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  • Govender, MelissaLinköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Medicinska fakulteten,ICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)

Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis

  • Article/chapterEnglish2018

Publisher, publication year, extent ...

  • AMER SOC MICROBIOLOGY,2018
  • printrdacarrier

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  • LIBRIS-ID:oai:DiVA.org:liu-153366
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-153366URI
  • https://doi.org/10.1128/IAI.00710-18DOI

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  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • 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]
  • 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.

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  • Hurdayal, RamonaICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)
  • Martinez-Salazar, BereniceICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Lausanne, Switzerland; Univ Lausanne, Switzerland (author)
  • Gqada, KayaICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)
  • Pillay, ShandreICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)
  • Gcanga, LornaICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)
  • Passelli, KatiuskaUniv Lausanne, Switzerland; Univ Lausanne, Switzerland (author)
  • Nieuwenhuizen, Natalie E.ICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Max Planck Inst Infect Biol, Germany (author)
  • Tacchini-Cottier, FabienneUniv Lausanne, Switzerland (author)
  • Guler, RetoICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)
  • Brombacher, FrankICGEB, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa; Univ Cape Town, South Africa (author)
  • Linköpings universitetAvdelningen för mikrobiologi och molekylär medicin (creator_code:org_t)

Related titles

  • In:Infection and Immunity: AMER SOC MICROBIOLOGY86:120019-95671098-5522

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