Treatment of candidiasis: insights from host genetics

References

• Gammelsrud KW, Sandven P, Høiby EA, Sandvik L, Brandtzaeg P, Gaustad P. Colonization by Candida in children with cancer, children with cystic fibrosis, and healthy controls. Clin. Microbiol. Infect. 17(12), 1875–1881 (2011).
   PubMed Web of Science ®Google Scholar
• Darwazeh AM, Hammad MM, Al-Jamaei AA. The relationship between oral hygiene and oral colonization with Candida species in healthy adult subjects. Int. J. Dent. Hyg. 8(2), 128–133 (2010).
   PubMedGoogle Scholar
• Yang YL, Leaw SN, Wang AH, Chen HT, Cheng WT, Lo HJ. Characterization of yeasts colonizing in healthy individuals. Med. Mycol. 49(1), 103–106 (2011).
   PubMed Web of Science ®Google Scholar
• Tortorano AM, Peman J, Bernhardt H et al.; ECMM Working Group on Candidaemia. Epidemiology of candidaemia in Europe: results of 28-month European Confederation of Medical Mycology (ECMM) hospital-based surveillance study. Eur. J. Clin. Microbiol. Infect. Dis. 23(4), 317–322 (2004).
   PubMed Web of Science ®Google Scholar
• Pappas PG, Rex JH, Lee J et al.; NIAID Mycoses Study Group. A prospective observational study of candidemia: epidemiology, therapy, and influences on mortality in hospitalized adult and pediatric patients. Clin. Infect. Dis. 37(5), 634–643 (2003).
   PubMed Web of Science ®Google Scholar
• Viscoli C, Girmenia C, Marinus A et al. Candidemia in cancer patients: a prospective, multicenter surveillance study by the Invasive Fungal Infection Group (IFIG) of the European Organization for Research and Treatment of Cancer (EORTC). Clin. Infect. Dis. 28(5), 1071–1079 (1999).
   PubMed Web of Science ®Google Scholar
• Wisplinghoff H, Bischoff T, Tallent SM, Seifert H, Wenzel RP, Edmond MB. Nosocomial bloodstream infections in US hospitals: analysis of 24,179 cases from a prospective nationwide surveillance study. Clin. Infect. Dis. 39(3), 309–317 (2004).
   PubMed Web of Science ®Google Scholar
• Gudlaugsson O, Gillespie S, Lee K et al. Attributable mortality of nosocomial candidemia, revisited. Clin. Infect. Dis. 37(9), 1172–1177 (2003).
   PubMed Web of Science ®Google Scholar
• Alonso-Valle H, Acha O, García-Palomo JD, Fariñas-Alvarez C, Fernández-Mazarrasa C, Fariñas MC. Candidemia in a tertiary care hospital: epidemiology and factors influencing mortality. Eur. J. Clin. Microbiol. Infect. Dis. 22(4), 254–257 (2003).
   PubMedGoogle Scholar
• Andes DR, Safdar N, Baddley JW et al.; Mycoses Study Group. Impact of treatment strategy on outcomes in patients with candidemia and other forms of invasive candidiasis: a patient-level quantitative review of randomized trials. Clin. Infect. Dis. 54(8), 1110–1122 (2012).
   PubMed Web of Science ®Google Scholar
• Romani L. Immunity to fungal infections. Nat. Rev. Immunol. 11(4), 275–288 (2011).
   PubMed Web of Science ®Google Scholar
• Gow NA, van de Veerdonk FL, Brown AJ, Netea MG. Candida albicans morphogenesis and host defence: discriminating invasion from colonization. Nat. Rev. Microbiol. 10(2), 112–122 (2012).
   PubMed Web of Science ®Google Scholar
• Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell 124(4), 783–801 (2006).
   PubMed Web of Science ®Google Scholar
• Netea MG, Van Der Graaf CA, Vonk AG, Verschueren I, Van Der Meer JW, Kullberg BJ. The role of Toll-like receptor (TLR) 2 and TLR4 in the host defense against disseminated candidiasis. J. Infect. Dis. 185(10), 1483–1489 (2002).
