A5102773240- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- T-cell and B-cell Immunology
- melanin and skin pigmentation
- Cancer Immunotherapy and Biomarkers
- Endoplasmic Reticulum Stress and Disease
- Autophagy in Disease and Therapy
- Phagocytosis and Immune Regulation
- Ginseng Biological Effects and Applications
- Biochemical Analysis and Sensing Techniques
- Cancer Cells and Metastasis
- Pancreatic and Hepatic Oncology Research
- TGF-β signaling in diseases
- Immune cells in cancer
- CAR-T cell therapy research
- Sports injuries and prevention
- Chemokine receptors and signaling
- Melanoma and MAPK Pathways
- Musculoskeletal pain and rehabilitation
- Balance, Gait, and Falls Prevention
- Pharmacological Receptor Mechanisms and Effects
- Adenosine and Purinergic Signaling
- Genetic factors in colorectal cancer
- Dermatology and Skin Diseases
- Circadian rhythm and melatonin
Cambridge Scientific (United States)
2019-2023
University of Arizona
2005-2020
Ohio University
2018
Infinity Pharmaceuticals (United States)
2016
University of Arizona Cancer Center
2015
University of Phoenix
2013-2015
Arizona Oncology
2010
Lafayette College
2004
University of Oklahoma
2002
CD39 (ENTPD1) is a key enzyme responsible for degradation of extracellular ATP and upregulated in the tumor microenvironment (TME). Extracellular accumulates TME from tissue damage immunogenic cell death, potentially initiating proinflammatory responses that are reduced by enzymatic activity CD39. Degradation other ectonucleotidases (e.g., CD73) results adenosine accumulation, constituting an important mechanism immune escape, angiogenesis induction, metastasis. Thus, inhibiting can inhibit...
Melanocyte differentiation Ags, including tyrosinase-related protein (TRP) 1, are relevant to both autoimmune skin depigmentation (vitiligo) and tumor immunity, because they expressed by benign melanocytes many malignant melanomas. Melanoma patients generate CD4(+) T cells that specifically recognize these proteins. TRP1 contains internal disulfide bonds is presented MHC class II molecules. Gamma-IFN-inducible lysosomal thiol reductase (GILT) facilitates the generation of II-binding peptides...
While the immune system has capacity to recognize and destroy melanoma, tolerance mechanisms often hinder development of effective anti-tumor responses. Since many melanoma antigens are self proteins expressed in normal melanocytes, antigen exposure before tumor can negatively impact function T cells specific for these self/tumor antigens. However, contribution anti-melanoma cell dysfunction remains largely unexplored. We have previously described a TCR transgenic (Tg) mouse model which...
Central tolerance prevents autoimmunity, but also limits T cell responses to potentially immunodominant tumor epitopes with limited expression in healthy tissues. In peripheral APCs, γ-IFN-inducible lysosomal thiol reductase (GILT) is critical for MHC class II-restricted presentation of disulfide bond-containing proteins, including the self-antigen and melanoma Ag tyrosinase-related protein 1 (TRP1). The role GILT thymic processing generation central has not been investigated. We found that...
In this study we were interested in investigating the extent to which stimulation through a chemokine receptor could modulate TCR function. We report that splenic T cells exposed secondary lymphoid‐tissue (SLC, CCL21) for 72, but not 2 or 24 hours, exhibited decreased ability produce IFN‐γ following CD3 crosslinking. Similar findings observed with CCL2 and CCL5. The decrease production was attributed cell viability, accompanied an increase IL‐4 production, be induced using G protein coupled...
Abstract Central tolerance is critical to prevent autoimmunity, but limits T cell responses tumor Ag that are self Ag. We have identified gamma-interferon-inducible lysosomal thiol reductase (GILT) required for thymic deletion of CD4+ cells specific the and melanoma Ag, tyrosinase-related protein 1 (TRP1). To define GILT’s role in central tolerance, we show GILT expression enriched APC capable mediating deletion, medullary epithelial (mTEC) dendritic cells. TRP1 restricted mTEC. facilitates...
Abstract Clonal deletion of thymocytes with high avidity for self-peptide:MHC complexes is critical the maintenance tolerance and prevention autoimmunity. We have shown that gamma-interferon-inducible lysosomal thiol reductase (GILT) required thymic T cells specific a self melanoma Ag, tyrosinase-related protein 1 (TRP1). To define GILT’s role in central tolerance, we show GILT expression enriched APC capable mediating deletion, medullary epithelial (mTEC) dendritic cells. TRP1 restricted to...
Abstract Regulating the balance between T cell activation and tolerance is essential for stimulating an anti-tumor immune response in controlling autoimmunity. We have shown that gamma-interferon-inducible lysosomal thiol reductase (GILT) required efficient MHC class II-restricted processing of epitope from melanoma antigen tyrosinase-related protein 1 (TRP1). Using CD4+ TRP1-specific receptor transgenic mice, here we demonstrate a novel function GILT regulation tolerance. cells are...
A concerted effort is underway to develop and deploy an open systems solution components of the Weather Surveillance Radar-1988 Doppler (WSR-88D). Several small working groups, or subteams, have been established focus on specific areas within each component. One these, Graphical User Interface (GUI) Team, consists a group individuals possessing specialized knowledge in some important aspect presently deployed WSR-88D Unit Control Position (UCP), human factors concepts, GUI design. The UCP...
Abstract Maintaining tolerance to skin-restricted antigens is critical for avoiding cutaneous autoimmunity. We have shown that gamma-interferon-inducible lysosomal thiol reductase (GILT) essential efficient MHC class II-restricted processing of the melanocyte differentiation antigen, tyrosinase-related protein 1 (TRP1). In GILT-/- TRP1-specific TCR transgenic (Tg) mice, CD4+ T cells escape thymic deletion, but do not induce autoimmune destruction melanocytes (vitiligo). Tg mice fewer...
Abstract Central tolerance prevents autoimmunity, but limits T cell responses to tumor antigens that are self antigens. In peripheral APCs, gamma-interferon-inducible lysosomal thiol reductase (GILT) is critical for MHC class II-restricted presentation of disulfide bond-containing proteins, including the and melanoma antigen tyrosinase-related protein 1 (TRP1). The role GILT in thymic processing generation central unknown. We found enhanced clonal deletion TRP1-specific thymocytes....
Abstract Central tolerance prevents autoimmunity, but also limits T cell responses to potentially immunodominant tumor epitopes with limited expression in healthy tissues. In peripheral antigen presenting cells (APCs), gamma-interferon-inducible lysosomal thiol reductase (GILT) is critical for MHC class II-restricted presentation of disulfide bond-containing proteins, including the self and melanoma tyrosinase-related protein 1 (TRP1). The role GILT thymic processing generation central has...