Stimulation of Camel Polyclonal Antibody against Human T cell Immunoglobulin and Mucin 3

Homayouni, Vida; Khanahmad, Hossein; Ganjalikhani‐Hakemi, Mazdak; Behdani, Mahdi; Ghasemi, Pouria; Rezaei, Abbas

doi:10.15171/ijb.1427

Cited by 4 publications

(7 citation statements)

References 22 publications

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“…TIM-3 as a co-inhibitory molecule plays important and complex roles in regulating immune responses and in inducing immune tolerance (7,13). The extracellular part of TIM-3 includes a mucin domain and an IgV domain, which have glycosylated sites and bind to ligands of TIM-3 (12,14,15).…”

Section: Ligands Of Tim-3mentioning

confidence: 99%

“…The TIM-3-Gal-9 interaction plays significant roles in the consequences of infection, inflammation, peripheral tolerance, tumor immunity, and autoimmunity, and evidence shows that this interaction suppresses the response of immune cells (14,17). Also, TIM-3 signaling induced by Gal-9 ligation causes exhaustion and apoptosis of antigen-specific Th1 cells and CTLs through the calcium-calpain-caspase-1 pathway, which correlates with the impaired antitumor immune response (7,13,18). Collectively, data show that the TIM-3-Gal-9 interaction can act via different mechanisms and on different cell types to suppress immune responses.…”

Section: Ligands Of Tim-3mentioning

confidence: 99%

“…The biological relationship between the TIM-3 and PtdSer in T cells is unknown as T cells do not have a role in removing apoptotic bodies, but it seems that the interaction of TIM-3 with PtdSer can be effective in the production of IL-10 by T cells because IL-10 has been demonstrated to be expressed by TIM-3 + T cells ( Figure 1B) (20). The HMGB1 as a damage-associated molecular pattern (DAMP) that binds to DNA released from dying cells boosts nucleic acid sensing by toll-like receptors (TLRs), but during chronic infection and cancers, due to HMGB1 binding to TIM-3 expressed on APCs, it seems that this interaction suppresses innate immune responses to the nucleic acid ( Figure 1A) (13,21). CEACAM1 is another newly identified ligand for TIM-3 that is co-expressed with TIM-3 in T cells and also is expressed by DCs and other APCs ( Figure 1B).…”

Section: Ligands Of Tim-3mentioning

confidence: 99%

“…Recent studies have shown that TIM-3 expressed on T cells and cancer stem cells also suppresses immune responses through inducing the development of myeloid-derived suppressor cells (MDSCs) that are a heterogeneous CD11b + Gr-1 + myeloid cell population. Blocking of TIM-3 has been shown to reduce the number of MDSCs; increase the production of IL-6, IFN-g, and TNF-a; and restore effector functions of exhausted CD8 + T cells and their antitumor activity (13,19,31). Furthermore, TIM-3 is expressed on Foxp3 + Tregs, and the interaction of Gal-9 with TIM-3 + in these cells enhances the regulatory function of Tregs, such as the robust expression of IL-10, perforin, granzyme A, granzyme G, and CD39 (9,18,20).…”

Section: The Effect Of Tim-3 On Adaptive Immune Cellsmentioning

confidence: 99%

“…For example, it has been seen that TIM-3 negative bone marrow-derived DCs (BMDCs), in comparison with TIM-3 + DCs, show an impaired function phenotype and exhibit a much poorer capacity to express IFN-b1, IFN-a, and IL-6 cytokines (9, 20). Also, in TME, TIM-3 expression is induced on resident DCs so TIM-3 + myeloid cells may act as a molecular sink for HGMB1, which can also be secreted by tumor cells (13,21). When TIM-3 binds to HMGB1, the transport of nucleic acids into endosomes is blocked; thus, the pattern-recognition receptor-mediated innate immune responses against tumor-derived nucleic acids is suppressed (55).…”

Section: The Effect Of Tim-3 On Innate Immune Cellsmentioning

confidence: 99%

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The Role of TIM-3 in Hepatocellular Carcinoma: A Promising Target for Immunotherapy?

et al. 2020

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One of the most common tumors in the world is hepatocellular carcinoma (HCC), and its mortality rates are still on the rise, so addressing it is considered an important challenge for universal health. Despite the various treatments that have been developed over the past decades, the prognosis for advanced liver cancer is still poor. Recently, tumor immunotherapy has opened new opportunities for suppression of tumor progression, recurrence, and metastasis. Besides this, investigation into this malignancy due to high immune checkpoint expression and the change of immunometabolic programming in immune cells and tumor cells is highly considered. Because anti-cytotoxic T lymphocyte–associated protein (CTLA)-4 antibodies and anti-programmed cell death protein (PD)-1 antibodies have shown therapeutic effects in various cancers, studies have shown that T cell immunoglobulin mucin-3 (TIM-3), a new immune checkpoint molecule, plays an important role in the development of HCC. In this review, we summarize the recent findings on signal transduction events of TIM-3, its role as a checkpoint target for HCC therapy, and the immunometabolic situation in the progression of HCC.