   PubMed Web of Science ®Google Scholar
• Netea MG, Brown GD, Kullberg BJ, Gow NA. An integrated model of the recognition of Candida albicans by the innate immune system. Nat. Rev. Microbiol. 6(1), 67–78 (2008).
   PubMed Web of Science ®Google Scholar
• Van der Graaf CA, Netea MG, Morré SA et al. Toll-like receptor 4 Asp299Gly/Thr399Ile polymorphisms are a risk factor for Candida bloodstream infection. Eur. Cytokine Netw. 17(1), 29–34 (2006).
   PubMedGoogle Scholar
• Woehrle T, Du W, Goetz A et al. Pathogen specific cytokine release reveals an effect of TLR2 Arg753Gln during Candida sepsis in humans. Cytokine 41(3), 322–329 (2008).
   PubMed Web of Science ®Google Scholar
• Plantinga TS, Johnson MD, Scott WK et al. Toll-like receptor 1 polymorphisms increase susceptibility to candidemia. J.Infect. Dis. 205(6), 934–943 (2012).
   PubMed Web of Science ®Google Scholar
• Gow NA, Netea MG, Munro CA et al. Immune recognition of Candida albicans beta-glucan by dectin-1. J. Infect. Dis. 196(10), 1565–1571 (2007).
   PubMed Web of Science ®Google Scholar
• Wells CA, Salvage-Jones JA, Li X et al. The macrophage-inducible C-type lectin, mincle, is an essential component of the innate immune response to Candida albicans. J. Immunol. 180(11), 7404–7413 (2008).
   PubMed Web of Science ®Google Scholar
• Robinson MJ, Osorio F, Rosas M et al. Dectin-2 is a Syk-coupled pattern recognition receptor crucial for Th17 responses to fungal infection. J. Exp. Med. 206(9), 2037–2051 (2009).
   PubMed Web of Science ®Google Scholar
• Ferwerda G, Meyer-Wentrup F, Kullberg BJ, Netea MG, Adema GJ. Dectin-1 synergizes with TLR2 and TLR4 for cytokine production in human primary monocytes and macrophages. Cell. Microbiol. 10(10), 2058–2066 (2008).
   PubMed Web of Science ®Google Scholar
• LeibundGut-Landmann S, Gross O, Robinson MJ et al. Syk- and CARD9-dependent coupling of innate immunity to the induction of T-helper cells that produce interleukin 17. Nat. Immunol. 8(6), 630–638 (2007).
   PubMed Web of Science ®Google Scholar
• Gringhuis SI, den Dunnen J, Litjens M et al. Dectin-1 directs T-helper cell differentiation by controlling noncanonical NF-kappaB activation through Raf-1 and Syk. Nat. Immunol. 10(2), 203–213 (2009).
   PubMed Web of Science ®Google Scholar
• Ferwerda B, Ferwerda G, Plantinga TS et al. Human dectin-1 deficiency and mucocutaneous fungal infections. N. Engl. J. Med. 361(18), 1760–1767 (2009).
   PubMed Web of Science ®Google Scholar
• Plantinga TS, van der Velden WJ, Ferwerda B et al. Early stop polymorphism in human DECTIN-1 is associated with increased Candida colonization in hematopoietic stem cell transplant recipients. Clin. Infect. Dis. 49(5), 724–732 (2009).
   PubMed Web of Science ®Google Scholar
• Rosentul DC, Plantinga TS, Oosting M et al. Genetic variation in the dectin-1/CARD9 recognition pathway and susceptibility to candidemia. J. Infect. Dis. 204(7), 1138–1145 (2011).
   PubMed Web of Science ®Google Scholar
• Brouwer N, Dolman KM, van Houdt M, Sta M, Roos D, Kuijpers TW. Mannose-binding lectin (MBL) facilitates opsonophagocytosis of yeasts but not of bacteria despite MBL binding. J. Immunol. 180(6), 4124–4132 (2008).
