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Статті в журналах з теми "Interleukin-12":
Дисертації з теми "Interleukin-12":
Interleukin-12 (IL-12) is a key cytokine in the development of a protective cellular Th1 immune response. It consists of a p40 and a p35 subunit. Following stimulation with IL-12, NK and T cells produce large amounts of IFN-gamma resulting in a type 1 immune response. The p40 subunit of IL-12 is also part of other biologically active proteins such as monomeric or homodimeric p40 or the heterodimeric IL-23 (in combination with a p19 subunit). While in this study the homodimeric p40 appears to antagonize IL-12, IL-23 was demonstrated to have agonistic effects. The aim of this study was to investigate p40-dependent effects which can be observed independently of IL-12, i.e. potential effects mediated by IL-23. For the experiments mutant mice were used so that IL-12 dependent mechanisms could not play a role but only p40-dependent proteins excluding IL-12. In a Salmonella Enteritidis infection model p35-gene deleted (p35-/-) and p40-/- mice were used. As the expression of p40 is induced by bacterial antigen, differences between the strains were caused by the p40 protein. During the infection p40 proteins induced IFN-gamma production thus improving the killing of intracellular pathogens. This resulted in a better control of the systemic infection and longer survival periods of the p35-/- mice as compared to p40-/- mice. For the experiments in the tumor model using the Lewis-Lung carcinoma and the Melanoma B16 as tumors, p35/40-/- mice which are unable to produce any p40 proteins, received gene therapy with DNA encoding for p40. This local gene therapy resulted in a reduced tumor growth. Immunohistochemical examination revealed an infiltration of the tumor tissue with macrophages and a reduced neoangiogenesis within the tumor. This effect could not be achieved by local administration of IL-23 or the p40-homodimer as a protein, indicating the existence of an as yet unknown heterodimeric p40 protein. In vitro experiments showed that IL-23 induces IFN-gamma production by splenocytes and this effect can be antagonized by the homodimer. Interestingly, IL-23 is also able to antagonize IL-12 in primary splenocyte cultures. In vitro infection with Salmonella resulted in an p40-dependent IFN-gamma production that could also be antagonized by the homodimer. The protective effects in the infection model might be caused by IL-23, which is supported by the in vitro results. On the other hand, in the tumor model IL-23 does not seem to be the player and it must be concluded that the protective effects are caused by an other as yet unknown p40-dependent protein p40-x
To analyse the role of interleukin-12p75 (IL-12p75) and interleukin-12p40 (IL-12p40) in the defence against Cryptococcus neoformans (C. neoformans) a murine infection model was established and studied. Mice of wild-tpye 129Sv/Ev background as well as IL-12p35-/- and IL-12p35/p40-/- 129Sv/Ev mice were infected intraperitoneally or intranasally with C. neoformans. The differences between the immune response of these genotypes were analysed. Comparing wild-type and IL-12p35-/--mice allows for conclusions related to the importance of IL-12p75, comparing IL-12p40-producing IL-12p35-/- mice with IL-12p35/p40-/- mice shows the importance of IL-12p40. Fungal organ burden, serum antigen levels, inflammatory cell responses, and antibody production were examined. The fungal organ load in wild-type mice was smaller than in both mutant IL-12-/--mice. In wild-type mice fewer cryptococci were found in organs and less cryptococcal antigen in serum than in IL-12p35-/- and IL-12p35/p40-/- mice. This underlines the importance of IL 12p75 for the control of the infection with C. neoformans. In addition, IL-12p40 was found to have a similar but weaker role as IL-12p75 in protection against C. neoformans. In the absence of IL-12p40 IL-12p35/p40-/- mice developed higher antigen titers than IL-12p35-/- and wild-type mice. The host response against infection with C. neoformans is associated with granuloma formation. Recruitment of inflammatory cells to granulomas was altered in the absence of IL 12p75. In addition, IL-12p40 contributed significantly to granuloma formation since IL 12p35/p40-/- mice developed no or only very poor granulomatous responses. Therefore, IL 12p40 is required for inflammatory cell responses. IL-12p40 was also found to be required for antibody production against C. neoformans. Infected IL-12p35/p40-/--mice had only very low levels of specific antibodies against C. neoformans. IL-12p75 is known to be essential for protective Th1 response against intracellular microorganisms. Th1 responses are commonly associated with the production of IgG2a. Infected wild-type mice produced 2-fold higher IgG2a levels than IL-12p35-/--mice. To adapt the infection model more to the natural infection mode the intraperitoneal infection route was changed to an intranasal route. Following intranasal infection IL-12p75 also proved to be necessary for control of the fungal organ load. Interestingly the organ load was higher in IL-12p35-/--mice than in IL-12p35/p40-/-mice which suggest a role of IL-12p40 in cell recruitment. Following intranasal application of cryptococci fungal dissemination to spleen and brain was reduced as compared to the intraperitoneal infection route. Without IL-12p75 dissemination of C. neoformans to the brain occured. This shows that IL-12p75 is involved in control of dissemination from lung to brain. The inflammatory response of IL-12p35-/--mice was stronger than the tissue response of wild-type mice. The massive tissue reactions of IL-12p35-/--mice caused big areas of diffuse cellular infiltration in their lungs. In IL-12p35/p40-/--mice inflammatory responses could be observed only in the peribronchial tissue. This shows that IL-12p40 is not only needed for a cellular inflammatory response following intraperitoneal but also following intranasal infection. Following intranasal infection IL-12p40 can induce immunopathological effects. Intranasal infection of mice with C. neoformans resulted in five to ten times higher antibody responses than intraperitoneal infection. This suggests that intranasal infection of mice results in a more Th2-biased humoral response. In summary, these experiments show that besides IL-12p75 also IL-12p40 contributes to cellular immunity against C. neoformans. The immunostimulatory properties of both, IL 12p75 and IL-12p40, can be observed after intraperitoneal and intranasal infection routes with similar but also distinct manifestations
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