Assistant Professor, Internal Medicine, Washington University School of Medicine
Rheumatology
Dr. Deborah J. Lenschow, MD
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Deborah J. Lenschow, MD works in the field of Rheumatology. She graduated from University of Chicago Pritzker School of Medicine. University of Chicago Pritzker School of Medicine has a rank of 10 in research and a 19 in primary care She received 2 awards: "Fellow (FACR)" and "Fellow". Deborah Lenschow is also a published physician. She has 40 publication published. The most recent publication is: Treatment with intact anti-B7-1 mAb during disease remission enhances epitope spreading and exacerbates relapses in R-EAE. Deborah Lenschow is registered with Medicare and accepts Medicare payments.
Publications
- Replication-competent fluorescent-expressing influenza B virus.
- Chikungunya viral Arthritis in the United States: a mimic of seronegative rheumatoid Arthritis.
- Type I Interferons Link Viral Infection to Enhanced Epithelial Turnover and Repair.
- A novel mode of ISG15 mediated protection against influenza A virus and Sendai virus in mice.
- Human Cytomegalovirus pUL79 Is an Elongation Factor of RNA Polymerase II for Viral Gene Transcription.
- ISG15 functions as an interferon-mediated antiviral effector early in the murine norovirus life cycle.
- Infection of Myofibers Contributes to Increased Pathogenicity during Infection with an Epidemic Strain of Chikungunya Virus.
- Rodent herpesvirus peru encodes a secreted chemokine decoy receptor.
- The Antiviral Activities of ISG15.
- Emerging Roles for Immunomodulatory Functions of Free ISG15.
- Identification of a candidate therapeutic autophagy-inducing peptide.
- Pillars article: ctla-4 can function as a negative regulator of T cell activation. Immunity. 1994. 1: 405-413.
- ISG15 Is Critical in the Control of Chikungunya Virus Infection Independent of UbE1L Mediated Conjugation.
- Increased cerebral protein ISGylation after focal ischemia is neuroprotective.
- Species-specific antagonism of host ISGylation by the influenza B virus NS1 protein.
- ISG15 Arg151 and the ISG15-conjugating enzyme UbE1L are important for innate immune control of Sindbis virus.
- Mice lacking the ISG15 E1 enzyme UbE1L demonstrate increased susceptibility to both mouse-adapted and non-mouse-adapted influenza B virus infection.
- Nitrosylation of ISG15 prevents the disulfide bond-mediated dimerization of ISG15 and contributes to effective ISGylation.
- Ovarian tumor domain-containing viral proteases evade ubiquitin- and ISG15-dependent innate immune responses.
- IFN-stimulated gene 15 functions as a critical antiviral molecule against influenza, herpes, and Sindbis viruses.
- Identification of interferon-stimulated gene 15 as an antiviral molecule during Sindbis virus infection in vivo.
- Proteomic identification of proteins conjugated to ISG15 in mouse and human cells.
- Anti-tumor necrosis factor therapy in patients with difficult to treat Takayasu arteritis.
- Polymyalgia rheumatica/temporal arteritis: recent advances.
- Antiviral Properties of ISG15.
- Inhibition of transplant rejection following treatment with anti-B7-2 and anti-B7-1 antibodies.
- IL-4 treatment of small splenic B cells induces costimulatory molecules B7-1 and B7-2.
- Differential up-regulation of the B7-1 and B7-2 costimulatory molecules after Ig receptor engagement by antigen.
- Differential effects of anti-B7-1 and anti-B7-2 monoclonal antibody treatment on the development of diabetes in the nonobese diabetic mouse.
- Immunomodulation of transplant rejection using monoclonal antibodies and soluble receptors.
- CTLA-4 can function as a negative regulator of T cell activation.
- T cell costimulation through the CD28 receptor.
- CD28/B7 system of T cell costimulation.
- Blockade of CD28/B7-1 interaction prevents epitope spreading and clinical relapses of murine EAE.
- CD28/B7 regulation of Th1 and Th2 subsets in the development of autoimmune diabetes.
- CD28/B7 regulation of autoimmune diabetes.
- Treatment with intact anti-B7-1 mAb during disease remission enhances epitope spreading and exacerbates relapses in R-EAE.
- B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes.
- CD28/B7 costimulation regulates autoimmune diabetes induced with multiple low doses of streptozotocin.
Schools
U Of Chgo Div Of Bio Sci Pritzker Sch Of Med
Washington UB JhSlch Conc
Procedures Preformed
- Joint Drainage
- Steroid Injection
- Trigger Point Injection
Conditions Treated
- Amyloidosis
- Antiphospholipid Syndrome (APS)
- Arthritis
- Carpal Tunnel Syndrome
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Doctors Specialties
- Rheumatology
Accepted Insurances
Awards
- Fellow (FACR)
- Fellow
Education
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Washington University -
Washington University - Barnes-Jewish Hospital -
University of Chicago Pritzker School of Medicine
Hospital
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Barnes-Jewish Hospital
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1669498895 |
| Last Name Of The Provider | LENSCHOW |
| First Name Of The Provider | DEBORAH |
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