   PubMed Web of Science ®Google Scholar
• Kozel TR, Weinhold LC, Lupan DM. Distinct characteristics of initiation of the classical and alternative complement pathways by Candida albicans. Infect. Immun. 64(8), 3360–3368 (1996).
   PubMed Web of Science ®Google Scholar
• Minchinton RM, Dean MM, Clark TR, Heatley S, Mullighan CG. Analysis of the relationship between mannose-binding lectin (MBL) genotype, MBL levels and function in an Australian blood donor population. Scand. J. Immunol. 56(6), 630–641 (2002).
   PubMed Web of Science ®Google Scholar
• Babovic-Vuksanovic D, Snow K, Ten RM. Mannose-binding lectin (MBL) deficiency. Variant alleles in a midwestern population of the United States. Ann. Allergy Asthma Immunol. 82(2), 134–138, 141; quiz 142 (1999).
   PubMed Web of Science ®Google Scholar
• Lipscombe RJ, Sumiya M, Summerfield JA, Turner MW. Distinct physicochemical characteristics of human mannose binding protein expressed by individuals of differing genotype. Immunology 85(4), 660–667 (1995).
   PubMed Web of Science ®Google Scholar
• Garred P, Thiel S, Madsen HO, Ryder LP, Jensenius JC, Svejgaard A. Gene frequency and partial protein characterization of an allelic variant of mannan binding protein associated with low serum concentrations. Clin. Exp. Immunol. 90(3), 517–521 (1992).
   PubMed Web of Science ®Google Scholar
• Madsen HO, Satz ML, Hogh B, Svejgaard A, Garred P. Different molecular events result in low protein levels of mannan-binding lectin in populations from southeast Africa and South America. J.Immunol. 161(6), 3169–3175 (1998).
   PubMed Web of Science ®Google Scholar
• Babula O, Lazdane G, Kroica J, Ledger WJ, Witkin SS. Relation between recurrent vulvovaginal candidiasis, vaginal concentrations of mannose-binding lectin, and a mannose-binding lectin gene polymorphism in Latvian women. Clin. Infect. Dis. 37(5), 733–737 (2003).
   PubMed Web of Science ®Google Scholar
• Giraldo PC, Babula O, Gonçalves AK et al. Mannose-binding lectin gene polymorphism, vulvovaginal candidiasis, and bacterial vaginosis. Obstet. Gynecol. 109(5), 1123–1128 (2007).
   PubMed Web of Science ®Google Scholar
• Donders GG, Babula O, Bellen G, Linhares IM, Witkin SS. Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis. BJOG 115(10), 1225–1231 (2008).
   PubMed Web of Science ®Google Scholar
• Liu F, Liao Q, Liu Z. Mannose-binding lectin and vulvovaginal candidiasis. Int. J. Gynaecol. Obstet. 92(1), 43–47 (2006).
   PubMed Web of Science ®Google Scholar
• Valdimarsson H, Stefansson M, Vikingsdottir T et al. Reconstitution of opsonizing activity by infusion of mannan-binding lectin (MBL) to MBL-deficient humans. Scand. J. Immunol. 48(2), 116–123 (1998).
   PubMed Web of Science ®Google Scholar
• Valdimarsson H, Vikingsdottir T, Bang P et al. Human plasma-derived mannose-binding lectin: a Phase I safety and pharmacokinetic study. Scand. J. Immunol. 59(1), 97–102 (2004).
   PubMed Web of Science ®Google Scholar
• Petersen KA, Matthiesen F, Agger T et al. Phase I safety, tolerability, and pharmacokinetic study of recombinant human mannan-binding lectin. J. Clin. Immunol. 26(5), 465–475 (2006).
   PubMed Web of Science ®Google Scholar
• Brouwer N, Frakking FN, van de Wetering MD et al. Mannose-binding lectin (MBL) substitution: recovery of opsonic function in vivo lags behind MBL serum levels. J.Immunol. 183(5), 3496–3504 (2009).
