Tim-3 Relieves Experimental Autoimmune Encephalomyelitis by Suppressing MHC-II

Tang, Lili; Li, Ge; Yang, Zheng; Hou, Chunmei; Gao, Yang; Hao, Ying; Gao, Zhenfang; Mo, Rongliang; Li, Yuxiang; Shen, Beifen; Wang, Renxi; Wang, Zhiding; Han, Gencheng

doi:10.3389/fimmu.2021.770402

Cited by 6 publications

(2 citation statements)

References 33 publications

(51 reference statements)

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“…During glioma progression, tumor cells modulate the expression profile of immune checkpoint molecules and their ligands [ 58 ]. TIM-3 receptor modulates microglia function and regulates the interaction of microglia with nerve cells [ 59 ]. Recent studies revealed that TIM-3 is a representative immune checkpoint molecule significantly overexpressed in gliomas [ 60 ].…”

Section: Tim-3 In Neoplasmsmentioning

confidence: 99%

TIM-3 as a promising target for cancer immunotherapy in a wide range of tumors

Sauer,

Janicka,

Szlasa

et al. 2023

Cancer Immunol Immunother

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T-cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) expression has been a trending topic in recent years due to its differential expression in a wide range of neoplasms. TIM-3 is one of the key immune checkpoint receptors that interact with GAL-9, PtdSer, HMGB1 and CEACAM1. Initially identified on the surface of T helper 1 (Th1) lymphocytes and later on cytotoxic lymphocytes (CTLs), monocytes, macrophages, natural killer cells (NKs), and dendritic cells (DCs), TIM-3 plays a key role in immunoregulation. Recently, a growing body of evidence has shown that its differential expression in various tumor types indicates a specific prognosis for cancer patients. Here, we discuss which types of cancer TIM-3 can serve as a prognostic factor and the influence of coexpressed immune checkpoint inhibitors, such as LAG-3, PD-1, and CTLA-4 on patients' outcomes. Currently, experimental medicine involving TIM-3 has significantly enhanced the anti-tumor effect and improved patient survival. In this work, we summarized clinical trials incorporating TIM-3 targeting monoclonal and bispecific antibodies in monotherapy and combination therapy and highlighted the emerging role of cell-based therapies.

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Section: Tim-3 In Neoplasmsmentioning

confidence: 99%

TIM-3 as a promising target for cancer immunotherapy in a wide range of tumors

Sauer,

Janicka,

Szlasa

et al. 2023

Cancer Immunol Immunother

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“…The role of Tim-3 in Mφs is complicated and controversial under different microenvironment conditions. For instance, it was reported that Tim-3 inhibits the autoantigen presentation of Mφs by suppressing MHC-II expression, inducing immune tolerance in multiple sclerosis [ 11 ]. Meanwhile, in diabetic nephropathy, Tim-3 was also found to promote Mφ activation and aggravate podocyte injury [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Tim-3 Coordinates Macrophage-Trophoblast Crosstalk via Angiogenic Growth Factors to Promote Pregnancy Maintenance

Cui

Sun

et al. 2023

IJMS

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T-cell immunoglobulin mucin-3 (Tim-3) is an important checkpoint that induces maternal–fetal tolerance in pregnancy. Macrophages (Mφs) play essential roles in maintaining maternal–fetal tolerance, remodeling spiral arteries, and regulating trophoblast biological behaviors. In the present study, the formation of the labyrinth zone showed striking defects in pregnant mice treated with Tim-3 neutralizing antibodies. The adoptive transfer of Tim-3+Mφs, rather than Tim-3-Mφs, reversed the murine placental dysplasia resulting from Mφ depletion. With the higher production of angiogenic growth factors (AGFs, including PDGF-AA, TGF-α, and VEGF), Tim-3+dMφs were more beneficial in promoting the invasion and tube formation ability of trophoblasts. The blockade of AGFs in Tim-3+Mφs led to the narrowing of the labyrinthine layer of the placenta, compromising maternal–fetal tolerance, and increasing the risk of fetal loss. Meanwhile, the AGFs-treated Tim-3-Mφs could resolve the placental dysplasia and fetal loss resulting from Mφ depletion. These findings emphasized the vital roles of Tim-3 in coordinating Mφs-extravillous trophoblasts interaction via AGFs to promote pregnancy maintenance and in extending the role of checkpoint signaling in placental development. The results obtained in our study also firmly demonstrated that careful consideration of reproductive safety should be taken when selecting immune checkpoint and AGF blockade therapies in real-world clinical care.

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