IL-2/IL-2R Antibody Complex Enhances Treg-Induced Neuroprotection by Dampening TNF-α Inflammation in an In Vitro Stroke Model

Borlongan, Mia C.; Kingsbury, Chase; Salazar, Felipe Esparza; Toledo, Alma R. Lezama; Monroy, Germán Rivera; Sadanandan, Nadia; Cozene, Blaise; Gonzales-Portillo, Bella; Saft, Madeline; Wang, Zhen-Jie; Moscatello, Alexa; Lee, Jea Y.

doi:10.1007/s12017-021-08656-0

Cited by 10 publications

(3 citation statements)

References 36 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Amoxicillin treatment demonstrates reduced infarct volumes and functional deficits 53 . Other methods targeting Treg differentiation from microbiome activation may be beneficial as well, such as IL‐2/IL‐2R antibody complexes 54 . Normalizing the microbiome may be a novel direction for research initiatives in regulating GBA communications following stroke.…”

Section: Managing the Microbiomementioning

confidence: 99%

Getting the guts to expand stroke treatment: The potential for microbiome targeted therapies

et al. 2022

View full text Add to dashboard Cite

Aims This review focuses on the recent literature regarding the role of the gut‐brain axis (GBA) following ischemic stroke. Discussion Stroke is the 5th leading cause of death and disability in the United States; however, few therapies have been developed to improve prognoses. There is a plethora of evidence suggesting peripheral inflammatory responses play a large role in the pathogenesis of stroke. Additionally, hyperglycemic conditions may play a significant role in worsening stroke outcomes due to microbiome dysbiosis. Conclusion Recent research has illuminated the vital role of the GBA in propagating poor clinical outcomes, such as hemorrhagic transformation, following ischemic stroke. Considering this detrimental consequence of stroke, and the apparent role of the GBA role, future therapeutics should aim to mitigate this peripheral contribution to stroke complications.

show abstract

Section: Managing the Microbiomementioning

confidence: 99%

Getting the guts to expand stroke treatment: The potential for microbiome targeted therapies

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Promotes neuroprotection and repair by enhancing the survival and differentiation of neural stem cells and neurons [12] IL-4…”

Section: Il-2mentioning

confidence: 99%

Autoimmune Neuroinflammatory Diseases: Role of Interleukins

Khan

Farooq

Hwang

et al. 2023

IJMS

View full text Add to dashboard Cite

Autoimmune neuroinflammatory diseases are a group of disorders resulting from abnormal immune responses in the nervous system, causing inflammation and tissue damage. The interleukin (IL) family of cytokines, especially IL-1, IL-6, and IL-17, plays a critical role in the pathogenesis of these diseases. IL-1 is involved in the activation of immune cells, production of pro-inflammatory cytokines, and promotion of blood-brain barrier breakdown. IL-6 is essential for the differentiation of T cells into Th17 cells and has been implicated in the initiation and progression of neuroinflammation. IL-17 is a potent pro-inflammatory cytokine produced by Th17 cells that plays a crucial role in recruiting immune cells to sites of inflammation. This review summarizes the current understanding of the roles of different interleukins in autoimmune neuroinflammatory diseases, including multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer’s disease, neuromyelitis optica, and autoimmune encephalitis, and discusses the potential of targeting ILs as a therapeutic strategy against these diseases. We also highlight the need for further research to better understand the roles of ILs in autoimmune neuroinflammatory diseases and to identify new targets for treating these debilitating diseases.

show abstract

“…In the meantime, the researchers are still working to develop other types of inhibitors to improve stroke outcomes. For example, the IL-2/IL-2R antibody complex enhances Treg-induced neuroprotective effects by inhibiting TNF-α induced inflammation [95]. Contreras et al proposed that the trimer TNF-R2 extracellular domain might be an innovative TNF-α antagonist [96].…”

Section: Tnf-α Inhibitorsmentioning

confidence: 99%

Tumor Necrosis Factor-α: The Next Marker of Stroke

Xue

Zeng

et al. 2022

Disease Markers

View full text Add to dashboard Cite

Although there is no shortage of research on the markers for stroke, to our knowledge, there are no clear markers that can meet the needs of clinical prediction and treatment. The inflammatory cascade is a critical process that persists and functions throughout the stroke process, ultimately worsening stroke outcomes and increasing mortality. Numerous inflammatory factors, including tumor necrosis factor (TNF), are involved in this process. These inflammatory factors play a dual role during stroke, and their mechanisms are complex. As one of the representatives, TNF is the primary regulator of the immune system and plays an essential role in the spread of inflammation. In researches done over the last few years, tumor necrosis factor-alpha (TNF-α) has emerged as a potential marker for stroke because of its essential role in stroke. This review summarizes the latest research on TNF-α in stroke and explores its potential as a therapeutic target.

show abstract

IL-2/IL-2R Antibody Complex Enhances Treg-Induced Neuroprotection by Dampening TNF-α Inflammation in an In Vitro Stroke Model

Cited by 10 publications

References 36 publications

Getting the guts to expand stroke treatment: The potential for microbiome targeted therapies

Getting the guts to expand stroke treatment: The potential for microbiome targeted therapies

Autoimmune Neuroinflammatory Diseases: Role of Interleukins

Tumor Necrosis Factor-α: The Next Marker of Stroke

Contact Info

Product

Resources

About