   PubMed Web of Science ®Google Scholar
• Frakking FN, Brouwer N, van de Wetering MD et al. Safety and pharmacokinetics of plasma-derived mannose-binding lectin (MBL) substitution in children with chemotherapy-induced neutropaenia. Eur. J. Cancer 45(4), 505–512 (2009).
   PubMedGoogle Scholar
• Glocker EO, Hennigs A, Nabavi M et al. A homozygous CARD9 mutation in a family with susceptibility to fungal infections. N.Engl. J. Med. 361(18), 1727–1735 (2009).
   PubMed Web of Science ®Google Scholar
• Gross O, Gewies A, Finger K et al. Card9 controls a non-TLR signalling pathway for innate anti-fungal immunity. Nature 442(7103), 651–656 (2006).
   PubMed Web of Science ®Google Scholar
• Le Bourhis L, Benko S, Girardin SE. Nod1 and Nod2 in innate immunity and human inflammatory disorders. Biochem. Soc. Trans. 35(Pt 6), 1479–1484 (2007).
   PubMedGoogle Scholar
• van der Graaf CA, Netea MG, Franke B, Girardin SE, van der Meer JW, Kullberg BJ. Nucleotide oligomerization domain 2 (Nod2) is not involved in the pattern recognition of Candida albicans. Clin. Vaccine Immunol. 13(3), 423–425 (2006).
   PubMedGoogle Scholar
• Hise AG, Tomalka J, Ganesan S et al. Anessential role for the NLRP3 inflammasome in host defense against the human fungal pathogen Candida albicans. Cell Host Microbe 5(5), 487–497 (2009).
   PubMed Web of Science ®Google Scholar
• Van De Veerdonk FL, Joosten LA, Devesa I et al. Bypassing pathogen-induced inflammasome activation for the regulation of interleukin-1β production by the fungal pathogen Candida albicans. J. Infect. Dis. 199(7), 1087–1096 (2009).
   PubMedGoogle Scholar
• Sutterwala FS, Ogura Y, Zamboni DS, Roy CR, Flavell RA. NALP3: a key player in caspase-1 activation. J. Endotoxin Res. 12(4), 251–256 (2006).
   PubMedGoogle Scholar
• Hoffman HM, Mueller JL, Broide DH, Wanderer AA, Kolodner RD. Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle–Wells syndrome. Nat. Genet. 29(3), 301–305 (2001).
   PubMed Web of Science ®Google Scholar
• Omi T, Kumada M, Kamesaki T et al. An intronic variable number of tandem repeat polymorphisms of the cold-induced autoinflammatory syndrome 1 (CIAS1) gene modifies gene expression and is associated with essential hypertension. Eur. J. Hum. Genet. 14(12), 1295–1305 (2006).
   PubMed Web of Science ®Google Scholar
• Lev-Sagie A, Prus D, Linhares IM, Lavy Y, Ledger WJ, Witkin SS. Polymorphism in a gene coding for the inflammasome component NALP3 and recurrent vulvovaginal candidiasis in women with vulvar vestibulitis syndrome. Am. J. Obstet. Gynecol. 200(3), 303.e1–303.e6 (2009).
   Web of Science ®Google Scholar
• Essner R, Rhoades K, McBride WH, Morton DL, Economou JS. IL-4 down-regulates IL-1 and TNF gene expression in human monocytes. J. Immunol. 142(11), 3857–3861 (1989).
   PubMed Web of Science ®Google Scholar
• Rosenwasser LJ, Klemm DJ, Dresback JK et al. Promoter polymorphisms in the chromosome 5 gene cluster in asthma and atopy. Clin. Exp. Allergy 25(Suppl. 2), 74–78; discussion 95 (1995).
   PubMed Web of Science ®Google Scholar
• Babula O, Lazdane G, Kroica J, Linhares IM, Ledger WJ, Witkin SS. Frequency of interleukin-4 (IL-4) -589 gene polymorphism and vaginal concentrations of IL-4, nitric oxide, and mannose-binding lectin in women with recurrent vulvovaginal candidiasis. Clin. Infect. Dis. 40(9), 1258–1262 (2005).
