CD4 T cell differentiation in type 1 diabetes

Walker, Lucy S. K.; Herrath, Matthias von

doi:10.1111/cei.12672

Cited by 153 publications

(119 citation statements)

References 171 publications

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“…Interestingly, in autoimmune diseases, a separate population of T H cells, the T H 1/T H 17 cells that co-produce both IL-17 and IFN-γ, has been found [54] . Several studies have found an increased polarization of IL-17+ cells to produce IFN-γ in children with T1D compared with healthy controls [55,56] . Thus, the presence of T H 1/T H 17 cells could potentially be a hallmark of T1D, even if further investigation is required.…”

Section: The Il-23/il-17 Axismentioning

confidence: 99%

Obesity, Type 1 Diabetes, and Psoriasis: An Autoimmune Triple Flip

Granata

Skarmoutsou²,

Trovato³

et al. 2016

Pathobiology

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Obesity, type 1 diabetes, and psoriasis are wide-ranging health problems. Genetics, epigenetics, and environmental factors together with immune disturbances are involved in these diseases. The white adipose tissue is an active endocrine organ, secreting a wide variety of soluble mediators called adipokines that have a central role in the relationship between adipose tissue and immune system. Inflammatory cytokines, including the IL-23/IL-17 and IL-18 axes, and microRNAs are involved in many processes, including immunity and inflammation, thus having a major role in the onset of these three diseases. In this review, we present an overview of the roles of adipokines, cytokines, and microRNAs in the pathogenesis and the progression of these three diseases.

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Section: The Il-23/il-17 Axismentioning

confidence: 99%

Obesity, Type 1 Diabetes, and Psoriasis: An Autoimmune Triple Flip

Granata

Skarmoutsou²,

Trovato³

et al. 2016

Pathobiology

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“…[H2] Involvement of TLRs T1DM is a well-established type 1 T helper (TH1) cell-mediated disease whereby pancreatic β cells are selectively injured and destroyed 29 . Many of the studies that have addressed the mechanisms of T1DM have mainly focused on the role of the adaptive immune system that is mediated by T lymphocytes.…”

Section: [H2] Inflammasomesmentioning

confidence: 99%

Innate immunity in diabetes and diabetic nephropathy

2015

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Abstract:The innate immune system consists of several classes of pattern recognition receptors (PRRs), including membrane-bound Toll-like receptors (TLRs) and nucleotide-binding domain leucine-rich oligomerization domain (NOD)-like receptors (NLRs).These receptors detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in the extracellular and intracellular space. Intracellular NLRs constitute inflammasomes, which activate and release caspase-1, IL1β, and IL18 and thus initiate an inflammatory response. Systemic and local low-grade inflammation and release of proinflammatory cytokines are implicated in the development and progression of diabetes mellitus and diabetic nephropathy. TLR2, TLR4, and the NLRP3 inflammasome are critically involved in the inflammatory responses in pancreatic islets, adipose, liver and kidney tissues. This Review discusses how innate immune system-driven inflammatory processes can lead to apoptosis, tissue fibrosis, and organ dysfunction to cause insulin resistance, impaired insulin secretion, and renal failure. We propose that careful targeting of TLR2, TLR4, and NLRP3 signalling pathways may be beneficial for the treatment of diabetes mellitus and diabetic nephropathy. 2 Key points The innate immune system consists of several classes of pattern recognition receptors, including TLRs and NLRs, which detect pathogen-associated and danger-associated molecular patterns and initiate an inflammatory response  TLR2 and TLR4 are the predominant toll-like receptors expressed on pancreatic β cells that trigger an inflammatory response in insulitis during type 1 diabetes mellitus  TLR2 and TLR4 signaling, and activation of NLRP3 inflammasomes results in production of various proinflammatory cytokines that can induce insulin resistance in type 2 diabetes mellitus (T2DM) and obesity  Innate immune responses in T2DM and obesity are modulated by the status of the gut microbiota, autophagy, and adipokines  TLR2, TLR4, NOD2, and NLRP3 inflammasome-mediated inflammation are involved in the perpetuation of inflammation in diabetic nephropathy  The activation of TLRs and NLRs stimulates the expression of MCP-1, which is associated with the progression of diabetic nephropathy [H1] IntroductionThe prevalence of diabetes mellitus is estimated to be 8.3%, affecting ~387 million people as of 2014. The number of patients living with diabetes mellitus is expected to increase to ~592 million by 2035, as reported by the International Diabetes Federation 1 . The incidence of end-stage renal disease (ESRD) is also rapidly increasing worldwide but varies up to 15-fold by country. In 2012, the number of new diagnoses of ESRD worldwide ranged from 25 to 467 patients per million. The proportion of new cases of ESRD with diabetes mellitus as the primary cause also differs by country, with 66% cases reported in Singapore and 12-16% cases reported in Ukraine, Romania, and the Netherlands 2 . Although intensified multifactorial intervention in patients with type 2 diabete...

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“…The role of CD8 1 T cells responding to ChgA autoantigen in the destruction of pancreatic islet b cells and diabetes development in NOD mice has not been documented. In NOD mice, both CD4 1 and CD8 1 T cells contribute to diabetes pathogenesis [8][9][10][11]. NOD mice deficient in major histocompatibility complex (MHC) class I molecules are resistant to diabetes development [12,13].…”

Section: Introductionmentioning

confidence: 99%