A5054560533- Immune Cell Function and Interaction
- Diabetes and associated disorders
- T-cell and B-cell Immunology
- Pancreatic function and diabetes
- Helicobacter pylori-related gastroenterology studies
- Immune Response and Inflammation
- Diabetes Management and Research
- Immunotherapy and Immune Responses
- CAR-T cell therapy research
- Cytokine Signaling Pathways and Interactions
- Digestive system and related health
- IL-33, ST2, and ILC Pathways
- Multiple Sclerosis Research Studies
- Erythrocyte Function and Pathophysiology
- Celiac Disease Research and Management
- Historical Medical Research and Treatments
- Systemic Lupus Erythematosus Research
- Gut microbiota and health
- Hepatitis B Virus Studies
- Eosinophilic Esophagitis
- Diet and metabolism studies
- Atherosclerosis and Cardiovascular Diseases
- Adipokines, Inflammation, and Metabolic Diseases
- RNA regulation and disease
- Metabolism, Diabetes, and Cancer
James Cook University
2014-2024
Monash University
2022-2024
National Archaeology Museum
2023
Royal Netherlands Institute of Southeast Asian and Caribbean Studies
2023
University of Ottawa
2020
Baxter (Australia)
2012
Nottingham Biomedical Research Centre
2011
Baxter (United States)
2009
San Antonio College
2009
The University of Melbourne
2004
We have previously shown that nonobese diabetic (NOD) mice are selectively deficient in α/β-T cell receptor (TCR)+CD4−CD8− NKT cells, a defect may contribute to their susceptibility the spontaneous development of insulin-dependent diabetes mellitus (IDDM). The role cells protection from IDDM NOD was studied by infusion thymocyte subsets into young female mice. A single intravenous injection 106 CD4−/lowCD8− or CD4−CD8− thymocytes (BALB/c × NOD)F1 donors protected intact onset clinical IDDM....
The development of CD1d-dependent natural killer T (NKT) cells is poorly understood. We have used both CD1d/α-galactosylceramide (CD1d/αGC) tetramers and anti-NK1.1 to investigate NKT cell in vitro vivo. Confirming the thymus-dependence these cells, we show that CD1d/αGC tetramer-binding including NK1.1+ NK1.1− subsets, develop fetal thymus organ culture (FTOC) are completely absent nude mice. Ontogenically, first appear thymus, at day 5 after birth, as CD4+CD8−NK1.1−cells. CD4+ CD4−CD8−...
NK1.1+α βTCR+ (NKT) cells have several important roles including tumor rejection and prevention of autoimmune disease. Although both CD4+ CD4–CD8– double-negative (DN) subsets NKT been identified, they are usually described as one population. Here, we show that phenotypically, functionally developmentally heterogeneous, three distinct (CD4+, DN CD8+) differentially distributed in a tissue-specific fashion. CD8+ present all tissues but the thymus, highly enriched for CD8α+β– cells. These...
NOD mice develop spontaneous IDDM as a result of T-cell–mediated autoimmune destruction pancreatic β-cells. It is not known why these T-cells become autoreactive, nor it clear whether the breakdown in self-tolerance reflects general problem T-cell development or selective defect an yet undefined regulatory cell population. In this study, we showed that mice, although relatively normal with regard to most thymocyte subsets, exhibit marked deficiency αβTCR+CD4−CD8− (αβ+DN) thymus and, lesser...
CD1d-restricted Valpha14-Jalpha281 invariant alphabetaTCR(+) (NKT) cells are well defined in the C57BL/6 mouse strain, but they remain poorly characterized non-NK1.1-expressing strains. Surrogate markers for NKT such as alphabetaTCR(+)CD4(-)CD8(-) and DX5(+)CD3(+) have been used many studies, although their effectiveness defining this lineage remains to be verified. Here, we compare among C57BL/6, NK1.1-congenic BALB/c, nonobese diabetic mice. were identified compared using a range of...
The secreted hexameric form of the dengue virus (DENV) non-structural protein 1 (NS1) has recently been shown to elicit inflammatory cytokine release and disrupt endothelial cell monolayer integrity. This suggests that circulating NS1 contributes vascular leak plays a major role in pathology haemorrhagic fever shock. Pathways activated by are thus great interest as potential therapeutic targets. Recent works have separately implicated both toll-like receptor 4 (TLR4) TLR2/6 heterodimer...
Defects in NK and NKT cell activities have been implicated the etiology of type 1 (autoimmune) diabetes NOD mice on basis experiments performed using surrogate phenotypes for identification these lymphocyte subsets. Here, we generated a congenic line (NOD.b-Nkrp1b) which express allelic NK1.1 marker, enabling direct study cells mice. Major deficiencies both populations were identified when NOD.b-Nkrp1b compared with C57BL/6 BALB.B6-Cmv1r by flow cytometry. The decrease numbers peripheral was...
Natural killer (NK) cells are thought to provide the first line of defence against tumors, particularly major histocompatibility complex (MHC) class I− variants. We have confirmed in C57BL/6 (B6) mice lacking perforin that peritoneal growth MHC RMA-S tumor unprimed is controlled by perforin-dependent cytotoxicity mediated CD3− NK1.1+ cells. Furthermore, we demonstrate B6 necrosis factor (TNF) also significantly defective their rejection RMA-S, despite fact insensitive TNF vitro and spleen NK...
Non–antigen-specific stimulatory cancer immunotherapies are commonly complicated by off-target effects. Antigen-specific immunotherapy, combining viral tumor antigen or personalized neoepitopes with immune targeting, offers a solution. However, the lack of flexible systems targeting antigens to cross-presenting dendritic cells (DCs) limits clinical development. Although antigen–anti-Clec9A mAb conjugates target DCs, adjuvant must be codelivered for cytotoxic T lymphocyte (CTL) induction. We...
Abstract The potential roles of TLRs in the cause and pathogenesis autoimmune CNS inflammation remain contentious. In this study, we examined effects targeted deletions TLR1, TLR2, TLR4, TLR6, TLR9, MyD88 on induction myelin oligodendrocyte glycoprotein 35–55 (MOG35–55) peptide/CFA/pertussis toxin-induced encephalomyelitis. Although C57BL/6.Tlr1−/−, C57BL/6.Tlr4−/− C57BL/6.Tlr6−/− mice showed normal susceptibility to disease, signs were alleviated female C57BL/6.Tlr2−/− C57BL/6.Tlr9−/−...
The NOD mouse is widely used as a model of organ-specific autoimmunity because it develops specific autoimmune destruction pancreatic β-cells. Although clear that T-cells and monocytes are necessary for β-cell destruction, humoral factors, such antibodies complement, may also contribute to tissue damage. Attempts cure diabetes in experimental models by immunoisolation transplanted islets has raised the need protect from relatively small components complement cascade. In this study, we report...