Shuhei Sakakibara

Assistant Professor

Osaka University

Japan

Research Interests

Explore related searches

Professors in Japan Professors in Immunology Immunology professors in Japan

Contact this professor

ORCID

Google Scholar

About

Shuhei Sakakibara is an Assistant Professor at Osaka University, Japan. His research areas include immune responses in viral infections, particularly COVID-19, and the role of innate immune cells in disease severity. He has contributed to studies exploring virus-specific T cells, plasmablast landscapes, and the effects of vaccination on memory B cells.

Shuhei Sakakibara

Research Interests

Explore related searches

Contact this professor

About

Articles (16)

Multifaceted profiling of virus-specific CD8 T cells reveals distinct immune signatures against cytomegalovirus infection states during pregnancy

Clonal landscape of autoantibody-secreting plasmablasts in COVID-19 patients

Atypical and non-classical CD45RBlo memory B cells are the majority of circulating SARS-CoV-2 specific B cells following mRNA vaccination or COVID-19

Threonine Phosphorylation and the Yin and Yang of STAT1: Phosphorylation-Dependent Spectrum of STAT1 Functionality in Inflammatory Contexts

Single-cell analyses and host genetics highlight the role of innate immune cells in COVID-19 severity

Opposing roles of RUBCN isoforms in autophagy and memory B cell generation

Antibody feedback contributes to facilitating the development of Omicron-reactive memory B cells in SARS-CoV-2 mRNA vaccinees

Consecutive BNT162b2 mRNA vaccination induces short-term epigenetic memory in innate immune cells

DOCK2 is involved in the host genetics and biology of severe COVID-19

Multiple tolerance checkpoints restrain affinity maturation of B cells expressing the germline precursor of a lupus patient-derived anti-dsDNA antibody in knock-in mice

Local production of broadly cross‐reactive IgE against multiple fungal cell wall polysaccharides in patients with allergic fungal rhinosinusitis

Glycan engineering of the SARS-CoV-2 receptor-binding domain elicits cross-neutralizing antibodies for SARS-related viruses

A SARS-CoV-2 antibody broadly neutralizes SARS-related coronaviruses and variants by coordinated recognition of a virus-vulnerable site

Publisher Correction: Tet2 and Tet3 in B cells are required to repress CD86 and prevent autoimmunity

Tet2 and Tet3 in B cells are required to repress CD86 and prevent autoimmunity

Self-reactive and polyreactive B cells are generated and selected in the germinal center during γ-herpesvirus infection

Collaborators (35)

Hiroyuki Satofuka

Yoshihiro Eriguchi

Janyerkye Tulyeu

Takeshi Inoue

Yohei Mikami

Yu-Diao Kuan

MITSUHIRO YAMADA

Taishi Onodera

Yuji Yamamoto

Kazuya Takeda

Junichi Sasaki

Yusuke Kawamura

Shuhei Nakamura

Akiyoshi Nakayama

Takahito Fukusumi

Yusuke Takeshima

Hiromu Tanaka

Tomomi Takano

Atsushi Yamanaka

Akira Ando

Hiroshi Ito

Hozaifa Metwally

Hiroki Kabata

Takayoshi Morita

Yoshinori Fukui

Yuhkoh Satouh

Yu-Chen Liu

Hideo Fukuhara

Hitoshi Kikutani

Keisuke Tabata

Toshihisa Anzai

Shunsuke Kita

Takeshi Noda

David Priest

Yoko Ito

How do I reach out?

Meet Kite AI