   PubMed Web of Science ®Google Scholar
• Johnson MD, Plantinga TS, van de Vosse E et al. Cytokine gene polymorphisms and the outcome of invasive candidiasis: a prospective cohort study. Clin. Infect. Dis. 54(4), 502–510 (2012).
   PubMed Web of Science ®Google Scholar
• Romani L, Mencacci A, Grohmann U et al. Neutralizing antibody to interleukin 4 induces systemic protection and T-helper type 1-associated immunity in murine candidiasis. J. Exp. Med. 176(1), 19–25 (1992).
   PubMed Web of Science ®Google Scholar
• Romani L, Puccetti P, Mencacci A et al. Neutralization of IL-10 up-regulates nitric oxide production and protects susceptible mice from challenge with Candida albicans. J. Immunol. 152(7), 3514–3521 (1994).
   PubMed Web of Science ®Google Scholar
• Heino M, Peterson P, Kudoh J et al.; Finnish–German APECED Consortium. An autoimmune disease, APECED, caused by mutations in a novel gene featuring two PHD-type zinc-finger domains. Nat. Genet. 17(4), 399–403 (1997).
   PubMedGoogle Scholar
• Ahonen P, Myllärniemi S, Sipilä I, Perheentupa J. Clinical variation of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) in a series of 68 patients. N.Engl. J. Med. 322(26), 1829–1836 (1990).
   PubMed Web of Science ®Google Scholar
• Kisand K, Bøe Wolff AS, Podkrajsek KT et al. Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines. J. Exp. Med. 207(2), 299–308 (2010).
   PubMed Web of Science ®Google Scholar
• Puel A, Döffinger R, Natividad A et al. Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I. J. Exp. Med. 207(2), 291–297 (2010).
   PubMed Web of Science ®Google Scholar
• Van De Veerdonk FL, Plantinga TS, Hoischen A et al. STAT1 mutations in autosomal dominant chronic mucocutaneous candidiasis. N. Engl. J. Med. 365(1), 54–61 (2011).
   PubMedGoogle Scholar
• Liu L, Okada S, Kong XF et al. Gain-of-function human STAT1 mutations impair IL-17 immunity and underlie chronic mucocutaneous candidiasis. J. Exp. Med. 208(8), 1635–1648 (2011).
   PubMed Web of Science ®Google Scholar
• Smeekens SP, Plantinga TS, van de Veerdonk FL et al. STAT1 hyperphosphorylation and defective IL12R/IL23R signaling underlie defective immunity in autosomal dominant chronic mucocutaneous candidiasis. PLoS ONE 6(12), e29248 (2011).
   PubMed Web of Science ®Google Scholar
• Davis SD, Schaller J, Wedgwood RJ. Job’s Syndrome. Recurrent, “cold”, staphylococcal abscesses. Lancet 1(7445), 1013–1015 (1966).
   PubMed Web of Science ®Google Scholar
• Holland SM, DeLeo FR, Elloumi HZ et al. STAT3 mutations in the hyper-IgE syndrome. N. Engl. J. Med. 357(16), 1608–1619 (2007).
   PubMed Web of Science ®Google Scholar
• Minegishi Y, Saito M, Tsuchiya S et al. Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome. Nature 448(7157), 1058–1062 (2007).
   PubMed Web of Science ®Google Scholar
• Engelhardt KR, McGhee S, Winkler S et al. Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal recessive form of hyper-IgE syndrome. J. Allergy Clin. Immunol. 124(6), 1289–302.e4 (2009).
   PubMed Web of Science ®Google Scholar
• Minegishi Y, Saito M, Morio T et al. Human tyrosine kinase 2 deficiency reveals its requisite roles in multiple cytokine signals involved in innate and acquired immunity. Immunity 25(5), 745–755 (2006).
   PubMed Web of Science ®Google Scholar
• de Beaucoudrey L, Puel A, Filipe-Santos O et al. Mutations in STAT3 and IL12RB1 impair the development of human IL-17-producing T cells. J. Exp. Med. 205(7), 1543–1550 (2008).
