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Paul V. Lehmann

Researcher at Case Western Reserve University

Publications -  167
Citations -  12081

Paul V. Lehmann is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: T cell & ELISPOT. The author has an hindex of 47, co-authored 162 publications receiving 11678 citations. Previous affiliations of Paul V. Lehmann include University Hospitals of Cleveland & University of California, Los Angeles.

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Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen.

TL;DR: In mice with chronic EAE, several additional determinants of MBP in peptides 35–47, 81–100 and 121–140 recall proliferative responses and reactivity to the latter determinants was also detected after induction of EAE with MBP peptide Ac1–11 alone, demonstrating priming by endogenous MBP determinants.
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Spontaneous loss of T-cell tolerance to glutamic acid decarboxylase in murine insulin-dependent diabetes.

TL;DR: It is reported here that a T-helper-1 response to glutamate decarboxylase develops in NOD mice at the same time as the onset of insulitis, and it is suggested that spontaneous autoimmune disease can be prevented by tolerization to the initiating target antigen.
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CpG oligodeoxynucleotides act as adjuvants that switch on T helper 1 (Th1) immunity.

TL;DR: CpG ODN provide a signal to switch on Th1-dominated responses to coadministered antigen and are potential adjuvants for human vaccines to elicit protective Th1 immunity.
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Dominance and Crypticity of T Cell Antigenic Determinants

TL;DR: In this paper, the structural constraints for binding a peptide to MHC class II molecules are considered, and the experimental evidence pertaining to this choice is reviewed for "MHC-guided processing", where the unfolding antigen can compete for determinants at an early stage of processing when the antigen is close to its original length.
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Induction of TH1 and TH2 Immunity in Neonatal Mice

TL;DR: The classic system for induction of neonatal tolerance to protein antigens was reexamined in mice and the presumably tolerogenic protocol was found to trigger a vigorous T helper cell type 2 (TH2) immune response.