Clinical Focus

  • Neurology

Academic Appointments

Professional Education

  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2024)
  • Residency: Stanford University Dept of Neurology (2024) CA
  • Internship: Santa Clara Valley Medical Center Dept of Medicine (2021) CA
  • Medical Education: University of California Davis School of Medicine (2020) CA

Contact

  • Academic
    jloe@stanford.edu
    University - Other Teaching/Research Department: Adult Neurology Position: Instructor
  • Clinical (Primary)  Neurology 300 Pasteur Dr Rm H3160 MC 5235 Stanford, CA 94305 (650) 723-7434 (fax)

Additional Clinical Info

Additional Info

  • Mail Code: 5327

All Publications

  • EBV reprograms autoreactive anti-CNS B cells as antigen presenting cells in multiple sclerosis. bioRxiv : the preprint server for biology Younis, S., Rasouli, S., Loeffler, J. W., Sattarnezhad, N., Courtney, Y., Moutusy, S. I., Jahanbani, S., Pandit, M., Tomczak, A., Wong, H. H., Sharpe, O., Utz, P. J., Meffre, E., Kipp, L. B., Dunn, J. E., Lanz, T. V., Steinman, L., Robinson, W. H. 2026

    Abstract

    Multiple sclerosis (MS) is a chronic autoimmune disease targeting the central nervous system (CNS). MS develops almost exclusively in individuals previously infected with Epstein-Barr virus (EBV)1, yet the mechanisms linking EBV infection to MS pathogenesis remain incompletely defined. Here we characterized EBV-infected B cells in MS and demonstrated that EBV directly infects autoreactive anti-CNS antigen B cells and reprograms them into pro-inflammatory antigen-presenting cells (APCs). EBV+ B cells in MS were enriched within the CD27+CD21low memory B-cell subset and exhibited upregulated B cell activation and APC transcriptional programs. Recombinant antibodies derived from MS blood and cerebrospinal fluid (CSF) EBV+ B cells bound brain tissue, and several cross-bound both MS-associated autoantigens and Epstein-Barr virus nuclear antigen-1 (EBNA1). In vitro, EBV+ B cells functioned as APCs that stimulated T peripheral helper cells, with associated activation of EBV- anti-CNS antigen B cells. Collectively, these findings support a mechanistic framework in which EBV infects and transcriptionally reprograms autoreactive anti-CNS antigen B cells into APCs that drive pathogenic anti-CNS antigen T cell and EBV- B cell responses in MS.

    View details for DOI 10.64898/2026.02.11.701910

    View details for PubMedID 41727017

    View details for PubMedCentralID PMC12919047

  • Influence of Body Mass Index on B Lymphocyte Repopulation in Multiple Sclerosis Patients Treated with Anti-CD20 Therapy Loeffler, J., Han, M. LIPPINCOTT WILLIAMS & WILKINS. 2023

    View details for DOI 10.1212/WNL.0000000000204140

    View details for Web of Science ID 001053672105186

  • HLA-DR4-positive Vogt-Koyanagi-Harada (VKH) Syndrome: Review of pathophysiology and clinical correlation (P1-1.Virtual) Loeffler, J., Nie, E., Han, M. LIPPINCOTT WILLIAMS & WILKINS. 2022

    View details for Web of Science ID 000894020500455

  • The contemporary management of renal artery aneurysms JOURNAL OF VASCULAR SURGERY Klausner, J. Q., Lawrence, P. F., Harlander-Locke, M. P., Coleman, D. M., Stanley, J. C., Fujimura, N., Vasc Low-Frequency Dis Consortium 2015; 61 (4): 978–84

    Abstract

    Renal artery aneurysms (RAAs) are rare, with little known about their natural history and growth rate or their optimal management. The specific objectives of this study were to (1) define the clinical features of RAAs, including the precise growth rate and risk of rupture, (2) examine the current management and outcomes of RAA treatment using existing guidelines, and (3) examine the appropriateness of current criteria for repair of asymptomatic RAAs.A standardized, multi-institutional approach was used to evaluate patients with RAAs at institutions from all regions of the United States. Patient demographics, aneurysm characteristics, aneurysm imaging, conservative and operative management, postoperative complications, and follow-up data were collected.A total of 865 RAAs in 760 patients were identified at 16 institutions. Of these, 75% were asymptomatic; symptomatic patients had difficult-to-control hypertension (10%), flank pain (6%), hematuria (4%), and abdominal pain (2%). The RAAs had a mean maximum diameter of 1.5 ± 0.1 cm. Most were unilateral (96%), on the right side (61%), saccular (87%), and calcified (56%). Elective repair was performed in 213 patients with 241 RAAs, usually for symptoms or size >2 cm; the remaining 547 patients with 624 RAAs were observed. Major operative complications occurred in 10%, including multisystem organ failure, myocardial infarction, and renal failure requiring dialysis. RAA repair for difficult-to-control hypertension cured 32% of patients and improved it in 26%. Three patients had ruptured RAA; all were transferred from other hospitals and underwent emergency repair, with no deaths. Conservatively treated patients were monitored for a mean of 49 months, with no acute complications. Aneurysm growth rate was 0.086 cm/y, with no difference between calcified and noncalcified aneurysms.This large, contemporary, multi-institutional study demonstrated that asymptomatic RAAs rarely rupture (even when >2 cm), growth rate is 0.086 ± 0.08 cm/y, and calcification does not protect against enlargement. RAA open repair is associated with significant minor morbidity, but rarely a major morbidity or mortality. Aneurysm repair cured or improved hypertension in >50% of patients whose RAA was identified during the workup for difficult-to-control hypertension.

    View details for DOI 10.1016/j.jvs.2014.10.107

    View details for Web of Science ID 000351776100021

    View details for PubMedID 25537277