NKT and NKT-like Cells in Autoimmune Neuroinflammatory Diseases—Multiple Sclerosis, Myasthenia Gravis and Guillain-Barre Syndrome

Zarobkiewicz, Michał K.; Morawska, Izabela; Michalski, Adam; Roliński, Jacek; Bojarska‐Junak, Agnieszka

doi:10.3390/ijms22179520

Cited by 18 publications

(10 citation statements)

References 112 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These specialised types of cells are usually reported in patients with high viral loads and cancer. 46,66,67 Additionally, we found here that immune dysregulation occurs for 18 months post-burn and does not appear to resolve, which is also contrary to the classic wound healing response. Proinflammatory mediators (Th17, TNF-a, NFjb, CCR6) remained in circulation at 18 months post-burn.…”

Section: Burn Injury Induces Changes In Effector T-cell Expression Of...contrasting

confidence: 62%

Unremitting pro‐inflammatory T‐cell phenotypes, and macrophage activity, following paediatric burn injury

Langley,

Zimmermann,

Krenske

et al. 2024

Clin & Trans Imm

View full text Add to dashboard Cite

ObjectivesThe aim of this study was to characterise the dynamic immune profile of paediatric burn patients for up to 18 months post‐burn.MethodsFlow cytometry was used to measure 25 cell markers, chemokines and cytokines which reflected both pro‐inflammatory and anti‐inflammatory immune profiles. Peripheral blood mononuclear cells from 6 paediatric burn patients who had returned for repeated burn and scar treatments for > 4 timepoints within 12 months post‐burn were compared to four age‐matched healthy controls.ResultsWhile overall proportions of T cells, NK cells and macrophages remained relatively constant, over time percentages of these immune cells differentiated into effector and proinflammatory cell phenotypes including Th17 and activated γδ T cells. Circulating proportions of γδ T cells increased their expression of pro‐inflammatory mediators throughout the burn recovery, with a 3–6 fold increase of IL‐17 at 1–3 weeks, and NFκβ 9–18 months post‐burn. T‐regulatory cell plasticity was also observed, and Treg phenotype proportions changed from systemically reduced skin‐homing T‐regs (CCR4+) and increased inflammatory (CCR6+) at 1‐month post‐burn, to double‐positive cell types (CCR4+CCR6+) elevated in circulation for 18 months post‐burn. Furthermore, Tregs were observed to proportionally express less IL‐10 but increased TNF‐α over 18 months.ConclusionOverall, these results indicate the circulating percentages of immune cells do not increase or decrease over time post‐burn, instead they become highly specialised, inflammatory and skin‐homing. In this patient population, these changes persisted for at least 18 months post‐burn, this ‘immune distraction’ may limit the ability of immune cells to prioritise other threats post‐burn, such as respiratory infections.

show abstract

Section: Burn Injury Induces Changes In Effector T-cell Expression Of...contrasting

confidence: 62%

Unremitting pro‐inflammatory T‐cell phenotypes, and macrophage activity, following paediatric burn injury

Langley,

Zimmermann,

Krenske

et al. 2024

Clin & Trans Imm

View full text Add to dashboard Cite

show abstract

“…NKT cells, which are innate-like T cells sharing features with both adaptive and innate cells, can be activated rapidly in response to self or foreign lipid antigens and adopt proinflammatory or immunoregulatory phenotypes in mice and human ( 39 ). In keeping with their modulatory functions, it has been noted that their levels are lower in the peripheral blood of MS patients ( 40 ), which can be restored during remission in patients undertaking IFN-β treatment ( 41 ).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Peripheral Immune Cell Counts on the Risk of Multiple Sclerosis: A Mendelian Randomization Study

Liu

Shen

et al. 2022

Front. Immunol.

View full text Add to dashboard Cite

ObjectivesMultiple sclerosis (MS) is a complex central nervous system (CNS) demyelinating disease, the etiology of which involves the interplay between genetic and environmental factors. We aimed to determine whether genetically predicted peripheral immune cell counts may have a causal effect on MS.MethodsWe used genetic variants strongly associated with cell counts of circulating leukocyte, lymphocyte, monocyte, neutrophil, eosinophil, and basophil, in addition to some subpopulations of T and B lymphocyte, as instrumental variables (IVs) to perform Mendelian randomization (MR) analyses. The effect of immune cell counts on MS risk was measured using the summary statistics from the International Multiple Sclerosis Genetics Consortium (IMSGC) genome-wide association studies (GWAS).ResultsOur findings indicated that higher leucocyte count [odds ratio (OR), 1.24; 95% confidence interval (CI), 1.07 - 1.43; p = 0.0039] and lymphocyte count (OR, 1.17; 95% CI, 1.01 – 1.35; p = 0.0317) were causally associated with MS susceptibility. In addition, we also found that increase of genetically predicted natural killer T (NKT) cell count is also associated with an increase MS risk (OR, 1.24; 95% CI, 1.06 - 1.45; p = 0.0082).ConclusionsThese findings show that the genetic predisposition to higher peripheral immune cell counts can exert a causal effect on MS risk, which confirms the crucial role played by peripheral immunity in MS. Particularly, the causal association between NKT cell count and MS underscores the relevance of exploring the functional roles of NKT cells in disease pathogenesis in future.

show abstract

“…In arthritis, some iNKT are promoted while others are suppressed. These findings suggest that iNKT-mediated regulation in autoimmune diseases is dependent, at least in part, on their ability to regulate macrophage inflammatory profiles ( 86 ).…”

Section: Invariant Natural Killer T (Inkt) Cellsmentioning

confidence: 99%

Novel potential therapeutic targets of alopecia areata

Wan

Xie

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

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.

show abstract

NKT and NKT-like Cells in Autoimmune Neuroinflammatory Diseases—Multiple Sclerosis, Myasthenia Gravis and Guillain-Barre Syndrome

Cited by 18 publications

References 112 publications

Unremitting pro‐inflammatory T‐cell phenotypes, and macrophage activity, following paediatric burn injury

Unremitting pro‐inflammatory T‐cell phenotypes, and macrophage activity, following paediatric burn injury

The Effect of Peripheral Immune Cell Counts on the Risk of Multiple Sclerosis: A Mendelian Randomization Study

Novel potential therapeutic targets of alopecia areata

Contact Info

Product

Resources

About