
Sudesh Pawaria - Boehringer Ingelheim - LinkedIn
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Sudesh Pawaria - Google Scholar
Interplay of Cyclic GMP-AMP Synthase/Stimulator of IFN Genes and Toll-Like Receptor Nucleic Acid Sensing Pathways in Autoinflammation and Abnormal Bone Formation due to DNaseII …
Sudesh PAWARIA | PostDoc | PhD | University of Massachusetts …
Sudesh PAWARIA, PostDoc | Cited by 639 | of University of Massachusetts Medical School, Massachusetts (UMMS) | Read 23 publications | Contact Sudesh PAWARIA
CD91-dependent programming of T-helper cell responses
Nov 1, 2011 · Specifically, CD91 is phosphorylated in response to HSPs in a unique pattern and phospho-CD91 triggers signalling cascades to activate nuclear factor-kappa B. Each HSP–CD91 interaction on APCs...
A role for the Heat Shock Protein-CD91 axis in initiation of …
In this chapter, we present evidence that heat shock protein-peptide complexes released by tumor cells are the entity responsible for initiating the immune responses. Interaction of the extracellular HSP with its receptor CD91 is necessary for priming the immune response.
Hierarchy of clinical manifestations in SAVI N153S and V154M …
Apr 4, 2019 · Recently, gain-of-function mutations in STING have been identified in patients with STING-associated vasculopathy with onset in infancy (SAVI). SAVI patients present with early-onset systemic inflammation and interstitial lung disease, resulting in pulmonary fibrosis and respiratory failure.
Taking the STING out of TLR-driven autoimmune diseases: good, …
Sudesh Pawaria * Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA; ‡ Program in Innate …
The Role of IFNγ-Producing Th1 Cells in a Type I IFN-Independent …
Pawaria S, Ramani K, Maers K, Liu Y, Kane LP, Levesque MC, et al. Complement component C5a permits the coexistence of pathogenic Th17 cells and type I IFN in lupus. J Immunol 2014; 193 :3288–3295. [ PubMed ] [ Google Scholar ]
Role of Interferon-γ-Producing Th1 Cells in a Murine Model of …
Objective: Patients with hypomorphic mutations in DNase II develop a severe and debilitating autoinflammatory disease.
Sudesh Pawaria and Robert J. Binder* Department of Immunology, University of Pittsburgh, Pittsburgh, PA 15261 Abstract
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