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dc.contributor.authorMakala, Levi HC
dc.date.accessioned2012-10-26T16:29:36Z
dc.date.available2012-10-26T16:29:36Z
dc.date.issued2012-01-9en_US
dc.identifier.citationJ Biomed Sci. 2012 Jan 9; 19(1):5en_US
dc.identifier.issn1423-0127en_US
dc.identifier.pmid22230608en_US
dc.identifier.doi10.1186/1423-0127-19-5en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/700
dc.description.abstractPathogen persistence in immune-competent hosts represents an immunological paradox. Increasing evidence suggests that some pathogens, such as, Leishmania major (L. major) have evolved strategies and mechanisms that actively suppress host adaptive immunity. If this notion is correct conventional vaccination therapies may be ineffective in enhancing host immunity, unless natural processes that suppress host immunity are also targeted therapeutically. The key problem is that the basis of pathogen persistence in immune-competent individuals is unknown, despite decades of intense research. This fact, coupled with poor health care and a dearth of effective treatments means that these diseases will remain a scourge on humans unless a better understanding of why the immune system tolerates such infections emerges from research. Indoleamine 2,3-dioxygenase (IDO) has been shown to act as a molecular switch regulating host responses, and IDO inhibitor drugs shown to possess potential in enhancing host immunity to established leishmania infections. It is hoped that this review will help stimulate and help generate critical new knowledge pertaining to the IDO mechanism and how to exploit it to suppress T cell mediated immunity, thus offer an innovative approach to studying the basis of chronic leishmania infection in mice.
dc.rightsCopyright ©2012 Makala; licensee BioMed Central Ltd.en_US
dc.subjectReviewen_US
dc.subject.meshAnimalsen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDendritic Cellsen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshHost-Parasite Interactionsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunity, Cellularen_US
dc.subject.meshIndoleamine-Pyrrole 2,3,-Dioxygenaseen_US
dc.subject.meshLeishmania majoren_US
dc.subject.meshLeishmaniasisen_US
dc.subject.meshMiceen_US
dc.subject.meshT-Lymphocytes, Regulatoryen_US
dc.titleThe role of indoleamine 2, 3 dioxygenase in regulating host immunity to leishmania infectionen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3295648en_US
dc.contributor.corporatenameDepartment of Pediatrics
refterms.dateFOA2019-04-10T00:37:27Z
html.description.abstractPathogen persistence in immune-competent hosts represents an immunological paradox. Increasing evidence suggests that some pathogens, such as, Leishmania major (L. major) have evolved strategies and mechanisms that actively suppress host adaptive immunity. If this notion is correct conventional vaccination therapies may be ineffective in enhancing host immunity, unless natural processes that suppress host immunity are also targeted therapeutically. The key problem is that the basis of pathogen persistence in immune-competent individuals is unknown, despite decades of intense research. This fact, coupled with poor health care and a dearth of effective treatments means that these diseases will remain a scourge on humans unless a better understanding of why the immune system tolerates such infections emerges from research. Indoleamine 2,3-dioxygenase (IDO) has been shown to act as a molecular switch regulating host responses, and IDO inhibitor drugs shown to possess potential in enhancing host immunity to established leishmania infections. It is hoped that this review will help stimulate and help generate critical new knowledge pertaining to the IDO mechanism and how to exploit it to suppress T cell mediated immunity, thus offer an innovative approach to studying the basis of chronic leishmania infection in mice.


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