1) The document discusses how dietary fatty acids can modulate cytokine production in T cells associated with Type 1 Diabetes (T1D) in NOD mice.
2) It reports on an experiment where T cells from NOD mice were polarized to become proinflammatory Th17 cells under conditions known to induce this differentiation.
3) The results showed that increasing concentrations of the fatty acid linoleic acid decreased production of the Th17 cytokine IL-17A, suggesting linoleic acid can modulate Th17 cell cytokine production.
1) The document discusses how dietary fatty acids can modulate cytokine production in T cells associated with Type 1 Diabetes (T1D) in NOD mice.
2) It reports on an experiment where T cells from NOD mice were polarized to become proinflammatory Th17 cells under conditions known to induce this differentiation.
3) The results showed that increasing concentrations of the fatty acid linoleic acid decreased production of the Th17 cytokine IL-17A, suggesting linoleic acid can modulate Th17 cell cytokine production.
1) The document discusses how dietary fatty acids can modulate cytokine production in T cells associated with Type 1 Diabetes (T1D) in NOD mice.
2) It reports on an experiment where T cells from NOD mice were polarized to become proinflammatory Th17 cells under conditions known to induce this differentiation.
3) The results showed that increasing concentrations of the fatty acid linoleic acid decreased production of the Th17 cytokine IL-17A, suggesting linoleic acid can modulate Th17 cell cytokine production.
Modulation of cytokine production by dietary fatty acids in T cells from Type 1
Diabetes-susceptible NOD mice
Maansi Gupta1 2, Jaileene,Hernandez Escalante2, Albert Jones IV2, Hans Dooms Ph.D.2 Johns Creek High School, 5575 State Bridge Rd, Johns Creek, GA 300221; Boston University School of Medicine: Rheumatology Section, 72 E Concord St, Boston, MA 021182. Type 1 Diabetes is an autoimmune disorder characterized by autoreactive T cells attacking beta cells in the pancreas. This causes insulin levels to decrease throughout an individual’s life until essentially no insulin is being produced. The instances of individuals with low-risk alleles for T1D acquiring the disease has been increasing, which shows that environmental factors have a role in the occurrence of T1D. One such environmental factor is one’s diet, more specifically, the amount of polyunsaturated fatty acids, such as omega-3, consumed. There are many T cell subsets, and of these subsets, experiments have shown that CD4+ and CD8+ T cells have been observed to produce less IL-10, an anti-inflammatory cytokine, when exposed to linoleic acid, a polyunsaturated fatty acid. It is possible that other T cell subsets could also be affected by fatty acids. In this experiment, conditions for CD4+ T cell polarization into proinflammatory Th17 cells were set. Th17 cells have two unique cytokines: IL-17A and IL-21. It has been observed that a high concentration of Th17 cells is associated with disease pathogenesis of T1D. As such, the goal of this experiment was to determine if a) Th17 polarization could occur given certain conditions; b) if fatty acid concentration could affect Th17 polarization; and c) how fatty acid concentration would affect cytokine production in Th17 cells. T cells were isolated from NOD mice (the standard mouse model for T1D) and exposed to Th17-specific cytokines and blocking antibodies to induce differentiation. These cells were then exposed to linoleic acid, a dietary fatty acid. The data generated by a flow cytometry (intracellular cytokine staining) showed that as fatty acid concentration increased, the abundance of IL-17A decreased, suggesting that linoleic acid can modulate cytokine production.