Mechanisms of autoimmunity in the non‐obese diabetic mouse: effector/regulatory cell equilibrium during peak inflammation

Askenasy, Nadir

doi:10.1111/imm.12581

Cited by 11 publications

(9 citation statements)

References 228 publications

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“…The major mouse model for this disease is the non obese diabetic (NOD) model; these mice develop an inflammatory autoimmunity against their pancreatic islet (insulin producing) β-cells [100]. Early in the disease process the pancreatic islets of NOD mice develop a transient influx of neutrophils [101].…”

Section: Neutrophils In Autoimmune Endocrine Conditionsmentioning

confidence: 99%

Neutrophils in animal models of autoimmune disease

Németh

Mócsai

Lowell

2016

Seminars in Immunology

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Neutrophils have traditionally been thought to play only a peripheral role in the genesis of many autoimmune and inflammatory diseases. However, recent studies in a variety of animal models suggest that these cells are central to the initiation and propagation of autoimmunity. The use of mouse models, which allow either deletion of neutrophils or the targeting of specific neutrophil functions, has revealed the many complex ways these cells contribute to autoimmune/inflammatory processes. This includes generation of self antigens through the process of NETosis, regulation of T-cell and dendritic cell activation, production of cytokines such as BAFF that stimulate self-reactive B-cells, as well as indirect effects on epithelial cell stability. In comparing the many different autoimmune models in which neutrophils have been examined, a number of common underlying themes emerge – such as a role for neutrophils in stimulating vascular permeability in arthritis, encephalitis and colitis. The use of animal models has also stimulated the development of new therapeutics that target neutrophil functions, such as NETosis, that may prove beneficial in human disease. This review will summarize neutrophil contributions in a number of murine autoimmune/inflammatory disease models.

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Section: Neutrophils In Autoimmune Endocrine Conditionsmentioning

confidence: 99%

Neutrophils in animal models of autoimmune disease

Németh

Mócsai

Lowell

2016

Seminars in Immunology

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“…A combination of CD4 + CD25 + and CD127 low expression is commonly used for the characterization of Tregs, regularly together with forkead box P3 (Foxp3) . In several studies, Tregs have been implicated as being part of the process in T1D . However, characterization and determination of the role of memory Tregs in T1D still need investigation.…”

Section: Introductionmentioning

confidence: 99%

“…7 In several studies, Tregs have been implicated as being part of the process in T1D. 8,9 However, characterization and determination of the role of memory Tregs in T1D still need investigation. Memory Tregs, sharing parts of phenotypic and functional characterization of Tregs, maintain long-lived tolerance to self-antigens and exhibit a more potent suppressive ability.…”

Section: Introductionmentioning

confidence: 99%

Altered expression of CD39 on memory regulatory T cells in type 1 diabetes patients

Jin

Zhang

Gong

et al. 2018

Journal of Diabetes

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Background Type 1 diabetes (T1D) is an autoimmune disease resulting from an attack by autoreactive T lymphocytes against pancreatic islet β‐ cells. In recent studies, regulatory T cells (Tregs) have been implicated in the process of T1D. Furthermore, cluster of differentiation 39 (CD39), which is involved in the suppression of inflammation, has been shown to be expressed on Tregs. However, the pathological importance of CD39 to the memory Treg population remains unclear. Methods This study investigated Treg subsets, focusing on resting, effector, and memory Tregs, and determined CD39 expression on Tregs. In addition, changes in Treg subsets and Treg‐associated cytokine secretion after CD3/CD28 stimulation of peripheral blood mononuclear cells were evaluated in diabetic patients and healthy controls. The suppressive function of Tregs was measured using the mixed lymphocyte reaction (MLR) test. Results There was a higher percentage of memory Tregs in T1D patients than healthy controls. However, Tregs in T1D patients showed impaired suppression, with low forkhead box P3 (Foxp3) expression and low serum interleukin (IL)‐10 levels. Furthermore, CD39 expression on Tregs, and on memory Tregs in particular, was lower in T1D patients than healthy controls. After stimulation, the percentage of resting Tregs was decreased and that of effector/memory Tregs was increased in both healthy controls and T1D patients, but CD39 expression on effector/memory Tregs was still lower and there was no increase in IL‐10 secretion in T1D patients. Conclusions The defective suppressive function of Tregs in T1D patients is due to lower expression of CD39 on memory Tregs.

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“…In splenocyte populations, the phagocytic cells' respiratory burst was examined by NBT dye reduction based on the partially modified previous description of the test [20][21][22]. Briefly, a mixture was prepared with splenocyte suspension (100 μL), Staphylococcus aureus suspension (10 8 cell/mL) of 0.1 mL, and 0.1% NBT of 0.1 mL in PBS (pH 7.4).…”

Section: Measuring Respiratory Burst In Splenocytesmentioning

confidence: 99%

Pistacia atlantica gum aqueous extract modulates humoral and cellular immune responses in BALB/c mice

Ghaleh¹,

Gandabeh²,

Motlagh³

et al. 2020

Turk J Vet Anim Sci

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Natural herbal products contain different compounds that can modulate immune and inflammatory diseases. This investigation aimed to examine the influence of Pistacia atlantica aqueous extract on cellular and humoral immunity in mice following the exposure to sheep red blood cells (SRBCs). For this purpose, male BALB/c mice (n = 40) were randomly assigned into 4 equivalent groups. The animals received 1 × 10 9 SRBCs in complete Freund's adjuvant (CFA) intraperitoneally 3 times with two-week intervals. Five days after the final injection, blood samples were taken from the animals. Additionally, 1 × 10 9 SRBCs were also injected into the mice's left hind footpad 48 h before the blood collection. Three groups of mice received various oral doses of the extract (100, 200, and 400 mg/kg) for 52 consecutive days after the study onset. Measurements were performed on the levels of humoral and cellular immune responses, splenocytes' ability to uptake neutral red, respiratory burst, and cell viability. The mice receiving Pistacia atlantica in all concentrations displayed significantly low delayed type hypersensitivity (DTH) reactions in a dose-dependent manner compared to the control animals. The treated mice also presented a dose-dependent, significantly lower average anti-SRBC titer than that in the control animals. IL-17 and IL-10 cytokine levels respectively decreased and increased significantly in the mice that received Pistacia atlantica compared to the control group. Splenocyte proliferation and respiratory burst declined significantly in mice treated with Pistacia atlantica as opposed to the normal control group but phagocytosis ability was significantly decreased. The immunomodulatory impacts of Pistacia atlantica might be partially caused by immunity diversion from proinflammatory cytokine IL-17 into antiinflammatory cytokine IL-10.

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Mechanisms of autoimmunity in the non‐obese diabetic mouse: effector/regulatory cell equilibrium during peak inflammation

Cited by 11 publications

References 228 publications

Neutrophils in animal models of autoimmune disease

Neutrophils in animal models of autoimmune disease

Altered expression of CD39 on memory regulatory T cells in type 1 diabetes patients

Pistacia atlantica gum aqueous extract modulates humoral and cellular immune responses in BALB/c mice

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