Publications by authors named "Pardeep S Taunk"

BACKGROUND Hemophagocytic lymphohistiocytosis (HLH) and Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) can trigger profound immune activation and systemic inflammation, leading to severe, often fatal, conditions. Simultaneously, HIV-infected patients, prone to immune dysregulation, face an increased risk of severe complications from SARS-CoV-2. The optimal timeline for initiating antiretroviral therapy (ART) in patients with severe SARS-CoV-2 and HIV co-infection, especially concerning the risk of HLH, remains uncertain.

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Article Synopsis
  • Pancreatic ductal adenocarcinoma (PDA) is resistant to immunotherapy and shows immune tolerance, making treatment challenging.
  • Researchers identified an increased level of RIP1 in tumor-associated macrophages in PDA and developed a specific RIP1 inhibitor that effectively targets these macrophages.
  • Inhibiting RIP1 leads to enhanced immune responses by activating cytotoxic T cells and promoting a beneficial immune environment, suggesting that targeting RIP1 could improve immunotherapy outcomes for PDA.
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We found that the cancerous pancreas harbors a markedly more abundant microbiome compared with normal pancreas in both mice and humans, and select bacteria are differentially increased in the tumorous pancreas compared with gut. Ablation of the microbiome protects against preinvasive and invasive pancreatic ductal adenocarcinoma (PDA), whereas transfer of bacteria from PDA-bearing hosts, but not controls, reverses tumor protection. Bacterial ablation was associated with immunogenic reprogramming of the PDA tumor microenvironment, including a reduction in myeloid-derived suppressor cells and an increase in M1 macrophage differentiation, promoting TH1 differentiation of CD4 T cells and CD8 T-cell activation.

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Small molecule interactions with amyloid proteins have had a huge impact in Alzheimer's disease (AD), especially in three specific areas: amyloid folding, metabolism and brain imaging. Amyloid plaque amelioration or prevention have, until recently, driven drug development, and only a few drugs have been advanced for use in AD. Amyloid proteins undergo misfolding and oligomerization via intermediates, eventually forming protease resistant amyloid fibrils.

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