell-(Lckcre), as well as pan T cell-(iLckcre) specific IL-4R deficient mice on a BALB/c background, unlike global IL-4R deficient mice are also not adversely affected in terms of resistance to primary infection with L. donovani. Our analysis suggested only a transient and tissue specific impact on disease course due to lack of IL4R on T cells, limited to a reduced hepatic parasite burden at day 30 post infection. Consequently, the protective role(s) demonstrated for IL-4 and IL-13 during L. donovani infection are mediated by IL-4R-responsive cell(s) other than macrophages, neutrophils and T cells.

@article{McFarlane2019,
abstract = {Previous studies infecting global IL-4R-/-, IL-4-/- and IL-13-/- mice on a BALB/c background with the visceralising parasite Leishmania donovani have shown that the T helper 2 cytokines, IL-4 and IL-13, play influential but not completely overlapping roles in controlling primary infection. Subsequently, using macrophage/neutrophil-specific IL-4R deficient BALB/c mice, we demonstrated that macrophage/neutrophil unresponsiveness to IL-4 and IL-13 did not have a detrimental effect during L. donovani infection. Here we expand on these findings and show that CD4+ T cell-(Lckcre), as well as pan T cell-(iLckcre) specific IL-4R deficient mice on a BALB/c background, unlike global IL-4R deficient mice are also not adversely affected in terms of resistance to primary infection with L. donovani. Our analysis suggested only a transient and tissue specific impact on disease course due to lack of IL4R on T cells, limited to a reduced hepatic parasite burden at day 30 post infection. Consequently, the protective role(s) demonstrated for IL-4 and IL-13 during L. donovani infection are mediated by IL-4R-responsive cell(s) other than macrophages, neutrophils and T cells.},
author = {McFarlane, Emma and Mokgethi, Thabang and Kaye, Paul M and Hurdayal, Ramona and Brombacher, Frank and Alexander, James and Carter, Katharine C},
doi = {10.3389/fimmu.2019.01957},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/McFarlane et al. - 2019 - IL-4 mediated resistance of BALBc mice to visceral Leishmaniasis is independent of IL-4R$\alpha$ signaling via T cell.pdf:pdf},
journal = {Frontiers in Immunology},
keywords = {OA,fund{\_}not{\_}ack,original},
mendeley-tags = {OA,fund{\_}not{\_}ack,original},
month = {aug},
pages = {1957},
pmid = {31475014},
publisher = {Frontiers},
title = {{IL-4 mediated resistance of BALB/c mice to visceral Leishmaniasis is independent of IL-4R$\alpha$ signaling via T cells}},
url = {https://www.frontiersin.org/article/10.3389/fimmu.2019.01957/full},
volume = {10},
year = {2019}
}

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