Immune system can protect host attacking from a variety of microorganism and virus through innate and adaptive immunities. The innate immune system can be activated by recognition of conserved carbohydrates on the cell surface of pathogen resulting in protection, immunity regulation and inflammation. Immunostimulating and anti-tumor ${eta}$-glucan, major cell wall component of many fungi, could be recognized as pathogen associated molecular pattern (PAMP) by C-type lectin such as pathogen recognition receptor (PRR) of host innate immunity cells. In spite of many studies of basidiomycetes ${eta}$-glucan on immunostimulation, little is known about the precise mechanism as molecular-level. Among C-type lectins, dectin-1 was cloned and reported as a ${eta}$-glucan receptor. In this report, we demonstrated induction of cytokine gene transcription by Ganoderma lucidum ${eta}$-glucan in the absence or presence of lipopolysaccharide (LPS) by RT-PCR analysis. The expression of murine dectin-1 (MD-1) on RAW264.7 macrophage by RT-PCR showing both the full length, 757 bp $(MD-1{alpha})$ and alternative spliced form, 620 bp $(MD-1{eta})$. Both $MD-1{alpha}$ and $MD-1{eta}$ mRNAs were induced by ${eta $-glucan both in the absence and presence of LPS. To explore expression of inflammatory cytokines by ${eta}$-glucan, RAW264.7 cells were treated with ${eta}$-glucan for 12 hours. As a result, the expressions of IL-1 IL-6, IL-l0 and $TNF-{alpha}$ were increased by ${eta}$-glucan treatment in a dose-dependent fashion. From these results, ${eta}$-glucan induced transcriptions of dectin-1 and immune activating cytokine genes, indicating induction of immune allertness by expressing dectin-1 and secreting inflammatory cytokines.