   PubMedGoogle Scholar
• Ma CS, Chew GY, Simpson N et al. Deficiency of Th17 cells in hyper IgE syndrome due to mutations in STAT3. J.Exp. Med. 205(7), 1551–1557 (2008).
   PubMed Web of Science ®Google Scholar
• Milner JD, Brenchley JM, Laurence A et al. Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome. Nature 452(7188), 773–776 (2008).
   PubMed Web of Science ®Google Scholar
• Coffman RL, Carty J. A T-cell activity that enhances polyclonal IgE production and its inhibition by interferon-γ. J. Immunol. 136(3), 949–954 (1986).
   PubMed Web of Science ®Google Scholar
• Pène J, Rousset F, Brière F et al. IgE production by normal human lymphocytes is induced by interleukin 4 and suppressed by interferons γ and α and prostaglandin E2. Proc. Natl Acad. Sci. USA 85(18), 6880–6884 (1988).
   PubMed Web of Science ®Google Scholar
• King CL, Gallin JI, Malech HL, Abramson SL, Nutman TB. Regulation of immunoglobulin production in hyperimmunoglobulin E recurrent-infection syndrome by interferon γ. Proc. Natl Acad. Sci. USA 86(24), 10085–10089 (1989).
   PubMed Web of Science ®Google Scholar
• Jeppson JD, Jaffe HS, Hill HR. Use of recombinant human interferon γ to enhance neutrophil chemotactic responses in Job syndrome of hyperimmunoglobulinemia E and recurrent infections. J. Pediatr. 118(3), 383–387 (1991).
   PubMedGoogle Scholar
• Segal BH, DeCarlo ES, Kwon-Chung KJ, Malech HL, Gallin JI, Holland SM. Aspergillus nidulans infection in chronic granulomatous disease. Medicine (Baltimore) 77(5), 345–354 (1998).
   PubMed Web of Science ®Google Scholar
• Winkelstein JA, Marino MC, Johnston RB Jr et al. Chronic granulomatous disease. Report on a national registry of 368 patients. Medicine (Baltimore) 79(3), 155–169 (2000).
   PubMed Web of Science ®Google Scholar
• Matute JD, Arias AA, Wright NA et al. Anew genetic subgroup of chronic granulomatous disease with autosomal recessive mutations in p40 phox and selective defects in neutrophil NADPH oxidase activity. Blood 114(15), 3309–3315 (2009).
   PubMed Web of Science ®Google Scholar
• Gallin JI, Alling DW, Malech HL et al. Itraconazole to prevent fungal infections in chronic granulomatous disease. N. Engl. J. Med. 348(24), 2416–2422 (2003).
   PubMed Web of Science ®Google Scholar
• Condino-Neto A, Newburger PE. Interferon-γ improves splicing efficiency of CYBB gene transcripts in an interferon-responsive variant of chronic granulomatous disease due to a splice site consensus region mutation. Blood 95(11), 3548–3554 (2000).
   PubMed Web of Science ®Google Scholar
• Ishibashi F, Mizukami T, Kanegasaki S et al. Improved superoxide-generating ability by interferon γ due to splicing pattern change of transcripts in neutrophils from patients with a splice site mutation in CYBB gene. Blood 98(2), 436–441 (2001).
   PubMed Web of Science ®Google Scholar
• Group TICGDCS. A controlled trial of interferon γ to prevent infection in chronic granulomatous disease. N. Engl. J. Med. 324(8), 509–516 (1991).
   PubMed Web of Science ®Google Scholar
• Seger RA. Hematopoietic stem cell transplantation for chronic granulomatous disease. Immunol. Allergy Clin. North Am. 30(2), 195–208 (2010).
   PubMedGoogle Scholar
• Ott MG, Seger R, Stein S, Siler U, Hoelzer D, Grez M. Advances in the treatment of chronic granulomatous disease by gene therapy. Curr. Gene Ther. 7(3), 155–161 (2007).
