Our observations corroborate a previous report, showing that TLR-2-deficient mice had enhanced resistance to L. braziliensis infection, but MyD88-deficient mice were susceptible to the infection [6]. In experimental Trypanosoma cruzi infection, the parasite load and mortality in wild-type or TLR-2-deficient mice on a C57BL/6 background were comparable, suggesting that TLR-2 might not play a role in T. cruzi infection [24]. Similarly, the L. major parasite loads in TLR-2-deficient mice on a Leishmania-resistant C57BL/6 background were comparable

to wild-type mice (data not shown). However, the addition of TLR-2 deficiency to TLR-9-deficient mice resulted in a higher parasite load and less survival compared to TLR-9 deficiency alone [24].

Taken Selleck AG-14699 together, these observations suggest that in susceptible hosts, the inhibitory or suppressive roles of TLR-2 in protozoan infections are clearly visible, whereas on an already resistant background the enhanced resistance due to lifting of the inhibitory functions of TLR-2 is not expressly apparent. Thus, although these two protozoan parasites are related closely, their interactions with the host cells with different genetic make-up can result in differences in parasite load and T cell responses. learn more In conclusion, as anti-TLR-2 antibody prevented the LPG-modulated expression of TLR-9 and enhanced

TLR-9-ligand-induced host protection significantly in a susceptible mouse strain, it is possible that TLR-2 modulates the anti-leishmanial immune response through altered expression of Sitaxentan TLR-9. Although observed in the context of L. major infection, this regulatory role of TLR-2 appears to have broader implications in other infections. The work is supported by the Department of Biotechnology, New Delhi (BT/PR/3288/BRB/10/966/2011). None. “
“Chronic asthma is an inflammatory disease of the airway wall that leads to bronchial smooth muscle hyperreactivity and airway obstruction, caused by inflammation, goblet cell metaplasia, and airway wall remodeling. In response to allergen presentation by airway DCs, T-helper lymphocytes of the adaptive immune system control many aspects of the disease through secretion of IL-4, IL-5, IL-13, IL-17, and IL-22, and these are counterbalanced by cytokines produced by Treg cells. Many cells of the innate immune system such as mast cells, basophils, neutrophils, eosinophils, and innate lymphoid cells also play an important role in disease pathogenesis.