title: Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection.
abstract: C-type lectin receptors (CLRs) are diverse, trans-membrane proteins that function as pattern recognition receptors (PRRs) which are necessary for orchestrating immune responses against pathogens. CLRs have been shown to play a major role in recognition and protection against fungal pathogens. Dectin-3 (also known as MCL, Clecsf8, or Clec4d) is a myeloid cell-specific CLR that recognizes mycobacterial trehalose 6,6'-dimycolate (TDM) as well as α-mannans present in the cell wall of fungal pathogens. To date, a potential role for Dectin-3 in the mediation of protective immune responses against C. neoformans has yet to be determined. Consequently, we evaluated the impact of Dectin-3 deficiency on the development of protective immune responses against C. neoformans using an experimental murine model of pulmonary cryptococcosis. Dectin-3 deficiency did not lead to increased susceptibility of mice to experimental pulmonary C. neoformans infection. Also, no significant differences in pulmonary leukocyte recruitment and cytokine production were observed in Dectin-3 deficient mice compared to wild type infected mice. In addition, we observed no differences in uptake and anti-cryptococcal activity of Dectin-3 deficient dendritic cells and macrophages. Altogether, our studies show that Dectin-3 is dispensable for mediating protective immune responses against pulmonary C. neoformans infection.
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, TX, United States of America.|South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, San Antonio, TX, United States of America.
authors.forename: Althea
authors.initials: A
authors.lastname: Campuzano
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, TX, United States of America.|South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, San Antonio, TX, United States of America.
authors.forename: Natalia
authors.initials: N
authors.lastname: Castro-Lopez
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, TX, United States of America.
authors.forename: Karen L
authors.initials: KL
authors.lastname: Wozniak
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, TX, United States of America.|South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, San Antonio, TX, United States of America.
authors.forename: Chrissy M
authors.initials: CM
authors.lastname: Leopold Wager
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, TX, United States of America.|South Texas Center for Emerging Infectious Diseases, The University of Texas at San Antonio, San Antonio, TX, United States of America.
authors.forename: Floyd L
authors.initials: FL
authors.lastname: Wormley
mesh_terms: D000818:Animals; D003453:Cryptococcosis / Q000382:microbiology / Q000517:prevention & control*; D003455:Cryptococcus neoformans / Q000472:pathogenicity*; D016207:Cytokines / Q000378:metabolism; D005260:Female; D037181:Lectins, C-Type / Q000235:genetics / Q000502:physiology*; D008168:Lung / Q000378:metabolism; D008172:Lung Diseases, Fungal / Q000276:immunology; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D011971:Receptors, Immunologic / Q000235:genetics / Q000502:physiology*
chemical_list: C584161:Clec4d protein, mouse; D016207:Cytokines; D037181:Lectins, C-Type; D011971:Receptors, Immunologic