β-1→3-D-glucans occur as a principal component of microbial cell walls or can be secreted from both, non-pathogenic and pathogenic fungi such as S. cerevisae and C. albicans [1]. These β-1→3-D-linked glucose polymers are characterized as a fungal pathogen-associated molecular pattern (PAMP) [2]. The primary cellular recognition of β-1→3-D-glucans is mediated by several β-1→3-D-glucan receptors on phagocytes [3,4] and other cells [5,6]. Human as well as murine Dectin-1 has been demonstrated to be the major pattern recognition receptor (PRR) for intact yeast and β-1→3-D-glucan-containing particles (i.e. zymosan) on monocytes/macrophages as well as neutrophils and on primary cells [7-11]. In the murine system, binding of zymosan to Dectin-1 resulted in production of TNFα through Toll-like receptor 2 and the adaptor protein MyD88 [12]. Another water-soluble β-1→3-D-glucan (PGG-glucan) has been described to activate NFκB and NFIL-6 in murine cell lines [13,14]. Similarly, it has been shown that β-1→3-D-glucans activate NFκB in a human monocyte-like cell line [15] and in human polymorphonuclear neutrophils (PMN), in the latter case without secretion of pro-inflammatory cytokines (IL-1, IL-6, TNFα) [16]. One study proposed that the production of the anti-inflammatory IL-1RA, but not IL-1 by human monocytes may be a potentially protective mechanism induced by β-1→3-D-glucan [17]. Three other investigations have reported that human leukocytes and human vascular endothelial cells produce IL-8 in response to zymosan [18] or a water-soluble β-1→3-D-glucan [6,19].