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https://www.arca.fiocruz.br/handle/icict/10906
IL-23 PROVIDES A LIMITED MECHANISM OF RESISTANCE TO ACUTE TOXOPLASMOSIS IN THE ABSENCE OF IL-12.
Toxoplasmose Animal/imunologia
Doença Aguda
Animais
Células Cultivadas/imunologia
Células Dendríticas/metabolismo
Dimerização
Feminino
Imunidade Inata
Interferon gama/biossíntese
Interleucina-12/deficiência
Subunidade p35 da Interleucina-12
Interleucinas/uso terapêutico
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Subunidades Proteicas/deficiência
Células Th1/imunologia
Toxoplasma/imunologia
Toxoplasmose Animal/quimioterapia
Author
Affilliation
University of Pennsylvania. School of Veterinary Medicine. Department of Pathobiology. Philadelphia, PA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
DNAX Research Institute. Discovery Research. Palo Alto, CA
DNAX Research Institute. Discovery Research. Palo Alto, CA
DNAX Research Institute. Discovery Research. Palo Alto, CA
DNAX Research Institute. Discovery Research. Palo Alto, CA
University of Pennsylvania. School of Veterinary Medicine. Department of Pathobiology. Philadelphia, PA
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
DNAX Research Institute. Discovery Research. Palo Alto, CA
DNAX Research Institute. Discovery Research. Palo Alto, CA
DNAX Research Institute. Discovery Research. Palo Alto, CA
DNAX Research Institute. Discovery Research. Palo Alto, CA
University of Pennsylvania. School of Veterinary Medicine. Department of Pathobiology. Philadelphia, PA
Abstract
IL-23 and IL-12 are heterodimeric cytokines which share the p40 subunit, but which have unique second subunits, IL-23p19 and
IL-12p35. Since p40 is required for the development of the Th1 type response necessary for resistance to Toxoplasma gondii,
studies were performed to assess the role of IL-23 in resistance to this pathogen. Increased levels of IL-23 were detected in mice
infected with T. gondii and in vitro stimulation of dendritic cells with this pathogen resulted in increased levels of mRNA for this
cytokine. To address the role of IL-23 in resistance to T. gondii, mice lacking the p40 subunit (common to IL-12 and IL-23) and
mice that lack IL-12 p35 (specific for IL-12) were infected and their responses were compared. These studies revealed that p40 /
mice rapidly succumbed to toxoplasmosis, while p35 / mice displayed enhanced resistance though they eventually succumbed to
this infection. In addition, the administration of IL-23 to p40 / mice infected with T. gondii resulted in a decreased parasite
burden and enhanced resistance. However, the enhanced resistance of p35 / mice or p40 / mice treated with IL-23 was not
associated with increased production of IFN- . When IL-23p19 / mice were infected with T. gondii these mice developed normal
T cell responses and controlled parasite replication to the same extent as wild-type mice. Together, these studies indicate that
IL-12, not IL-23, plays a dominant role in resistance to toxoplasmosis but, in the absence of IL-12, IL-23 can provide a limited
mechanism of resistance to this infection.
DeCS
Interleucinas/fisiologiaToxoplasmose Animal/imunologia
Doença Aguda
Animais
Células Cultivadas/imunologia
Células Dendríticas/metabolismo
Dimerização
Feminino
Imunidade Inata
Interferon gama/biossíntese
Interleucina-12/deficiência
Subunidade p35 da Interleucina-12
Interleucinas/uso terapêutico
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Subunidades Proteicas/deficiência
Células Th1/imunologia
Toxoplasma/imunologia
Toxoplasmose Animal/quimioterapia
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