[1] Goughenour KD, Rappleye CA. Antifungal therapeutics for dimorphic fungal pathogens[J]. Virulence,2017,8(2):211-221. [2] Emma C, Niño-Vega GA. Paracoccidioides spp.:virulence factors and immune-evasion strategies[J]. Mediators Inflamm, 2017, 2017:1-19. [3] Fernandes CM, Goldman GH, Del Poeta M, et al. Biological roles played by sphingolipids in dimorphic and filamentous fungi[J]. mBio, 2018, 9(3):e00642-18. [4] Cleare LG, Zamith-Miranda D, Nosanchuk JD. Heat shock proteins in Histoplasma and Paracoccidioides[J]. 2017, 24(11):e00221-17-e00221-17. [5] Viriyakosol S, Walls L, Okamoto S, et al. Myeloid differentiation factor 88 and interleukin-1R1 signaling contribute to resistance to Coccidioides immitis[J]. Infect Immun,2018,86(6):e00028-18. [6] Kirkland TN, Fierer J.Coccidioides immitis and posadasii; A review of their biology, genomics, pathogenesis, and host immunity[J]. Virulence, 2018, 9(1):1426-1435. [7] McBride JA, Gauthier GM, Klein BS. Turning on virulence:Mechanisms that underpin the morphologic transition and pathogenicity of Blastomyces[J]. Virulence,2019,10(1):801-809. [8] Zhang Z, Hou B, Wu Y Z, et al. Two component histidine kinase DRK1 is required for pathogenesis in Sporothrix schenckii[J]. Mol Med Rep, 2017, 17(1):721-728. [9] Martinez R. New trends in Paracoccidioidomycosis epidemiology[J]. J Fungi (Basel), 2017,3(1):1. [10] Singulani JL, Scorzoni L, de Oliveira HC, et al. Applications of invertebrate animal models to dimorphic fungal infections[J]. J Fungi (Basel),2018,4(4):118. [11] Thind SK, Taborda CP, Nosanchuk JD. Dendritic cell interactions with Histoplasma and Paracoccidioides[J]. Virulence,2015,6(5):424-32. [12] Kauffman CA, Miceli MH. Histoplasmosis and blastomycosis in solid organ transplant recipients[J]. J Fungi (Basel), 2015;1(2):94-106. [13] Muñoz JF, Mcewen JG, Clay OK, et al. Genome analysis reveals evolutionary mechanisms of adaptation in systemic dimorphic fungi[J]. Sci Rep, 2018, 8(1):4473. [14] Susanna L, Chi-Ching T, Patrick W.Talaromyces marneffei genomic, transcriptomic, proteomic and metabolomic studies reveal mechanisms for environmental adaptations and virulence[J]. Toxins, 2017, 9(6):192. [15] Kujoth GC, Sullivan TD, Merkhofer R, et al. CRISPR/Cas9-mediated gene disruption reveals the importance of zinc metabolism for fitness of the dimorphic fungal pathogen Blastomyces dermatitidis[J]. mBio, 2018, 9(2):e00412-18. [16] Tamayo D, Muñoz JF, Almeida AJ, et al.Paracoccidioides spp. catalases and their role in antioxidant defense against host defense responses[J]. Fungal Genet Biol, 2017,100:22-32. [17] Woo P, Lau S, Lau C, et al. Mp1p is a virulence factor inTalaromyces (Penicillium) marneffei[J]. PLoS Negl Trop Dis, 2016, 10(8):e0004907. [18] Lorenzini J, Fites J S, Nett J, et al. Blastomyces dermatitidis\, serine protease dipeptidyl peptidase IVA (DppIVA) cleaves ELR\, +\, CXC chemokines altering their effects on neutrophils[J]. Cell Microbiol, 2017,19(9):10.1111/cmi.12741. [19] Mills CD. M1 and M2 macrophages:oracles of health and disease[J]. Crit Rev Immunol, 2012, 32(6):463-488. [20] Dai X, Mao C, Lan X, et al. Acute Penicillium marneffei infection stimulates host M1/M2a macrophages polarization in BALB/C mice[J]. BMC Microbiol, 2017, 17(1):177. [21] Mosser DM. The many faces of macrophage activation[J]. J Leukoc Biol, 2003, 73(2):209. |