ArticleClinical and experimental immunology2014
Blockade of the T cell immunoglobulin and mucin domain protein 3 pathway exacerbates sepsis-induced immune deviation and immunosuppression.
Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Serine protease inhibitor from Trichinella spiralis ameliorates diet-induced obesity and adipose tissue inflammation through TIM-3-dependent macrophage reprogramming.PLoS pathogens · 2026Article
- TIM-3, a potential target for sepsis therapy.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Review
- Tim-3 pathway dysregulation and targeting in sepsis-induced immunosuppression.European journal of medical research · 2024Review
- Lymphopenia in sepsis: a narrative review.Critical care (London, England) · 2024Review
- Review
- Clinical practice of sepsis-induced immunosuppression: Current immunotherapy and future options.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2024Review
- The role of TIM-3 in sepsis: a promising target for immunotherapy?Frontiers in immunology · 2024Review
- The Impact of Colistin Resistance on the Activation of Innate Immunity by Lipopolysaccharide Modification.Infection and immunity · 2023Article
- Tim-3 regulates sepsis-induced immunosuppression by inhibiting the NF-κB signaling pathway in CD4 T cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Early detection of soluble CD27, BTLA, and TIM-3 predicts the development of nosocomial infection in pediatric burn patients.Frontiers in immunology · 2022Observational
- TIM-3 Genetic Variants Are Associated with Altered Clinical Outcome and Susceptibility to Gram-Positive Infections in Patients with Sepsis.International journal of molecular sciences · 2020Article
- Immunological Endotyping of Chronic Critical Illness After Severe Sepsis.Frontiers in medicine · 2020Review
- Immune Checkpoints: Novel Therapeutic Targets to Attenuate Sepsis-Induced Immunosuppression.Frontiers in immunology · 2020Review
- Pathological alteration and therapeutic implications of sepsis-induced immune cell apoptosis.Cell death & disease · 2019Review
- Galectin-9 Alleviates LPS-Induced Preeclampsia-Like Impairment in Rats via Switching Decidual Macrophage Polarization to M2 Subtype.Frontiers in immunology · 2018Article
- Innate Immunity in the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome and Its Implications for Therapy.Frontiers in immunology · 2018Review
- Targeting Immune Cell Checkpoints during Sepsis.International journal of molecular sciences · 2017Review
- Sepsis and septic shock.Nature reviews. Disease primers · 2016Review
- Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening condition, but the pathophysiological basis and biomarkers for the monitoring of sepsis and as targets for therapy remain to be determined. We have shown previously that T cell immunoglobulin and mucin domain protein 3 (Tim-3), a negative immune regulator, is involved in the physiopathology of sepsis, but the underlying mechanisms remain unclear. In the present study, we showed that Tim-3 signalling modulated the response patterns of both macrophages and T helper cells in sepsis. Blockade of the Tim-3 pathway exacerbated sepsis-induced proinflammatory macrophage responses and lymphocyte apoptosis during the early phase of sepsis, and enhanced the shift to anti-inflammatory responses for both macrophages and T helper cells during the late phase of sepsis. Tim-3 signalling was found to regulate CD80 and CD86 expression on macrophages both in vivo and in vitro. Co-culture of T cells with Tim-3 knock-down macrophages led to a biased T helper type 2 (Th2) response, partially explaining how Tim-3 signalling shapes inflammation patterns in vivo. Further studies on this pathway might shed new light on the pathogenesis of sepsis and suggest new approaches for intervention.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.