Hancing the Th1 response via stimulation of DCs with IFN and co-stimulatory molecules through C. pneumoniae infection. Chlamydia muridarum may be the mouse model for Chlamydia trachomatis infection, a sexually transmitted infection which can cause critical damage for the female reproductive tract. The outcomes from two current research indicate this organism has an antigen for iNKT cells [21, 22], even though its structure is unknown. Also, infected epithelial cells degrade CD1d, suggestive of an immune evasion mechanism [23]. In spite of this, there isn’t any consensus on the function of iNKT cells inside the host response to C. muridarum, 1 report suggesting that iNKT cells improve the growth of this organism by inducing a Th2 cytokine milieu [19], when other studies recommend iNKT cells can promote clearance of bacteria, but additionally immune pathology [22]. iNKT cells might also play a role in stopping stroke-associated bacterial infection. In comparison to WT mice, CD1dKO mice were very susceptible to bacterial infection soon after transient midcerebral artery occlusion induced brain injury, a rodent model of stroke [24]. Protective liver iNKT cell function was suppressed by noradrenergic neurotransmitter(s) immediately after stroke. Blockade of this innervation offered protection from bacterial infection in WT mice but not in CD1dKO mice [24]. In addition, activation of iNKT cells with alCer induced inflammatory cytokine production and prevented bacterial infections immediately after stroke.Formula of 1260663-68-0 These information suggest that stroke-associated bacterial infections may be induced by suppression of iNKT cell function.Fungal infectionsiNKT cells happen to be shown to play an essential part in host defense against several fungal infections. For instance, following pulmonary infection with Cryptococus neoformans, iNKT cells accumulated inside the lungs, which was dependent on the C-C motif chemokine-2 (CCL-2)/macrophage chemoattractant protein-1 (MCP-1) within the early phase of infection [25]. The Th1 response that’s critical for C. neoformans elimination was lowered in J?8KO mice resulting in delayed clearance of C. neoformans. It was also shown that CD1dKO mice manage Aspergillus fumigatus infection poorly [26]. iNKT cells developed IFN activated by a mixture of self-antigen recognition and IL-12 from antigenJ Infect Chemother. Author manuscript; obtainable in PMC 2014 August 01.Kinjo et al.Pagepresenting cells (APCs). Production of IL-12 by APCs was induced by means of recognition of fungal cell wall -1,3 glucans by Dectin-1, a C-type lectin receptor that binds this glycan.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptProtozoan parasite infectionsiNKT cells also participate in immune response against some protozoan parasites.725728-43-8 web For instance, J?8KO mice showed improved parasite burden in skin lesions and draining lymph nodes following subcutaneous infection with Leishmania key, a reason for sand flytransmitted Leishmaniasis that ranges from cutaneous lesions to visceral infection.PMID:23614016 Decreased cytokine production, NK cell cytotoxicity and elevated splenic parasite burden had been observed in J?8KO mice following intravenous infection, suggesting that iNKT cells play significant roles in host defense against L. key [27, 28]. In addition, CD1dKO mice have been also shown to be extra susceptible to L. donovani infection [29]. iNKT cells are also involved in regulating excessive inflammation triggered by parasite infection. J?8KO mice created severe inflammation in numerous organs, such as spleen, liver and mu.
