-Omic Approaches and Treatment Response in Rheumatoid Arthritis

Madrid-Paredes, Adela; Martín, Javier; Márquez, Ana

doi:10.3390/pharmaceutics14081648

Cited by 6 publications

(4 citation statements)

References 108 publications

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“…DNA methylation changes were also found in patients after methotrexate treatment (113). Multiomics techniques will allow new development of therapeutic strategies (114). Increased proinflammatory cytokines production in monocytes, upregulated glycolysis, and methylation changes are features of trained immunity.…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

Trained immunity as a possible newcomer in autoinflammatory and autoimmune diseases pathophysiology

Beignon

Galeotti²,

Schvartz³

2023

Front. Med.

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Autoimmune disorders have been well characterized over the years and many pathways—but not all of them–have been found to explain their pathophysiology. Autoinflammatory disorders, on the other hand, are still hiding most of their molecular and cellular mechanisms. During the past few years, a newcomer has challenged the idea that only adaptive immunity could display memory response. Trained immunity is defined by innate immune responses that are faster and stronger to a second stimulus than to the first one, being the same or not. In response to the trained immunity inducer, and through metabolic and epigenetic changes of hematopoietic stem and progenitor cells in the bone marrow that are transmitted to their cellular progeny (peripheral trained immunity), or directly of tissue-resident cells (local innate immunity), innate cells responsiveness and functions upon stimulation are improved in the long-term. Innate immunity can be beneficial, but it could also be detrimental when maladaptive. Here, we discuss how trained immunity could contribute to the physiopathology of autoimmune and autoinflammatory diseases.

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Section: Rheumatoid Arthritismentioning

confidence: 99%

Trained immunity as a possible newcomer in autoinflammatory and autoimmune diseases pathophysiology

Beignon

Galeotti²,

Schvartz³

2023

Front. Med.

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“…López-Rodríguez et al (2018) provide evidence that the methotrexate treatment efficacy is associated with the polymorphism of the A-allele MTRR-rs1801394 in the patient [37]. It is also related to genetic variants SLC19A1-rs1051266, DHFR-rs836788 and TYMS-rs2244500 [38]. Methotrexate is an antimetabolite, similar in structure to folic acid, and its accumulation in the body provokes an antiproliferative effect by depleting the intracellular folate depot [39].…”

Section: Ra Therapy Strategy: Principles and Mechanisms The Significa...mentioning

confidence: 99%

Peripheral blood lymphocytes apoptosis role in rheumatoid arthritis progressing

Aringazina,

Seitmaganbetova,

Mussina

et al. 2023

J CLIN MED KAZ

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Rheumatoid arthritis (RA) is an autoimmune, chronic, and genetically linked inflammatory lesion of joint tissues that is accompanied by extra-articular systemic pathologies. The disease progression leads to joints immobilization, and eventually, the patient's disability occurs approximately ten years from the first clinical manifestation. RA pathogenesis involves various mechanisms: specific joint-related damage, nonspecific adaptive, and vessel-related pathological changes. Our research aimed to study the role of peripheral blood lymphocyte apoptosis in RA pathogenesis. We have analyzed research data from Google Scholar, PubMed, Web of Science, and Scopus databases to investigate the role of lymphocyte apoptosis in RA progression. Clinical manifestations in RA are caused by autoreactive T- and B-lymphocyte activity supported by humoral and cellular immune factors activity. Disease pathogenesis is caused by an imbalance in the process of programmed cell death (apoptosis): a proportion of immune cells are rapidly destroyed. In contrast, apoptosis is inhibited in the other classes of immune cells. High infiltration of the joint by autoreactive sensitized lymphocytes worsens the patient's condition. Apoptosis inhibition is especially noticeable in the early stages of RA and correlates with the concentration of the anti-apoptotic molecule Bcl-2 in the synovia. Activating the apoptotic destruction of lymphocytes (by drug action) allows a positive therapeutic effect and sustained remission. However, it should be noted that genetic factors play a significant role in the onset, progression and drug response of RA. In addition, environmental and behavioral factors can activate RA progression and influence treatment efficacy.

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“…Systematic literature reviews and meta-analyses of clinical studies continue to highlight the heterogeneity in RA and the need for new biomarkers predictive of therapeutic response beyond data available to clinicians when selecting a new RA therapy at the point of care [ 2 – 6 ]. Several biomarkers and clinical factors may be weakly predictive in groups of patients; yet singly or in combination these are not strong enough to guide treatment selection for individuals.…”

Section: Main Commentarymentioning

confidence: 99%

Commentary on Cohen et al.: Role of Clinical Factors in Precision Medicine Test to Predict Nonresponse to TNFi Therapies in Rheumatoid Arthritis

Cohen

Curtis

Mellors³

et al. 2022

Rheumatol Ther

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A 2021 study described the development and validation of a blood-based precision medicine test called the molecular signature response classifier (MSRC) that uses 23 features to identify rheumatoid arthritis (RA) patients who are likely nonresponders to tumor necrosis factor-a inhibitor (TNFi) therapy. Both the gene expression features and clinical components (sex, body mass index, patient global assessment, and anti-cyclic citrullinated protein) included in the MSRC were statistically significant contributors to MSRC results. In response to continued inquiries on this topic, we write this letter to provide additional insights into the contribution of clinical components to the MSRC on the Network-004 validation cohort.

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-Omic Approaches and Treatment Response in Rheumatoid Arthritis

Cited by 6 publications

References 108 publications

Trained immunity as a possible newcomer in autoinflammatory and autoimmune diseases pathophysiology

Trained immunity as a possible newcomer in autoinflammatory and autoimmune diseases pathophysiology

Peripheral blood lymphocytes apoptosis role in rheumatoid arthritis progressing

Commentary on Cohen et al.: Role of Clinical Factors in Precision Medicine Test to Predict Nonresponse to TNFi Therapies in Rheumatoid Arthritis

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