The Toll-like receptors (TLRs) in mammals comprise a family of transmembrane proteins characterized by multiple copies of leucine rich repeats in the extracellular domain and an IL-1 receptor motif in the cytoplasmic domain. Like its counterparts in Drosophila, TLRs signal through adaptor molecules (1). The TLR family is a phylogenetically conserved mediator of innate immunity that is essential for microbial recognition (2). Ten human homologs of TLRs (TLR1-10) have been described (3). TLR2 is differentially expressed in human cells. TLR2 is expressed in tonsils, lymph nodes, and appendices, activated B-cells in germinal centers. CD14+ monocytes expressed the highest level of TLR2 followed by CD15+ granulocytes, and CD19+ B-cells, CD3+ T-cells, and CD56+ NK cells did not express TLR2. The expression of TLR2 in different cell types is regulated by different immune response modifiers. For example, LPS, GM-CSF, IL-1, and IL-10 up regulates TLR2 whereas IL-4, IFN-gamma, and TNF down regulate TLR2 expression in monocytes (4).