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Nutrition and Immune Modulation in Autoimmune Diseases

A Special Issue of Nutrients (ISSN 2072-6643) belonging to the section "Nutritional Immunology".

Deadline for manuscript submissions: 5 March 2027 | Viewed by 3435

Editors


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Guest Editor
Independent Laboratory of Rheumatic Diagnostics, Pomeranian Medical University in Szczecin, Unii Lubelskiej 1, 71-252 Szczecin, Poland
Interests: systemic connective tissue diseases; cardiovascular disease; metabolic syndrome; atherosclerosis; systemic lupus erythematosus; autoimmunity
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Gastroenterology, Pomeranian Medical University in Szczecin, Unii Lubelskiej 1, 71-252 Szczecin, Poland
Interests: microbiota; disorders of gut-brain interactions; mental health; probiotics; gastroscopy; colonoscopy; IBD; IBS

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Guest Editor
Department of Human Nutrition and Metabolomics, Pomeranian Medical University in Szczecin, Władysława Broniewskiego 24, 71-460 Szczecin, Poland
Interests: nutrients; diet; metabolomics; microbiome; probiotics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autoimmune diseases are extremely heterogenous in terms of frequency, clinical manifestations and pathogenic mechanisms. Epidemiologic data show that about 10% of the global population suffers from these disorders, and the number of cases is increasing. More than 100 disease entities have been defined, with a prevalence ranging from 1% to < 1/106. These diseases are typically characterized by a chronic course with periods of exacerbation and remission, leading—in the most dramatic cases—to multi-organ involvement, permanent disability or even death.

Diet plays a pivotal role in influencing the course of autoimmune diseases by directly affecting immune system function and inflammation. Certain dietary components have been identified as triggers that exacerbate autoimmune conditions. On the other hand, a well-balanced anti-inflammatory diet provides significant benefits by regulating the immune system, reducing the production of autoantibodies, and supporting overall health.

Taking into account the vast heterogeneity of autoimmune diseases with regard to etiopathogenic mechanisms, clinical phenotype and disease progression, as well as the response to applied drugs, there is an critical need to individualize health care and therapeutic approach. As tailored dietary interventions can significantly reduce symptoms and improve quality of life, the current Special Issue aims to direct attention to the complex interplay between nutrients, lifestyle and immunological and inflammatory factors to offer more comprehensive and effective care, enhancing both clinical outcomes and the overall quality of life for individuals suffering from autoimmune conditions.

Dr. Katarzyna Fischer
Prof. Dr. Wojciech Marlicz
Prof. Dr. Ewa Stachowska
Guest Editors

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Keywords

  • diet
  • nutrients
  • immune system
  • autoimmunity
  • inflammation
  • systemic connective tissue disease
  • organ-specific autoimmune disease
  • atherosclerosis
  • cardiovascular disease
  • metabolic syndrome
  • metabolomics
  • microbiome
  • exercise
  • lifestyle
  • quality of life

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Published Papers (2 papers)

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Review

22 pages, 1142 KB  
Review
Refractory Celiac Disease: Nutritional Failure, Immune Dysregulation, and Lymphomagenesis
by Ioanna Aggeletopoulou, Ploutarchos Pastras, Maria Kalafateli and Christos Triantos
Nutrients 2026, 18(15), 2479; https://doi.org/10.3390/nu18152479 - 31 Jul 2026
Viewed by 827
Abstract
Refractory celiac disease (RCeD) is a rare but severe complication of celiac disease characterized by persistent or recurrent malabsorptive symptoms and villous atrophy despite a strict gluten-free diet, after exclusion of ongoing gluten exposure, alternative enteropathies, and overt lymphoma. RCeD comprises two biologically [...] Read more.
Refractory celiac disease (RCeD) is a rare but severe complication of celiac disease characterized by persistent or recurrent malabsorptive symptoms and villous atrophy despite a strict gluten-free diet, after exclusion of ongoing gluten exposure, alternative enteropathies, and overt lymphoma. RCeD comprises two biologically distinct entities. RCeD-I is associated with phenotypically normal, polyclonal intraepithelial lymphocytes and generally reflects persistent gluten-independent mucosal inflammation with a relatively favorable prognosis. RCeD-II is defined by expansion of aberrant clonal intraepithelial lymphocytes lacking normal surface T-cell markers and is increasingly regarded as a low-grade intraepithelial lymphoma or in situ lymphomatous disorder, with substantial risk of progression to enteropathy-associated T-cell lymphoma (EATL). Mechanistic studies identify epithelial stress, IL-15-driven IEL survival, stromal and innate immune amplification, and cytotoxic epithelial injury as central drivers of refractory mucosal damage. In RCeD-II, aberrant IELs acquire a hybrid T/NK-like phenotype, persist through anti-apoptotic IL-15/JAK–STAT signaling, and induce enterocyte killing, while molecular alterations involving JAK1, STAT3, JAK/STAT regulators, NF-κB signaling, epigenetic regulators, and chromosomal abnormalities support stepwise lymphomagenesis. Recent single-cell multiomic studies further reveal genetically altered intestinal lymphocyte clones and intratumoral heterogeneity across the RCeD-II–EATL continuum. From a nutritional immunology perspective, RCeD illustrates a setting in which removal of the initiating dietary antigen is insufficient to restore mucosal immune homeostasis. This review summarizes the pathogenic processes that distinguish RCeD-I from RCeD-II and link failed mucosal recovery after gluten withdrawal to persistent immune-mediated epithelial injury, aberrant IEL expansion, clonal evolution, and lymphoma progression. Full article
(This article belongs to the Special Issue Nutrition and Immune Modulation in Autoimmune Diseases)
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30 pages, 1450 KB  
Review
The Role of Microbiome and Diet on Disease Activity and Immune–Inflammatory Status in Rheumatoid Arthritis
by Aleksandra Rodziewicz and Ewa Bryl
Nutrients 2026, 18(9), 1325; https://doi.org/10.3390/nu18091325 - 22 Apr 2026
Cited by 1 | Viewed by 1711
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune background and unknown etiology. The importance of genetic factors in RA development is well-established. Environmental factors have also been extensively researched in relation to risk of RA and managing its symptoms. Smoking, physical [...] Read more.
Rheumatoid arthritis (RA) is a chronic inflammatory disease of autoimmune background and unknown etiology. The importance of genetic factors in RA development is well-established. Environmental factors have also been extensively researched in relation to risk of RA and managing its symptoms. Smoking, physical activity, diet, and gut microbiota are considered to be the most essential modifiable factors in RA. Among dietary interventions, the most researched is Mediterranean diet, monounsaturated fatty acids, fish consumption, and fish oil (EPA, eicosapentaenoic acid and DHA, that is, docosahexaenoic acid). Others concerned gluten-free and vegan or vegetarian diet, salt intake, supplementation with vitamin D, antioxidants, prebiotics, and probiotics. Diet modifications can alter the gut environment, and the association between RA development or severity and the composition of gut bacteria has already been shown. This review focuses on effectiveness and usefulness of various dietary approaches and supplements in RA prevention and management, including the influence on disease activity and inflammatory status. The composition of gut microbiota and its changes in response to dietary factors are also considered. There is a great need for further research into mutual dependencies of diet, microbiome, and RA activity. The current state of knowledge provides promising evidence for future nutrition and microbial therapies. Full article
(This article belongs to the Special Issue Nutrition and Immune Modulation in Autoimmune Diseases)
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