   PubMed Web of Science ®Google Scholar
• Kang EM, Choi U, Theobald N et al. Retrovirus gene therapy for X-linked chronic granulomatous disease can achieve stable long-term correction of oxidase activity in peripheral blood neutrophils. Blood 115(4), 783–791 (2010).
   PubMed Web of Science ®Google Scholar
• Stein S, Ott MG, Schultze-Strasser S et al. Genomic instability and myelodysplasia with monosomy 7 consequent to EVI1 activation after gene therapy for chronic granulomatous disease. Nat. Med. 16(2), 198–204 (2010).
   PubMed Web of Science ®Google Scholar
• Riddell LA, Pinching AJ, Hill S et al. APhase III study of recombinant human interferon γ to prevent opportunistic infections in advanced HIV disease. AIDS Res. Hum. Retroviruses 17(9), 789–797 (2001).
   PubMed Web of Science ®Google Scholar
• Baltch AL, Bopp LH, Smith RP, Ritz WJ, Carlyn CJ, Michelsen PB. Effects of voriconazole, granulocyte–macrophage colony-stimulating factor, and interferon γ on intracellular fluconazole-resistant Candida glabrata and Candida krusei in human monocyte-derived macrophages. Diagn. Microbiol. Infect. Dis. 52(4), 299–304 (2005).
   PubMed Web of Science ®Google Scholar
• Dignani MC, Rex JH, Chan KW et al. Immunomodulation with interferon-γ and colony-stimulating factors for refractory fungal infections in patients with leukemia. Cancer 104(1), 199–204 (2005).
   PubMed Web of Science ®Google Scholar
• Poynton CH, Barnes RA, Rees J. Interferon γ and granulocyte–macrophage colony-stimulating factor for the treatment of hepatosplenic candidosis in patients with acute leukemia. Clin. Infect. Dis. 26(1), 239–240 (1998).
   PubMed Web of Science ®Google Scholar
• Bodasing N, Seaton RA, Shankland GS, Pithie A. γ-interferon treatment for resistant oropharyngeal candidiasis in an HIV-positive patient. J. Antimicrob. Chemother. 50(5), 765–766 (2002).
   PubMed Web of Science ®Google Scholar
• Gadish M, Kletter Y, Flidel O, Nagler A, Slavin S, Fabian I. Effects of recombinant human granulocyte and granulocyte–macrophage colony-stimulating factors on neutrophil function following autologous bone marrow transplantation. Leuk. Res. 15(12), 1175–1182 (1991).
   PubMed Web of Science ®Google Scholar
• Vazquez JA, Gupta S, Villanueva A. Potential utility of recombinant human GM-CSF as adjunctive treatment of refractory oropharyngeal candidiasis in AIDS patients. Eur. J. Clin. Microbiol. Infect. Dis. 17(11), 781–783 (1998).
   PubMed Web of Science ®Google Scholar
• Rókusz L, Liptay L, Kádár K. Successful treatment of chronic disseminated candidiasis with fluconazole and a granulocyte–macrophage colony-stimulating factor combination. Scand. J. Infect. Dis. 33(10), 784–786 (2001).
   PubMed Web of Science ®Google Scholar
• Roilides E, Holmes A, Blake C, Pizzo PA, Walsh TJ. Effects of granulocyte colony-stimulating factor and interferon-γ on antifungal activity of human polymorphonuclear neutrophils against pseudohyphae of different medically important Candida species. J. Leukoc. Biol. 57(4), 651–656 (1995).
   PubMed Web of Science ®Google Scholar
• Kullberg Bj VK, Herbrecht R, Jacobs F, Aoun M, Kujath P. A double-blind, randomized, placebo-controlled Phase II study of filgrastim (recombinant granulocyte colony-stimulating factor) incombination with fluconazole for treatment of invasive candidiasis and candidemia in nonneutropenic patients. Presented at: The 38th Interscience Conference on Antimicrobial Agents and Chemotherapy. San Diego, CA, USA, 24–27 September (1998) (abstract no. J-100).
   Google Scholar