Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis-Reference-Cited by-同舟云学术

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

Published:2018-12 Issue:12 Volume:86 Page:
ISSN:0019-9567
Container-title:Infection and Immunity
language:en
Short-container-title:Infect Immun

Author:

Govender Melissa¹²³⁴^ORCID,Hurdayal Ramona¹²³⁵,Martinez-Salazar Berenice¹²³⁶,Gqada Kaya¹²³,Pillay Shandre¹²³,Gcanga Lorna¹²³,Passelli Katiuska⁶,Nieuwenhuizen Natalie E.¹²³⁷,Tacchini-Cottier Fabienne⁶,Guler Reto¹²³,Brombacher Frank¹²³

Affiliation:

1. International Center for Genetic Engineering and Biotechnology (ICGEB), Cape Town Component, Cape Town, South Africa

2. Institute of Infectious Diseases and Molecular Medicine (IDM), Department of Pathology, Division of Immunology, and South African Medical Research Council (SAMRC) on Immunology of Infectious Diseases, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa

3. Wellcome Center for Infectious Diseases Research in Africa, Institute of Infectious Diseases and Molecular Medicine (IDM), Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa

4. Department of Clinical and Experimental Medicine, Division of Molecular Virology, Linköping University, Linköping, Sweden

5. Department of Molecular and Cell Biology, University of Cape Town, Cape Town, South Africa

6. Department of Biochemistry, and WHO Immunology Research and Training Collaborative Center, University of Lausanne, Epalinges, Switzerland

7. Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany

Abstract

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.

Funder

Swiss National Science Foundation (SNF) and South African National Research Foundation

Swiss National Science Foundation

South African National Research Foundation

South African Research Chair Initiative

Department of Science and Technology (DST) of South Africa and NRF for the Swiss-South African Joint Research Programme

South African Medical Council

Department of Science and Technology (DST) of South Africa/South African National Research Foundation (NRF) Postgraduate Training Programme

Wellcome Trust CIDRI-Africa

Department of Science and Technology, Republic of South Africa

Publisher

American Society for Microbiology