Tissue-resident immune cells in the pathogenesis of multiple sclerosis

Tian, Jie; Jiang, Lingli; Chen, Zixiang; Yuan, Qingfang; Liu, Chang; He, Longfeng; Jiang, Feng; Rui, Ke

doi:10.1007/s00011-022-01677-w

Cited by 3 publications

(3 citation statements)

References 102 publications

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“…The innate immune system, composed mainly of macrophages and microglia, is an effective defense system that can maintain homeostasis and protect the body from harmful stress. Its over-activation is known to be one of the main causes of various types of disorders, such as sepsis (Wen et al ., 2022), multiple sclerosis (Tian et al ., 2023), Alzheimer’s disease (Princiotta Cariddi et al ., 2022), and Parkinson’s disease (Lee et al ., 2022). In the pathogenesis of depression, over-activation of macrophages or microglia-mediated innate immune response in the brain, which may be associated with an abnormal hypothalamic-pituitary-adrenal (HPA) axis response that cues a higher risk to treatment resistance (Berardelli et al ., 2020), is also considered an important pathological process for the progression of depressive symptoms (Gallagher et al ., 2019; Wang et al ., 2022a).…”

Section: Introductionmentioning

confidence: 99%

Immunization with a low dose of zymosan A confers resistance to depression-like behavior and neuroinflammatory responses in chronically stressed mice

Liu,

Zhu,

Zhang

et al. 2024

Behavioural Pharmacology

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Stimulation of the innate immune system prior to stress exposure is a possible strategy to prevent depression under stressful conditions. Based on the innate immune system stimulating activities of zymosan A, we hypothesize that zymosan A may prevent the development of chronic stress-induced depression-like behavior. Our results showed that a single injection of zymosan A 1 day before stress exposure at a dose of 2 or 4 mg/kg, but not at a dose of 1 mg/kg, prevented the development of depression-like behaviors in mice treated with chronic social defeat stress (CSDS). The prophylactic effect of a single zymosan A injection (2 mg/kg) on CSDS-induced depression-like behaviors disappeared when the time interval between zymosan A and stress exposure was extended from 1 day or 5 days to 10 days, which was rescued by a second zymosan A injection 10 days after the first zymosan A injection and 4 days (4×, once daily) of zymosan A injections 10 days before stress exposure. Further analysis showed that a single zymosan A injection (2 mg/kg) 1 day before stress exposure could prevent the CSDS-induced increase in pro-inflammatory cytokines in the hippocampus and prefrontal cortex. Inhibition of the innate immune system by pretreatment with minocycline (40 mg/kg) abolished the preventive effect of zymosan A on CSDS-induced depression-like behaviors and CSDS-induced increase in pro-inflammatory cytokines in the brain. These results suggest that activation of the innate immune system triggered by zymosan A prevents the depression-like behaviors and neuroinflammatory responses in the brain induced by chronic stress.

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Section: Introductionmentioning

confidence: 99%

Immunization with a low dose of zymosan A confers resistance to depression-like behavior and neuroinflammatory responses in chronically stressed mice

Liu,

Zhu,

Zhang

et al. 2024

Behavioural Pharmacology

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“…8 In those circumstances, such as multiple sclerosis, rheumatoid arthritis, autoimmune hepatitis, psoriasis, and vitiligo, TRM cells can attack healthy cells and tissues, leading to chronic inflammation and tissue damage. [9][10][11][12][13] In recent years, the study of TRM cells has gained significant attention in the field of cancer immunotherapy. It has been shown that TRM cells are critical in providing protection against tumors, and their presence in tumor tissues is associated with better clinical outcomes.…”

Section: Introductionmentioning

confidence: 99%

“…However, autoreactive or aberrantly activated TRM cells contribute to the development of autoimmune or autoinflammation disorders 8 . In those circumstances, such as multiple sclerosis, rheumatoid arthritis, autoimmune hepatitis, psoriasis, and vitiligo, TRM cells can attack healthy cells and tissues, leading to chronic inflammation and tissue damage 9–13 …”

Section: Introductionmentioning

confidence: 99%

Tissue‐resident memory T cells in immunotherapy and immune‐related adverse events by immune checkpoint inhibitor

Xiong,

Shen

2024

Intl Journal of Cancer

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Tissue‐resident memory T cells (TRM) are a specialized subset of T cells that reside in tissues and provide long‐term protective immunity against pathogens that enter the body through that specific tissue. TRM cells have specific phenotype and reside preferentially in barrier tissues. Recent studies have revealed that TRM cells are the main target of immune checkpoint inhibitor immunotherapy since their role in cancer immunosurveillance. Furthermore, TRM cells also play a crucial part in pathogenesis of immune‐related adverse events (irAEs). Here, we provide a concise review of biological characteristics of TRM cells, and the major advances and recent findings regarding their involvement in immune checkpoint inhibitor immunotherapy and the corresponding irAEs.

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Cognate antigen-independent differentiation of resident memory T cells in chronic kidney disease

Moore,

Erman,

Traylor

et al. 2024

American Journal of Physiology-Renal Physiology

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Resident memory T cells (TRMs), which are memory T cells that are retained locally within tissues, have recently been described as antigen-specific frontline defenders against pathogens in barrier and non-barrier epithelial tissues. They have also been noted for perpetuating chronic inflammation. The conditions responsible for TRM differentiation are still poorly understood, and their contributions, if any, to sterile models of chronic kidney disease (CKD) remain a mystery. In this study we subjected male C57BL/6J mice and OT-1 transgenic mice to five consecutive days of 2mg/kg Aristolochic acid (AA) injections i.p. to induce CKD or saline injections as a control. We evaluated their kidney immune profiles at two weeks, six weeks, and six months after treatment. We identified a substantial population of TRMs in the kidneys of mice with AA-induced CKD. Flow cytometry of injured kidneys showed T cells bearing TRM surface markers and single cell RNA sequencing revealed these cells as expressing well-known TRM transcription factors and receptors responsible for TRM differentiation and maintenance. While kidney TRMs expressed Cd44, a marker of antigen experience and T cell activation, their derivation was independent of cognate antigen-T cell receptor interactions, as the kidneys of transgenic OT-1 mice still harbored considerable proportions of TRMs after injury. Our results suggest a non-antigen-specific or antigen-independent mechanism capable of generating TRMs in the kidney and highlight the need to better understand TRMs and their involvement in CKD.

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Tissue-resident immune cells in the pathogenesis of multiple sclerosis

Cited by 3 publications

References 102 publications

Immunization with a low dose of zymosan A confers resistance to depression-like behavior and neuroinflammatory responses in chronically stressed mice

Immunization with a low dose of zymosan A confers resistance to depression-like behavior and neuroinflammatory responses in chronically stressed mice

Tissue‐resident memory T cells in immunotherapy and immune‐related adverse events by immune checkpoint inhibitor

Cognate antigen-independent differentiation of resident memory T cells in chronic kidney disease

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