J Interferon Cytokine Res. 2016 Apr;36(4):267-76. doi: 10.1089/jir.2015.0040. Epub 2016 Jan 27.
Ifrim, DC; Quintin, J; Courjol, F; Verschueren, I; van Krieken, JH; Koentgen, F; Fradin, C; Gow, NA; Joosten, LA; van der Meer, JW; van de Veerkonk, F; Netea, MG
Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands; Inserm U995, Lille, France; Université de Lille, Faculté de Médecine, Lille, France; Ozgene Pty Ltd, Bentley, WA, Australia; Institute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom.
Despite the fact that Candida albicans is an important human fungal pathogen and Dectin-2 is a major pattern recognition receptor for fungi, our knowledge regarding the role of Dectin-2 for the host defense against disseminated candidiasis is limited. Dectin-2 deficient (Dectin-2(-/-)) mice were more susceptible to systemic candidiasis, and the susceptibility was mirrored by an elevated fungal load in the kidneys that correlated with the presence of large inflammatory foci. Phagocytosis of Candida by the macrophages lacking the Dectin-2 receptor was moderately decreased, while production of most of the macrophage-derived cytokines from Dectin-2(-/-) mice with systemic candidiasis was decreased. No striking differences among several Candida mutants defective in mannans could be detected between naïve wild-type and Dectin-2(-/-) mice, apart from the β-mannan-deficient bmt1Δ/bmt2Δ/bmt5Δ triple mutant, suggesting that β-mannan may partially mask α-mannan detection, which is the major fungal structure recognized by Dectin-2. Deciphering the mechanisms responsible for host defense against the majority of C. albicans strains represents an important step in understanding the pathophysiology of systemic candidiasis, which might lead to the development of novel immunotherapeutic strategies.
The team at Ozgene has over two decades of experience creating customised knockout and knock-in mice for pivotal medical research globally. Over 400 scientific publications are based on research using Ozgene mice.