Introduction: Adult human bone marrow-derived mesenchymal stem cells (hMSCs) are as therapeutic delivery agents that assist in the repair of damaged tissues. To achieve the desired clinical outcomes for this strategy requires a better understanding of the mechanisms that drive the recruitment, migration and engraftment of hMSCs to the targeted tissues. It is known that hMSCs are recruited to sites of stress or inflammation to fulfill their repair function. It is recognized that toll-like receptors (TLRs) mediate stress responses of other bone marrow-derived cells. Toll-like receptors (TLRs) are a conserved family of receptors that recognize pathogen-associated molecular patterns and promote the activation of immune cells. Nowadays, several TLR (numbered 1−11) have been identified in humans. Initially, research on TLRs focused on their expression and signaling consequences in immune cells. However, recent reports indicate that other bone marrow-derived cells including mesenchymal stem/progenitor cells (MSCs) are among the cells that express TLR proteins. These cells specifically home to damaged and inflammed tissues and triggers the induction of cytokines, chemokines and other TLR-regulated genes. Objective: Human MSCs (hMSCs) are very attractive candidates in stem cell-based strategies for tissue repair and gene therapy and TLRs within hMSCs leads to the activation of established TLR signaling pathways. Interestingly, these activated pathways mediate the secretion of discrete patterns of cytokines and chemokines depending on the TLR-ligand employed, since these receptors in the immune modulating function established for hMSCs. Furthermore, recent reports concerning adult adipose tissue-derived, mesenchymal, and hematopoietic stem cells suggest that TLRs play a role in stem cell biology and are expressed in human mesenchymal stem cells (hMSCs). Conclusions: because that TLRs, specially TLR3 stimulation within hMSCs triggers their enhanced migration. Thus, TLR-stimulation may be one mechanism that specifically drives the recruitment, migration and immune modulating function of the hMSCs at injured or stressed sites. These observations determined that TLR stimulation within hMSCs may be one critical mechanism that specifically drives their stress responses and to play an important role in the therapeutic efficacy of MSCs in injured tissues. Future prospectives: Along with establishing a new aspect of their biology, the identification of TLRs as critical mediators of stress responses within hMSCs also provides a novel target to exploit in the improvement of stem cell-based therapeutic strategies.

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