Immunopathogenesis of Cerebral Toxoplasmosis Export

@article{citeulike:5856158, abstract = {doi: 10.1086/344276 PMID: 12424703 Interferon (IFN)‐γ is an absolute requirement for resistance against acute acquired infection with Toxoplasma gondii and development of toxoplasmic encephalitis (TE) during the late stage of infection. Multiple populations of both T and non–T cells are important sources of IFN‐γ in resistance. In the absence of IFN‐γ–producing non–T cells, T cells cannot prevent TE. Interleukin‐12, Bcl‐3, NF‐κB(2), and CD40‐CD40L ligand interaction are important for up‐regulation of IFN‐γ production. T. gondii infects a variety of host cells, and IFN‐γ–mediated immune responses control the parasite in both phagocytic and nonphagocytic cells through at least five different mechanisms, most likely depending on the types of cells responding to IFN‐γ. Such effector functions involve production of NO by iNOS, tryptophan degradation by the enzyme IDO (indolamine 2,3‐dioxygenase), unidentified mechanism(s) mediated by 47‐ to 48‐kDa proteins encoded by an IFN‐γ responsive gene family, limiting the availability of intracellular iron to the parasite, and production of reactive oxygen intermediates.}, author = {Suzuki, Yasuhiro}, citeulike-article-id = {5856158}, citeulike-linkout-0 = {http://dx.doi.org/10.1086/344276}, citeulike-linkout-1 = {http://www.journals.uchicago.edu/doi/abs/10.1086/344276}, day = {1}, doi = {10.1086/344276}, journal = {The Journal of Infectious Diseases}, keywords = {and, gondi, iron, toxoplasma}, month = {December}, number = {s2}, pages = {S234--S240}, posted-at = {2009-09-29 21:34:49}, priority = {2}, title = {Immunopathogenesis of Cerebral Toxoplasmosis}, url = {http://dx.doi.org/10.1086/344276}, volume = {186}, year = {2002} }

TY - JOUR ID - citeulike:5856158 L3 - citeulike-article-id:5856158 N2 - doi: 10.1086/344276 PMID: 12424703 Interferon (IFN)‐γ is an absolute requirement for resistance against acute acquired infection with Toxoplasma gondii and development of toxoplasmic encephalitis (TE) during the late stage of infection. Multiple populations of both T and non–T cells are important sources of IFN‐γ in resistance. In the absence of IFN‐γ–producing non–T cells, T cells cannot prevent TE. Interleukin‐12, Bcl‐3, NF‐κB(2), and CD40‐CD40L ligand interaction are important for up‐regulation of IFN‐γ production. T. gondii infects a variety of host cells, and IFN‐γ–mediated immune responses control the parasite in both phagocytic and nonphagocytic cells through at least five different mechanisms, most likely depending on the types of cells responding to IFN‐γ. Such effector functions involve production of NO by iNOS, tryptophan degradation by the enzyme IDO (indolamine 2,3‐dioxygenase), unidentified mechanism(s) mediated by 47‐ to 48‐kDa proteins encoded by an IFN‐γ responsive gene family, limiting the availability of intracellular iron to the parasite, and production of reactive oxygen intermediates. IS - s2 JF - The Journal of Infectious Diseases EP - S240 TI - Immunopathogenesis of Cerebral Toxoplasmosis VL - 186 SP - S234 KW - and KW - gondi KW - iron KW - toxoplasma AU - Suzuki, Yasuhiro PY - 2002/12/01/ UR - http://dx.doi.org/10.1086/344276 ER -