Tissue-Resident T Cells in Chronic Relapsing–Remitting Intestinal Disorders

Albuquerque, Juliana Barreto de; Mueller, Christoph; Gungor, Bilgi

doi:10.3390/cells10081882

Cited by 3 publications

(2 citation statements)

References 131 publications

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“…Tissue-specific signals influence its differentiation ( 45 ). T RM cells are predominantly generated by T cell-mediated immunological responses ( 46 ). Simultaneously, T RM cells can recirculate memory T cells through the blood and lymphoid organs ( 47 ).…”

Section: Tissue-resident Memory T Cells (T Rm Cells)mentioning

confidence: 99%

Novel potential therapeutic targets of alopecia areata

Wan

Xie

et al. 2023

Front. Immunol.

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Alopecia areata (AA) is a non-scarring hair loss disorder caused by autoimmunity. The immune collapse of the hair follicle, where interferon-gamma (IFN-γ) and CD8+ T cells accumulate, is a key factor in AA. However, the exact functional mechanism remains unclear. Therefore, AA treatment has poor efficacy maintenance and high relapse rate after drug withdrawal. Recent studies show that immune-related cells and molecules affect AA. These cells communicate through autocrine and paracrine signals. Various cytokines, chemokines and growth factors mediate this crosstalk. In addition, adipose-derived stem cells (ADSCs), gut microbiota, hair follicle melanocytes, non-coding RNAs and specific regulatory factors have crucial roles in intercellular communication without a clear cause, suggesting potential new targets for AA therapy. This review discusses the latest research on the possible pathogenesis and therapeutic targets of AA.

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Section: Tissue-resident Memory T Cells (T Rm Cells)mentioning

confidence: 99%

Novel potential therapeutic targets of alopecia areata

Wan

Xie

et al. 2023

Front. Immunol.

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“…Based on these works on cytokines, our present theory is that GDD is primarily an immune-mediated inflammatory disease (IMID) that has a principal effect on tissue-resident memory T cells (NT), which have been described as the principal mediating cell in Crohn disease 18,19 and asthma 17 . Other researchers have looked at other cell products elevated in GBCA exposure and GDD, and have shown elevated serum biomarkers for mitochondrial damage 5,20,21 …”

Section: Diagnosismentioning

confidence: 99%

Gadolinium Deposition Disease

Semelka¹,

Ramalho²

2023

Invest Radiol

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This review describes the current knowledge of a form of gadolinium toxicity termed gadolinium deposition disease (GDD), supplemented with the opinions of the authors developed during 6 years of clinical experience treating GDD. Gadolinium deposition disease can also be considered a subset under the symptoms associated with gadolinium exposure rubric. Young and middle-aged White women of central European genetic origin are the most affected. The most common symptoms are fatigue, brain fog, skin pain, skin discoloration, bone pain, muscle fasciculations, and pins and needles, but a long list of additional symptoms is reported herein. The time of onset of symptoms ranges from immediate to 1 month after gadolinium-based contrast agent (GBCA) administration. The primary treatment is to avoid further GBCAs and metal removal through chelation. Presently, the most effective chelating agent is DTPA because of its high affinity with gadolinium. Flare development is an expected outcome, amenable to concurrent immune dampening. We emphasize in this review the critical nature of recognizing GDD when it first arises, as the disease becomes progressively more severe with each subsequent GBCA injection. It is generally very treatable after the first symptoms of GDD, often arising after the first GBCA injection. Future directions of disease detection and treatment are discussed.

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Effects of Gadolinium Retention in the Brains of Type 2 Diabetic Rats after Repeated Administration of Gadolinium‐Based MRI Contrast Agents on Neurobiology and NLRP3 Inflammasome Activation

Yao,

Zhang,

et al. 2024

Magnetic Resonance Imaging

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BackgroundThe neurotoxic potential of gadolinium (Gd)‐based contrast agents (GBCAs) retention in the brains of patients with type 2 diabetes mellitus (T2DM) is unclear.PurposeTo determine the deposition and clearance of GBCAs in T2DM rats and the mechanism by which Gd enhances nucleotide‐binding oligomerization domain‐3 (NLRP3) inflammasome activation.Study TypeCross‐sectional, prospective.Animal Model104 T2DM male Wistar rats.Field Strength/Sequence9.4‐T, T1‐weighted fast spin echo sequence.AssessmentT2DM (male Wistar rats, n = 52) and control group (healthy, male Wistar rats, n = 52) rats received saline, gadodiamide, Gd‐diethylenetriaminepentaacetic acid, and gadoterate meglumine for four consecutive days per week for 7 weeks. The distribution and clearance of Gd in the certain brain were assessed by MRI (T1 signal intensity and relaxation rate R1, on the last day of each week), inductively coupled plasma mass‐spectroscopy, ultraperformance liquid chromatography mass spectrometry, and transmission electron microscopy. Behavioral tests, histopathological features, and the effects of GBCAs on neuroinflammation were also analyzed.Statistical TestsOne‐way analysis of variance, bonferroni method, and unpaired t‐test. A P‐value <0.05 was considered statistically significant.ResultsThe movement distance and appearance time in the open field test of the T2DM rats in the gadodiamide group were significantly shorter than in the other groups. Furthermore, the expression of NLRP3, Pro‐Caspase‐1, interleukin‐1β (IL‐1β), and apoptosis‐associated speck‐like protein containing a CARD protein in neurons was significantly higher in the gadodiamide group than in the saline group, as shown by Western blot. Gadodiamide also induced differentiation of microglia into M1 type, decreased the neuronal mitochondrial membrane potential, and significantly increased neuronal apoptosis from flow cytometry.Data ConclusionT2DM may affect both the deposition and clearance of GBCAs in the brain. Informed by the T2DM model, gadodiamide could mediate the neuroinflammatory response by NLRP3 inflammasome activation.Level of Evidence1Technical EfficacyStage 1

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Tissue-Resident T Cells in Chronic Relapsing–Remitting Intestinal Disorders

Cited by 3 publications

References 131 publications

Novel potential therapeutic targets of alopecia areata

Novel potential therapeutic targets of alopecia areata

Gadolinium Deposition Disease

Effects of Gadolinium Retention in the Brains of Type 2 Diabetic Rats after Repeated Administration of Gadolinium‐Based MRI Contrast Agents on Neurobiology and NLRP3 Inflammasome Activation

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