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Section: Ligands Of Tim-3mentioning

confidence: 99%

Section: Ligands Of Tim-3mentioning

confidence: 99%

Section: Ligands Of Tim-3mentioning

confidence: 99%

Section: The Effect Of Tim-3 On Adaptive Immune Cellsmentioning

confidence: 99%

Section: The Effect Of Tim-3 On Innate Immune Cellsmentioning

confidence: 99%

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The Role of TIM-3 in Hepatocellular Carcinoma: A Promising Target for Immunotherapy?

et al. 2020

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Cancer Stem Cells—Origins and Biomarkers: Perspectives for Targeted Personalized Therapies

et al. 2020

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The use of biomarkers in diagnosis, therapy and prognosis has gained increasing interest over the last decades. In particular, the analysis of biomarkers in cancer patients within the pre- and post-therapeutic period is required to identify several types of cells, which carry a risk for a disease progression and subsequent post-therapeutic relapse. Cancer stem cells (CSCs) are a subpopulation of tumor cells that can drive tumor initiation and can cause relapses. At the time point of tumor initiation, CSCs originate from either differentiated cells or adult tissue resident stem cells. Due to their importance, several biomarkers that characterize CSCs have been identified and correlated to diagnosis, therapy and prognosis. However, CSCs have been shown to display a high plasticity, which changes their phenotypic and functional appearance. Such changes are induced by chemo- and radiotherapeutics as well as senescent tumor cells, which cause alterations in the tumor microenvironment. Induction of senescence causes tumor shrinkage by modulating an anti-tumorigenic environment in which tumor cells undergo growth arrest and immune cells are attracted. Besides these positive effects after therapy, senescence can also have negative effects displayed post-therapeutically. These unfavorable effects can directly promote cancer stemness by increasing CSC plasticity phenotypes, by activating stemness pathways in non-CSCs, as well as by promoting senescence escape and subsequent activation of stemness pathways. At the end, all these effects can lead to tumor relapse and metastasis. This review provides an overview of the most frequently used CSC markers and their implementation as biomarkers by focussing on deadliest solid (lung, stomach, liver, breast and colorectal cancers) and hematological (acute myeloid leukemia, chronic myeloid leukemia) cancers. Furthermore, it gives examples on how the CSC markers might be influenced by therapeutics, such as chemo- and radiotherapy, and the tumor microenvironment. It points out, that it is crucial to identify and monitor residual CSCs, senescent tumor cells, and the pro-tumorigenic senescence-associated secretory phenotype in a therapy follow-up using specific biomarkers. As a future perspective, a targeted immune-mediated strategy using chimeric antigen receptor based approaches for the removal of remaining chemotherapy-resistant cells as well as CSCs in a personalized therapeutic approach are discussed.

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Nanobodies: Next Generation of Cancer Diagnostics and Therapeutics

2020

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The development of targeted medicine has greatly expanded treatment options and spurred new research avenues in cancer therapeutics, with monoclonal antibodies (mAbs) emerging as a prevalent treatment in recent years. With mixed clinical success, mAbs still hold significant shortcomings, as they possess limited tumor penetration, high manufacturing costs, and the potential to develop therapeutic resistance. However, the recent discovery of “nanobodies,” the smallest-known functional antibody fragment, has demonstrated significant translational potential in preclinical and clinical studies. This review highlights their various applications in cancer and analyzes their trajectory toward their translation into the clinic.

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Stimulation of Camel Polyclonal Antibody against Human T cell Immunoglobulin and Mucin 3

Cited by 4 publications

References 22 publications

The Role of TIM-3 in Hepatocellular Carcinoma: A Promising Target for Immunotherapy?

The Role of TIM-3 in Hepatocellular Carcinoma: A Promising Target for Immunotherapy?

Cancer Stem Cells—Origins and Biomarkers: Perspectives for Targeted Personalized Therapies

Nanobodies: Next Generation of Cancer Diagnostics and Therapeutics

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