TY  - JOUR
AU  - Saksida, Tamara
AU  - Koprivica, Ivan
AU  - Vujičić, Milica
AU  - Stošić-Grujičić, Stanislava
AU  - Perović, Milka
AU  - Kanazir, Selma
AU  - Stojanović, Ivana D.
PY  - 2018
UR  - http://www.ncbi.nlm.nih.gov/pubmed/29254086
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2948
AB  - Alzheimer's disease (AD) is characterized by accumulation of amyloid-β plaques that further promotes microglia-mediated neuroinflammatory responses and inflammation in the brain. Emerging data are revealing the relation between gut-associated lymphoid tissue (GALT) cells and CNS, as effector cells primed in the gut might home to the brain. This study aimed to determine cell composition of GALT in 5xFAD mice, an established model for AD. Immune cells isolated from Peyer's patches (PP) and mesenteric lymph nodes (MLN) were stained with surface and intracellular markers for T helper (Th) subpopulations, B lymphocytes and macrophages and analyzed cytofluorimetrically, while cytokine expression and production were determined by qPCR and ELISA, respectively. Inflammation was detected in GALT of 5xFAD mice with established AD pathology. Although the production of IFN-γ, IL-4, and IL-10 was comparable between the strains, lower IL-17 production was observed in PP and MLN cells. This phenomenon could not be attributed to a lower abundance of Th17 cells, or cytokines that initiate their formation or propagation (TGF-β, IL-6, and IL-23). Also, reduced IL-17 production was not a consequence of altered Il-17 mRNA transcription or deficiency of Rorγt, a key transcription factor for IL-17. However, the expression of miR-155 (a non-coding micro RNA that promotes the development of Th17 cells), was significantly lower in MLN cells of 5xFAD mice. In contrast, mice without AD neuropathology did not have inflammation in GALT or altered Th17 numbers, nor decreased IL-17 production. In conclusion, the observed changes in GALT of 5xFAD mice mirror the disease progression and might reflect inadequate immune surveillance in the gut and lead to enhanced AD pathology.
T2  - Journal of Alzheimer's disease : JAD
T2  - Journal of Alzheimer's disease : JAD
T1  - Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology
IS  - 2
VL  - 61
DO  - 10.3233/JAD-170538
SP  - 619
EP  - 630
ER  - 

@article{
author = "Saksida, Tamara and Koprivica, Ivan and Vujičić, Milica and Stošić-Grujičić, Stanislava and Perović, Milka and Kanazir, Selma and Stojanović, Ivana D.",
year = "2018",
abstract = "Alzheimer's disease (AD) is characterized by accumulation of amyloid-β plaques that further promotes microglia-mediated neuroinflammatory responses and inflammation in the brain. Emerging data are revealing the relation between gut-associated lymphoid tissue (GALT) cells and CNS, as effector cells primed in the gut might home to the brain. This study aimed to determine cell composition of GALT in 5xFAD mice, an established model for AD. Immune cells isolated from Peyer's patches (PP) and mesenteric lymph nodes (MLN) were stained with surface and intracellular markers for T helper (Th) subpopulations, B lymphocytes and macrophages and analyzed cytofluorimetrically, while cytokine expression and production were determined by qPCR and ELISA, respectively. Inflammation was detected in GALT of 5xFAD mice with established AD pathology. Although the production of IFN-γ, IL-4, and IL-10 was comparable between the strains, lower IL-17 production was observed in PP and MLN cells. This phenomenon could not be attributed to a lower abundance of Th17 cells, or cytokines that initiate their formation or propagation (TGF-β, IL-6, and IL-23). Also, reduced IL-17 production was not a consequence of altered Il-17 mRNA transcription or deficiency of Rorγt, a key transcription factor for IL-17. However, the expression of miR-155 (a non-coding micro RNA that promotes the development of Th17 cells), was significantly lower in MLN cells of 5xFAD mice. In contrast, mice without AD neuropathology did not have inflammation in GALT or altered Th17 numbers, nor decreased IL-17 production. In conclusion, the observed changes in GALT of 5xFAD mice mirror the disease progression and might reflect inadequate immune surveillance in the gut and lead to enhanced AD pathology.",
journal = "Journal of Alzheimer's disease : JAD, Journal of Alzheimer's disease : JAD",
title = "Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology",
number = "2",
volume = "61",
doi = "10.3233/JAD-170538",
pages = "619-630"
}

Saksida, T., Koprivica, I., Vujičić, M., Stošić-Grujičić, S., Perović, M., Kanazir, S.,& Stojanović, I. D.. (2018). Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology. in Journal of Alzheimer's disease : JAD, 61(2), 619-630.
https://doi.org/10.3233/JAD-170538

Saksida T, Koprivica I, Vujičić M, Stošić-Grujičić S, Perović M, Kanazir S, Stojanović ID. Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology. in Journal of Alzheimer's disease : JAD. 2018;61(2):619-630.
doi:10.3233/JAD-170538 .

Saksida, Tamara, Koprivica, Ivan, Vujičić, Milica, Stošić-Grujičić, Stanislava, Perović, Milka, Kanazir, Selma, Stojanović, Ivana D., "Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology" in Journal of Alzheimer's disease : JAD, 61, no. 2 (2018):619-630,
https://doi.org/10.3233/JAD-170538 . .