A5069651542- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- Immune Response and Inflammation
- Immunotherapy and Immune Responses
- Artificial Intelligence in Healthcare and Education
- Systemic Lupus Erythematosus Research
- Diabetes and associated disorders
- Neonatal Respiratory Health Research
- Cytomegalovirus and herpesvirus research
- Neuroinflammation and Neurodegeneration Mechanisms
- Modernist Literature and Criticism
- RNA regulation and disease
- Chromatin Remodeling and Cancer
- Explainable Artificial Intelligence (XAI)
- Glioma Diagnosis and Treatment
- Autophagy in Disease and Therapy
- NF-κB Signaling Pathways
- Immune responses and vaccinations
- Malaria Research and Control
- AI in cancer detection
- Hedgehog Signaling Pathway Studies
- Samuel Beckett and Modernism
- Mosquito-borne diseases and control
Hospital of the University of Pennsylvania
2024
University of Alabama at Birmingham
2008-2023
Although B cells expressing the IFNγR or IFNγ-inducible transcription factor T-bet promote autoimmunity in Systemic Lupus Erythematosus (SLE)-prone mouse models, role for IFNγ signaling human antibody responses is unknown. We show that elevated levels of SLE patients correlate with expansion IgDnegCD27negCD11c+CXCR5neg (DN2) pre-antibody secreting cell (pre-ASC) subset. demonstrate naïve form T-bethi pre-ASCs following stimulation either Th1 IFNγ, IL-2, anti-Ig and TLR7/8 ligand IL-21...
Multiple mechanisms restrain inflammation in neonates, most likely to prevent tissue damage caused by overly robust immune responses against newly encountered pathogens. Here, we identify a population of pulmonary dendritic cells (DCs) that express intermediate levels CD103 (CD103
Abstract Although B cells expressing the IFNγR or IFNγ-inducible transcription factor T-bet drive autoimmunity in Systemic Lupus Erythematosus (SLE)-prone mouse models, role for IFNγ signaling human antibody responses is unknown. We show that elevated levels of SLE patients correlate with expansion IgD neg CD27 CD11c + CXCR5 (DN2) pre-antibody secreting cell (pre-ASC) subset. demonstrate naïve form hi pre-ASCs following stimulation either Th1 IFNγ, IL-2, anti-Ig and TLR7/8 ligand IL-21...
As Artificial Intelligence (AI) making advancements in medical decision-making, there is a growing need to ensure doctors develop appropriate reliance on AI avoid adverse outcomes. However, existing methods enabling might encounter challenges while being applied the domain. With this regard, work employs and provides validation of an alternative approach – majority voting facilitate decision-making. This achieved by multi-institutional user study involving 32 professionals with various...
As Artificial Intelligence (AI) making advancements in medical decision-making, there is a growing need to ensure doctors develop appropriate reliance on AI avoid adverse outcomes. However, existing methods enabling might encounter challenges while being applied the domain. With this regard, work employs and provides validation of an alternative approach -- majority voting facilitate decision-making. This achieved by multi-institutional user study involving 32 professionals with various...
Abstract The germinal center (GC) is composed of distinct regions with proliferation and affinity maturation GC B cells (GCB) occurring in the dark zone (DZ) antigen-mediated selection commitment long-lived plasma cell (LL-PCs) precursors light (LZ). Despite key role for GCs establishing enduring humoral immunity, we know little about dynamics GCB response. We showed that transcription factor T-bet expressed by intrinsic required LL-PC response following influenza (flu) infection. To test...
Abstract Long-lived plasma cells (LLPC) arise from germinal center B (GCB). The transcription factor Bcl6, which is required for GCB cell survival, inhibits LLPC development by repressing the Blimp1, normally initiates development. To date, it not clear how these opposing factors are regulated in cells. In T lymphocytes, T-bet modulates balance between Blimp1 and Bcl6 controls subsequent differentiation of into memory effector When naïve activated vitro with helper 1 (Th1) cells,...
Abstract Memory B cells (Bmem) and long-lived plasma (LLPC) arise from germinal center (GCB). The transcription factor Bcl6 is required for GCB cell survival the development of Bmem. By contrast, inhibits LLPC by repressing Blimp1. To date, it not clear how these opposing factors are regulated in cells. In T cells, T-bet modulates balance between Blimp1 controls their subsequent differentiation into memory effector We recently defined a B-cell subset, referred to as B-effector 1 (Be-1...
Abstract Understanding the factors that drive differentiation of long-lived plasma cells (LLPCs) remains a significant roadblock en route to rationale vaccine design. Our lab previously described prominent role for cytokine-induced transcription factor, T-bet, in driving LLPC during pulmonary viral infection. We observed T-bet is upregulated by proportion virus-specific germinal center B (GCBs), which are precursors LLPCs. However, and signals responsible inducing transcriptional program...
Abstract Neonates are susceptible to respiratory tract infections, possibly due immature pulmonary dendritic cells (cDCs). Here we assessed the development and function of conventional DCs in lung lung-draining mediastinal lymph node (MedLN). We found that neonatal lungs, from days 3 10 life, contained a higher proportion CD103+ cDC1 than adult lungs these could be divided into small population CD103hi larger CD103int cDC1, which were not lungs. A similar expansion was observed MedLN...
Abstract Memory B cells(Bmem), which can rapidly differentiate into antibody secreting cells (ASC) upon secondary challenge, are key mediators of humoral immunity. However, the signals that govern formation and function these remain poorly understood. To date, most Bmem studies have been performed with alum-adjuvanted proteins induce type 2 immune responses. This differs significantly from I II interferon (IFN) response generated after viral infection. Using a murine model influenza, we...