[1] Chang HT, Tsai PW, Huang HH, et al. LL37 and hBD-3 elevate the beta-1,3-exoglucanase activity of Candida albicans Xog1p, resulting in reduced fungal adhesion to plastic[J]. Biochem J, 2012, 441(3):963-970.
[2] Tsai PW, Yang CY, Chang HT, et al. Human antimicrobial peptide LL-37 inhibits adhesion of Candida albicans by interacting with yeast cell-wall carbohydrates[J]. PloS one, 2011, 6(3):e17755.
[3] Wong JH, Ng TB, Legowska A, et al. Antifungal action of human cathelicidin fragment (LL13-37) on Candida albicans[J]. Peptides, 2011, 32(10):1996-2002.
[4] Chairatana P, Chiang IL, Nolan EM. Human alpha-defensin 6 self-assembly prevents adhesion and suppresses virulence traits of Candida albicans[J]. Biochemistry, 2017, 56(8):1033-1041.
[5] Tomalka J, Azodi E, Narra HP, et al. beta-defensin 1 plays a role in acute mucosal defense against Candida albicans[J]. J Immunol, 2015, 194(4):1788-1795.
[6] Jarva M, Phan TK, Lay FT, et al. Human beta-defensin 2 kills Candida albicans through phosphatidylinositol 4,5-bisphosphate-mediated membrane permeabilization[J]. Sci Adv, 2018, 4(7):eaat0979.
[7] Kumar R, Chadha S, Saraswat D, et al. Histatin 5 uptake by Candida albicans utilizes polyamine transporters Dur3 and Dur31 proteins[J]. J Biol Chem, 2011, 286(51):43748-43758.
[8] Brauner A, Alvendal C, Chromek M, et al. Psoriasin, a novel anti-Candida albicans adhesin[J]. J Mol Med (Berl), 2018, 96(6):537-545.
[9] Ling Y, Cypowyj S, Aytekin C, et al. Inherited IL-17RC deficiency in patients with chronic mucocutaneous candidiasis[J]. J Exp Med, 2015, 212(5):619-631.
[10] Boisson B, Wang C, Pedergnana V, et al. An ACT1 mutation selectively abolishes interleukin-17 responses in humans with chronic mucocutaneous candidiasis[J]. Immunity, 2013, 39(4):676-686.
[11] Conti HR, Peterson AC, Brane L, et al. Oral-resident natural Th17 cells and gammadelta T cells control opportunistic Candida albicans infections[J]. J Exp Med, 2014, 211(10):2075-2084.
[12] Verma AH, Richardson JP, Zhou C, et al. Oral epithelial cells orchestrate innate type 17 responses to Candida albicans through the virulence factor candidalysin[J]. Sci Immunol, 2017, 2(17):eaam8834.
[13] Pietrella D, Rachini A, Pines M, et al. Th17 cells and IL-17 in protective immunity to vaginal candidiasis[J]. PloS one, 2011, 6(7):e22770.
[14] Yano J, Kolls JK, Happel KI, et al. The acute neutrophil response mediated by S100 alarmins during vaginal Candida infections is independent of the Th17-pathway[J]. PloS one, 2012, 7(9):e46311.
[15] Moyes DL, Wilson D, Richardson JP, et al. Candidalysin is a fungal peptide toxin critical for mucosal infection[J]. Nature, 2016, 532(7597):64.
[16] Zhu W, Phan QT, Boontheung P, et al. EGFR and HER2 receptor kinase signaling mediate epithelial cell invasion by Candida albicans during oropharyngeal infection[J]. Proc Natl Acad Sci U S A., 2012, 109(35):14194-14199.
[17] Swidergall M, Solis NV, Lionakis MS, et al. EphA2 is an epithelial cell pattern recognition receptor for fungal β-glucans[J]. Nat Microbiol, 2018, 3(1):53-61.
[18] Netea MG, Brown GD, Kullberg BJ, et al. An integrated model of the recognition of Candida albicans by the innate immune system[J]. Nat Rev Microbiol, 2008, 6(1):67-78.
[19] Branzk N, Lubojemska A, Hardison SE, et al. Neutrophils sense microbe size and selectively release neutrophil extracellular traps in response to large pathogens[J]. Nat Immunol, 2014, 15(11):1017-1025.
[20] Urban CF, Ermert D, Schmid M, et al. Neutrophil extracellular traps contain calprotectin, a cytosolic protein complex involved in host defense against Candida albicans[J]. PLoS Pathog, 2009, 5(10):e1000639.
[21] Hopke A, Nicke N, Hidu EE, et al. Neutrophil attack triggers extracellular trap-dependent Candida cell wall remodeling and altered immune recognition[J]. PLoS Pathog, 2016, 12(5):e1005644.
[22] Ermert D, Niemiec MJ, Rohm M, et al. Candida albicans escapes from mouse neutrophils[J]. J Leukoc Biol, 2013, 94(2):223-236.
[23] Wellington M, Koselny K, Sutterwala FS, et al. Candida albicans triggers NLRP3-mediated pyroptosis in macrophages[J]. Eukaryot Cell, 2014, 13(2):329-340.
[24] Krysan DJ, Sutterwala FS, Wellington M. Catching fire:Candida albicans, macrophages, and pyroptosis[J]. PLoS Pathog, 2014, 10(6):e1004139.
[25] Zhao X, Guo Y, Jiang C, et al. JNK1 negatively controls antifungal innate immunity by suppressing CD23 expression[J]. Nat Med, 2017, 23(3):337-346.
[26] Vylkova S, Lorenz MC. Modulation of phagosomal pH by Candida albicans promotes hyphal morphogenesis and requires Stp2p, a regulator of amino acid transport[J]. PLoS Pathog, 2014, 10(3):e1003995.
[27] Uwamahoro N, Verma-Gaur J, Shen HH, et al. The pathogen Candida albicans hijacks pyroptosis for escape from macrophages[J]. Mbio, 2014, 5(2):00003-00014.
[28] Cua DJ, Tato CM. Innate IL-17-producing cells:the sentinels of the immune system[J]. Nat Rev Immunol, 2010, 10(7):479-489.
[29] Gladiator A, Wangler N, Trautwein-Weidner K, et al. Cutting edge:IL-17-secreting innate lymphoid cells are essential for host defense against fungal infection[J]. J Immunol, 2013, 190(2):521-525.
[30] Kashem SW, Riedl MS, Yao C, et al. Nociceptive sensory fibers drive interleukin-23 production from CD301b(+) dermal dendritic cells and drive protective cutaneous immunity[J]. Immunity, 2015, 43(3):515-526.
[31] Taylor PR, Roy S, Leal SM Jr, et al. Activation of neutrophils by autocrine IL-17A-IL-17RC interactions during fungal infection is regulated by IL-6, IL-23, RORgammat and dectin-2[J]. Nat Immunol, 2014, 15(2):143-151.
[32] Huppler AR, Verma AH, Conti HR, et al. Neutrophils do not express IL-17A in the context of acute oropharyngeal candidiasis[J]. Pathogens, 2015, 4(3):559-572.
[33] Tamassia N, Arruda-Silva F, Calzetti F, et al. A reappraisal on the potential ability of human neutrophils to express and produce IL-17 family members in vitro:failure to reproducibly detect it[J]. Front Immunol, 2018, 9:795.