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Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity [TCR-Seq]

ABSTRACT: To investigate the clonality of tumor Treg cells, we performed TCRseq on tumor Treg cells from Apc Min/+ mice versus normal colonic Treg cells from WT mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE271765 | GEO | 2024/07/18

REPOSITORIES: GEO

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Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity [RNA-seq]

Project description:To investigate the mechanism by which Treg cell positioning is regulated in our manuscript,we performed RNAseq on tumor Treg cells from Apc Min/+ Foxp3 DTR mice versus normal colonic Treg cells from Foxp3 DTR mice.

2024-07-18 | GSE234180 | GEO

Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity [scRNA-seq]

Project description:Tumor microenvironment (TME) plays critical roles in both tumor progression and immunotherapeutic efficacy. Here using single-cell RNA sequencing (scRNA-seq), we described the TME heterogeneity and found a specific state of CCL22+ dendritic cell (mregDC) cross talk close to regulatory T cells (Treg). We analyzed cell–cell communication mediated by ligand–receptor interactions and finally found that mregDCs probably attract Treg cells via chemotaxis and physically interact with them in tumor. Within this cross talk, Treg cells received activation signals from mregDCs and upregulated suppressive and adhesion molecules, including PD-1, ICOS, CTLA-4 and OX-40, further enhancing their interaction with mregDCs. In turn, the association of Treg cells with mregDCs restrained the trafficking of tumor antigen-bearing dendritic cells to draining mesenteric lymph nodes and thus dampened the presentation of tumor antigens to initiate anti-tumor immune responses in a cell contact dependent manner.

2024-07-18 | GSE234182 | GEO

Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-18 | GSE234186 | GEO

Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity [TCR-Seq]

Project description:Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity [TCR-Seq]

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Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity

Project description:Lymphatic-localized Treg-mregDC crosstalk limits antigen trafficking and restrains anti-tumor immunity

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AIM2 in regulatory T (Treg) cells restrains autoimmune diseases

Project description:The inflammasome initiates innate defense and inflammatory response by activating caspase-1 and pyroptotic cell death in myeloid cells1,2. It is comprised of an innate immune receptor/effector, pro-caspase-1 and a common adaptor molecule, ASC (apoptotic speck-containing protein with a CARD). Consistent with their pro-inflammatory function, inflammasome components including caspase-1, ASC and NLRP3, are known to exacerbate autoimmunity during experimental autoimmune encephalomyelitis (EAE) by enhancing IL-1 and IL-18 secretion in myeloid cells3-6. Here we show an unexpected function of a DNA-binding inflammasome effector, AIM2 (Absent in Melanoma 2)7-10, in restraining autoimmunity by performing EAE in both whole body and Treg-specific deletion of Aim2–/– mice. AIM2 is highly expressed by human and mouse Treg cells and it is essential to attenuate EAE. RNA-seq, biochemical and metabolic analyses revealed that AIM2 attenuates mTOR, Myc and immune-metabolic functions in both Treg cells isolated in vivo and Treg cells induced in vitro with TGF-. Importantly, we found AIM2 physically interacted with RACK1 in Treg cells to facility the PP2A/RACK1/Akt-mTOR signaling, which is identified as a central component downstream of AIM2 that controls Treg cell function and stability. While AIM2 is generally accepted as an inflammasome effector in myeloid cells, this report reveals a previously unappreciated T cell-intrinsic role of AIM2 in maintaining Treg cell function to restrain autoimmunity. This is achieved by diminishing Akt-mTOR signaling to regulate Treg stability under inflammation, and altering immune-metabolism in Treg cells.

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Project description:In the musculoskeletal system, lymphatic vessels (LVs), which are interdigitated with blood vessels, travel and form an extensive transport network. Blood vessels in bone regulate osteogenesis and hematopoiesis, however, whether LVs in bone affect fracture healing is unclear. Here, we investigate the lymphatic draining function at the tibial fracture sites using near-infrared indocyanine green lymphatic imaging (NIR-ICG) and discover that lymphatic drainage insufficiency (LDI) starts on day one and persists for up to two weeks following the fracture in male mice. Sufficient lymphatic drainage facilitates fracture healing in male mice. Furthermore, we identify that lymphatic platelet thrombosis (LPT) blocks the draining lymphoid sinus and LVs, causes LDI, and inhibits fracture healing in male mice, which can be rescued by a blood thinner. Moreover, unblocked lymphatic drainage decreases neutrophils and increases M2-type macrophages of the hematoma niche to support osteoblast (OB) survival and bone marrow-derived mesenchymal stem cell (BMSC) proliferation via transporting damage-associated molecular patterns (DAMPs) in male rats. Lymphatic platelet thrombolysis also benefits senile fracture healing in female mice. These findings demonstrate that LPT limits bone regeneration by impeding lymphatic transporting DAMPs. Together, these findings represent a way forward in the treatment of bone repair.

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