functional members of the TLR family have been described in humans so far. Studies have been conducted on TLR11 as well, and it has been shown that it recognizes flagellin and profilin-like proteins in mice. Nonetheless, TLR11 is only a pseudogene in humans without direct function or functional protein expression. Each of the TLR has been shown to interact with a specific PAMP. TLR signaling TLRs tend to dimerize, TLR4 forms homodimers, and TLR6 can dimerize with either TLR1 or TLR2. Interaction of TLRs with their specific PAMP is mediated through either MyD88- dependent pathway and triggers the signaling through NF-κB and the MAP kinase pathway and therefore the secretion of pro-inflammatory cytokines and co-stimulatory molecules or TRIF - dependent signaling pathway. MyD88 - dependent pathway is induced by various PAMPs stimulating the TLRs on macrophages and dendritic cells. MyD88 attracts the IRAK4 molecule, IRAK4 recruits IRAK1 and IRAK2 to form a signaling complex. The signaling complex reacts with TRAF6 which leads to TAK1 activation and consequently the induction of inflammatory cytokines. The TRIF-dependent pathway is induced by macrophages and DCs after TLR3 and TLR4 stimulation. Molecules released following TLR activation signal to other cells of the immune system making TLRs key elements of innate immunity and adaptive immunity. C-type lectin receptors (CLR) Many different cells of the innate immune system express a myriad of CLRs which shape innate immunity by virtue of their pattern recognition ability. Even though, most classes of human pathogens are covered by CLRs, CLRs are a major receptor for recognition of fungi: nonetheless, other PAMPs have been identified in studies as targets of CLRs as well e.g. mannose is the recognition motif for many viruses, fungi and mycobacteria; similarly fucose presents the same for certain bacteria and helminths; and glucans are present on mycobacteria and fungi. In addition, many of acquired nonself surfaces e.g. carcinoembryonic/oncofetal type neoantigens carrying "internal danger source"/"self turned nonself" type pathogen pattern are also identified and destroyed (e.g. by complement fixation or other cytotoxic attacks) or sequestered (phagocytosed or ensheathed) by the immune system by virtue of the CLRs. The name lectin is a bit misleading because the family includes proteins with at least one C-type lectin domain (CTLD) which is a specific type of carbohydrate recognition domain. CTLD is a ligand binding motif found in more than 1000 known proteins (more than 100 in humans) and the ligands are often