Timothy L. Ratliff
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View article: Folate receptor β performs an immune checkpoint function in activated macrophages
Folate receptor β performs an immune checkpoint function in activated macrophages Open
Monocytes and macrophages are sentinels of the immune system that distinguish themselves from other cells by expressing the beta isoform of the folate receptor (FRβ). Because FRβ does not bind folate until the monocyte/macrophage is expose…
View article: Immune dysregulation in the prostates of C57BL/6<sup>Aire-/-</sup>mice mirrors that seen in human benign prostatic hyperplasia
Immune dysregulation in the prostates of C57BL/6<sup>Aire-/-</sup>mice mirrors that seen in human benign prostatic hyperplasia Open
Benign prostatic hyperplasia (BPH) is the most common urologic disease in aging men, resulting in significant morbidity. The etiologies of BPH are unknown, though chronic prostatic inflammation is known to promote hyperplasia, fibrotic rem…
View article: Immune cell single-cell RNA sequencing analyses link an age-associated T cell subset to symptomatic benign prostatic hyperplasia
Immune cell single-cell RNA sequencing analyses link an age-associated T cell subset to symptomatic benign prostatic hyperplasia Open
Introduction Benign prostatic hyperplasia (BPH) is among the most common age-associated diseases in men. Prostatic immune cell infiltration is frequently observed with aging coincident with BPH; however, the contribution of age-related cha…
View article: Infiltrating lipid-rich macrophage subpopulations identified as a regulator of increasing prostate size in human benign prostatic hyperplasia
Infiltrating lipid-rich macrophage subpopulations identified as a regulator of increasing prostate size in human benign prostatic hyperplasia Open
Introduction Macrophages exhibit marked phenotypic heterogeneity within and across disease states, with lipid metabolic reprogramming contributing to macrophage activation and heterogeneity. Chronic inflammation has been observed in human …
View article: Immune cell single-cell RNA sequencing analyses link an age-associated T cell subset to symptomatic benign prostatic hyperplasia
Immune cell single-cell RNA sequencing analyses link an age-associated T cell subset to symptomatic benign prostatic hyperplasia Open
Benign prostatic hyperplasia (BPH) is among the most common age-associated diseases in men; however, the contribution of age-related changes in immune cells to BPH is not clear. The current study determined that an age-associated CD8 + T c…
View article: Infiltrating lipid-rich macrophage subpopulations identified as a regulator of increasing prostate size in human benign prostatic hyperplasia
Infiltrating lipid-rich macrophage subpopulations identified as a regulator of increasing prostate size in human benign prostatic hyperplasia Open
Macrophages exhibit marked phenotypic heterogeneity within and across disease states, with lipid metabolic reprogramming contributing to macrophage activation and heterogeneity. Chronic inflammation has been observed in human benign prosta…
View article: Tumor-specific activation of folate receptor beta enables reprogramming of immune cells in the tumor microenvironment
Tumor-specific activation of folate receptor beta enables reprogramming of immune cells in the tumor microenvironment Open
Folate receptors can perform folate transport, cell adhesion, and/or transcription factor functions. The beta isoform of the folate receptor (FRβ) has attracted considerable attention as a biomarker for immunosuppressive macrophages and my…
View article: Systemic Delivery of Paclitaxel by Find-Me Nanoparticles Activates Antitumor Immunity and Eliminates Tumors
Systemic Delivery of Paclitaxel by Find-Me Nanoparticles Activates Antitumor Immunity and Eliminates Tumors Open
Local delivery of immune-activating agents has shown promise in overcoming an immunosuppressive tumor microenvironment (TME) and stimulating antitumor immune responses in tumors. However, systemic therapy is ultimately needed to treat tumo…
View article: Supplementary Figures from Pharmacologic Inhibition of FGFR Modulates the Metastatic Immune Microenvironment and Promotes Response to Immune Checkpoint Blockade
Supplementary Figures from Pharmacologic Inhibition of FGFR Modulates the Metastatic Immune Microenvironment and Promotes Response to Immune Checkpoint Blockade Open
Supplementary Figures 1-8
View article: Supplementary Figure S1 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S1 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Combination of SHP099 and α-PD-L1 delays D2.A1 pulmonary growth in vivo
View article: Supplementary Figure S13 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S13 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Inhibition or depletion of SHP2 and PD-L1 blockade rescue T cell cytotoxicity.
View article: Supplementary Figure S10 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S10 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Representative dot plots for data shown in figure 4D-F and additional exhaustion marker analysis of CD8+ T cells in mice bearing SHP2 manipulated 4T1 metastases.
View article: Supplementary Tables S1-S7 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Tables S1-S7 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
These are supplementary tables to provide detailed information about the materials used in the study including cell, culture conditions, growth factors, inhibitors, and antibodies.
View article: Supplementary Figure S9 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S9 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Representative dot plots for data shown in figure 4B-C and additional exhaustion marker analysis of CD4+ T cells in mice bearing SHP2 manipulated 4T1 metastases.
View article: Supplementary Figure S15 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S15 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Growth factors and 3D culture environment induce PD-L1 in MBC cells.
View article: Supplementary Figure S6 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S6 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Depletion of SHP2 in tumor cells delays 4T1 pulmonary metastasis in vivo
View article: Supplementary Figure S2 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S2 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
The gating ancestry for the populations in the study of D2.A1 model
View article: Supplementary Figure S4 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S4 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Corresponding representative dot plots for the quantification in figure 2B-C and additional T cell exhaustion marker analysis in the study of D2.A1 model.
View article: Supplementary Figure S5 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S5 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Corresponding representative dot plots for the quantification in figure 2D-F and additional myeloid composition analysis in the study of D2.A1 model.
View article: Data from Pharmacologic Inhibition of FGFR Modulates the Metastatic Immune Microenvironment and Promotes Response to Immune Checkpoint Blockade
Data from Pharmacologic Inhibition of FGFR Modulates the Metastatic Immune Microenvironment and Promotes Response to Immune Checkpoint Blockade Open
The effectiveness of immunotherapy as a treatment for metastatic breast cancer is limited due to low numbers of infiltrating lymphocytes in metastatic lesions. Herein, we demonstrated that adjuvant therapy using FIIN4, a covalent inhibitor…
View article: Supplementary Figure S12 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S12 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Analyses of Tregs and macrophage scores in clinical datasets with respect to SHP2 phosphorylation.
View article: Supplementary Figure S16 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S16 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
SHP2 regulates MHC class I expression via the balance between MAPK and STAT1 signaling in human MBC cells.
View article: Supplementary Figure S1 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S1 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Combination of SHP099 and α-PD-L1 delays D2.A1 pulmonary growth in vivo
View article: Supplementary Tables S1-S7 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Tables S1-S7 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
These are supplementary tables to provide detailed information about the materials used in the study including cell, culture conditions, growth factors, inhibitors, and antibodies.
View article: Supplementary Figure S14 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S14 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
PD-L1 expression is induced by growth factor stimulation in the D2.A1 cells.
View article: Supplementary Figure S16 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S16 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
SHP2 regulates MHC class I expression via the balance between MAPK and STAT1 signaling in human MBC cells.
View article: Supplementary Figure S7 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S7 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
The gating ancestry for the populations in the study of 4T1 model
View article: Supplementary Figure S3 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer
Supplementary Figure S3 from Tumor Cell–Autonomous SHP2 Contributes to Immune Suppression in Metastatic Breast Cancer Open
Corresponding representative dot plots for the quantification in figure 2A and additional T cell composition analysis in the study of D2.A1 model.