CD4<sup>+</sup> TSCMs in the Bone Marrow Assist in Maturation of Antibodies against Influenza in Mice

Wu, Kang; Wang, Fei; Guo, Guangwu; Li, Yuqing; Qiu, Lijun; Li, Xuefeng

doi:10.1155/2019/3231696

Cited by 4 publications

(6 citation statements)

References 45 publications

(44 reference statements)

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“…Cluster 7 is composed of M1-like macrophages that express CD64, F4-80, MHCII, and CX3CR1. Cluster 5 was characterized by CD90.2 + Sca1 + CD45 + , with lower levels of CD44, CD69, and CD86 expression, indicating they could be CD8 + memory T cells or NKT cells ( 54 , 55 ). Because the myeloid panel lacks CD4 or CD8, it is still unclear whether cluster 5 was composed of CD4 or CD8 subsets.…”

Section: Resultsmentioning

confidence: 99%

“…tumors appear to be selectively depleted of stem-like CD8 + T cells and NK cells, both important for tumor control when activated. ( 50), ( 51), ( 52 Cluster 5 was characterized by CD90.2 + Sca1 + CD45 + , with lower levels of CD44, CD69 and CD86 expression, indicating they could be CD8 + memory T cells or NKT cells (54), (55). Because the myeloid panel lacks CD4 or CD8, it is still unclear whether the cluster 5 comprised of CD4 or CD8 subsets.…”

Section: Overexpression Of Mmp2 In B16 Cells Accelerates Tumor Growth and Promotes A Protumorigenic Tmementioning

confidence: 99%

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MMP2 and TLRs modulate immune responses in the tumor microenvironment

et al. 2021

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The presence of an immunosuppressive tumor microenvironment is a major obstacle in the success of cancer immunotherapies. Because extracellular matrix components can shape the microenvironment, we investigated the role of matrix metalloproteinase 2 (MMP2) in melanoma tumorigenesis. Significantly, we found that MMP2 signals pro-inflammatory pathways on antigen presenting cells which requires both toll-like receptor (TLR) 2 and TLR4. B16 melanoma cells that express MMP2 at baseline have slower kinetics in Tlr2 -/-Tlr4 -/mice, implicating MMP2 in promoting tumor growth. Indeed, Mmp2 overexpression in B16 cells potentiated rapid tumor growth which was accompanied by reduced intra-tumoral cytolytic cells and increased M2 macrophages. In contrast, knockdown of Mmp2 slowed tumor growth, and enhanced T cell proliferation and NK cell recruitment. Finally we found that these effects of MMP2 are mediated through dysfunctional dendritic cell (DC) -T cell cross-talk as they are lost in Batf3 -/and Rag2 -/mice, respectively. These findings provide insights into the detrimental role of endogenous alarmins like MMP2 in modulating immune responses in the tumor microenvironment.

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Section: Resultsmentioning

confidence: 99%

Section: Overexpression Of Mmp2 In B16 Cells Accelerates Tumor Growth and Promotes A Protumorigenic Tmementioning

confidence: 99%

MMP2 and TLRs modulate immune responses in the tumor microenvironment

et al. 2021

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“…Immunofluorescence staining was performed as previously described ( Wu et al, 2019b ). Briefly, tumor and animal tissues were fixed with paraformaldehyde, dehydrated, and cleared with a gradient of alcohol solutions and xylene, respectively.…”

Section: Methodsmentioning

confidence: 99%

Targeting TIGIT Inhibits Bladder Cancer Metastasis Through Suppressing IL-32

Zeng

Xiao-li

et al. 2022

Front. Pharmacol.

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Bladder cancer is a highly metastatic tumor and one of the most common malignancies originating in the urinary tract. Despite the efficacy of immune checkpoints, including programmed cell death-1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), the effect of immunotherapy for bladder cancer remains unsatisfactory. Therefore, it is urgent to develop new targets to expand immunotherapeutic options. In this study, we utilized single-cell sequencing to explore the cell composition of tumors and detected a subset of Treg cells with high expression of T-cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) and interleukin (IL)-32. The antitumor immune response was suppressed by this subset of Treg cells, while IL-32 promoted bladder cancer metastasis. Nevertheless, targeting TIGIT not only reversed immunosuppression by restoring the antitumor immune response mediated by T cells but also suppressed the secretion of IL-32 and inhibited the metastasis of bladder cancer cells. Thus, our study provided novel insights into immunosuppression in bladder cancer and highlighted TIGIT as a novel target for immunotherapy of bladder cancer. We also illustrated the mechanism of the dual effect of targeting TIGIT and revealed the metastasis-promoting effect of IL-32 in bladder cancer. Collectively, these findings raise the possibility of utilizing TIGIT as a target against bladder cancer from the bench to the bedside.

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“…They express stem cell antigen-1 (Sca-1, CD122) and B-cell lymphoma protein-2 (Bcl-2), and they relocate, after their vigorous response to blood-borne antigens, to the BM by adhesion molecules VCAM-1, P-selectin glycoprotein 1, and P-selectin or E-selectin [49]. The natural CD4+ TSCMs in the BM colocalize with VCAM-1+, IL-15+, IL-7+, and CXCL-12+ stromal cells [50]. In contrast to spleen-resident CD4+ TSCMs, the BM resident TSCMs are able to assist in the maturation of antibodies [50].…”

Section: Stem-like Memory T Cells In Bm Parenchymamentioning

confidence: 99%

Bone Marrow: The Central Immune System

Schirrmacher¹

2023

Immuno

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Bone marrow is known as the site of hematopoiesis. What is not being described in textbooks of immunology is the fact that bone marrow is not only a generative, but also an antigen-responsive, immune organ. It is also a major storage site for antigen-specific memory B and T cells. That bone marrow is a priming site for T cell responses to blood borne antigens was discovered exactly 20 years ago. This review celebrates this important discovery. The review provides a number of examples of medical relevance of bone marrow as a central immune system, including cancer, microbial infections, autoimmune reactions, and bone marrow transplantation. Bone marrow mesenchymal stem cell-derived stromal cells provide distinct bone marrow niches for stem cells and immune cells. By transmitting anti-inflammatory dampening effects, facilitating wound healing and tissue regeneration mesenchymal stem cells contribute to homeostasis of bone and other tissues. Based on the evidence presented, the review proposes that bone marrow is a multifunctional and protective immune system. In an analogy to the central nervous system, it is suggested that bone marrow be designated as the central immune system.

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CD4⁺ TSCMs in the Bone Marrow Assist in Maturation of Antibodies against Influenza in Mice

Cited by 4 publications

References 45 publications

MMP2 and TLRs modulate immune responses in the tumor microenvironment

MMP2 and TLRs modulate immune responses in the tumor microenvironment

Targeting TIGIT Inhibits Bladder Cancer Metastasis Through Suppressing IL-32

Bone Marrow: The Central Immune System

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CD4+ TSCMs in the Bone Marrow Assist in Maturation of Antibodies against Influenza in Mice

Cited by 4 publications

References 45 publications

MMP2 and TLRs modulate immune responses in the tumor microenvironment

MMP2 and TLRs modulate immune responses in the tumor microenvironment

Targeting TIGIT Inhibits Bladder Cancer Metastasis Through Suppressing IL-32

Bone Marrow: The Central Immune System

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Product

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CD4⁺ TSCMs in the Bone Marrow Assist in Maturation of Antibodies against Influenza in Mice