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Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis
Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine. Linköping University, Faculty of Medicine and Health Sciences. ICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa.
ICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa.
ICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Lausanne, Switzerland; Univ Lausanne, Switzerland.
ICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa.
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2018 (English)In: Infection and Immunity, ISSN 0019-9567, E-ISSN 1098-5522, Vol. 86, no 12, article id e00710-18Article in journal (Refereed) Published
Abstract [en]

The skin microenvironment at the site of infection plays a role in the early events that determine protective T helper 1/type 1 immune responses during cutaneous leishmaniasis (CL) infection. During CL in nonhealing BALB/c mice, early interleukin-4 (IL-4) can instruct dendritic cells for protective Th1 immunity. Additionally, keratinocytes, which are the principal cell type in the skin epidermis, have been shown to secrete IL-4 early after Leishmania major infection. Here, we investigated whether IL-4/1L-13 signaling via the common IL-4 receptor alpha chain (IL-4R alpha) on keratinocytes contributes to susceptibility during experimental CL. To address this, keratinocyte-specific IL-41R alpha-deficient (KRT14(cre) IL-4R alpha(-/lox)) mice on a BALB/c genetic background were generated by gene targeting and site-specific recombination (Cre/loxP) under the control of the keratinocyte-specific krt14 locus. Following high-dose infection with L. major IL-81 and LV39 promastigotes subcutaneously in the footpad, footpad swelling, parasite burden, IFN-gamma/IL-4/IL-13 cytokine production, and type 1 and type 2 antibody responses were similar between KRT14(cre) IL-4R alpha(-)(lox) and littermate control IL-4R alpha(-) (lox) BALB/c mice. An intradermal infection with low-dose L. major IL-81 and LV39 promastigotes in the ear showed results in infected KRT14(cre) IL-4R alpha(-)(/)(lox) BALB/c mice similar to those of littermate control IL-4R alpha(-)(/)(lox) BALB/c mice, with the exception of a significant decrease observed in parasite burden only at the site of LV39 infection in the ear. Collectively, our results show that autocrine and paracrine signaling of IL-4/1L-13 through the IL-4R alpha chain on keratinocytes does not influence the establishment of a nonhealing Th2 immune response in BALB/c mice during L. major infection.

Place, publisher, year, edition, pages
AMER SOC MICROBIOLOGY , 2018. Vol. 86, no 12, article id e00710-18
Keywords [en]
IL-4 receptor alpha signaling; keratinocytes; Leishmania major; skin
National Category
Immunology
Identifiers
URN: urn:nbn:se:liu:diva-153366DOI: 10.1128/IAI.00710-18ISI: 000450630200019PubMedID: 30275010OAI: oai:DiVA.org:liu-153366DiVA, id: diva2:1271833
Note

Funding Agencies|Swiss National Science Foundation (SNF); South African National Research Foundation (NRF); SNF [3100030_166651/1]; NRF; Department of Science and Technology; South African Research Chair Initiative (SARCHi); South Africa Medical Research Council (SAMRC); Department of Science and Technology (DST)/NRF for the Swiss-South African Joint Research Program (SSAJRP) [UID 87399]; DST/NRF postgraduate training program [UID 92532]; Wellcome Trust CIDRI-Africa [203135Z/16/Z]; National Research Foundation; Oppenheimer Memorial Trust; University of Cape Town; South African Association of Women Graduates; [IZLSZU3_14906]

Available from: 2018-12-18 Created: 2018-12-18 Last updated: 2018-12-18

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