Author

J. H. Reed

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 5

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 5 Approach:experimental assay· 5 Research Focus:differential expression· 4 Organism:mouse· 4 Research Focus:cancer & tumor microenvironment· 3 Research Focus:cell signaling & trafficking· 2 Research Focus:gene regulatory network inference· 2 Organism:human· 2

Frequent Co-Authors

C. C. Goodnow· 4 shared T. J. Peters· 4 shared D. Suan· 3 shared E. Masle-Farquhar· 3 shared M. Singh· 3 shared R. Brink· 3 shared C. Young· 2 shared G. Al-Eryani· 2 shared

Activity by Year

2021-2024 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 42 mutual co-author links

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4 shared papersImmunology

C. C. Goodnow

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Author profile →

5 papers

Recent·Most cited

Self-reactive B cells traverse a perfect storm of somatic mutagenesis to cause a virus-induced autoimmune disease

C. Young, M. Singh, K. J. Jackson, M. A. Field, T. J. Peters, S. Angioletti-Uberti, D. Frenkel, S. Ravishankar, M. Gupta, J. J. Wang, D. Agapiou, M. L. Faulks, G. Al-Eryani, F. Luciani, T. P. Gordon, , C. C. Goodnow

The paper traces the evolution of autoantibodies in HCV-CV patients, revealing convergent somatic mutations and compromised solubility in pathogenic B cells.

bioRxiv · Jan 7, 2024Immunology

STAT3 gain-of-function mutations connect leukemia with autoimmune disease by pathological dysregulation of NKG2Dhi CD8 killer T cells

E. Masle-Farquhar, K. J. L. Jackson, T. J. Peters, G. Al-Eryani, M. Singh, K. J. Payne, G. Rao, G. Apps, J. Kingham, C. J. Jara, K. Skvortsova, A. Swarbrick, C. Ma, D. Suan, G. Uzel, , C. C. Goodnow

This study shows that STAT3 gain-of-function mutations in leukemia drive autoimmune pathology by causing NKG2Dhi CD8 T cell oligoclonal expansion and cytotoxic activity.

bioRxiv · Feb 11, 2022 · PreprintImmunology

Overactive STAT3 drives accumulation of disease-associated CD21low B cells

E. Masle-Farquhar, T. J. Peters, K. J. Jackson, M. Singh, C. S. Ma, D. Suan, G. Uzel, I. Chua, J. W. Leiding, K. Heiskanen, K. Preece, L. Kainulainen, M. O Sullivan, M. A. Cooper, M. R. Seppänen, , C. C. Goodnow

This study shows that overactive STAT3 leads to the accumulation of disease-associated CD21low B cells in both humans and mice.

bioRxiv · Dec 20, 2021 · PreprintImmunology

Uncontrolled CD21low age-associated and B1 B cell accumulation caused by failure of an EGR2/3 tolerance checkpoint

E. Masle-Farquhar, T. J. Peters, L. A. Miosge, I. A. Parish, C. Weigel, C. C. Oakes, J. H. Reed, C. Goodnow

This study identifies EGR2 and EGR3 as critical transcription factors that suppress CD21low and B1 B cell accumulation by repressing plasma cell differentiation and follicular germinal center formation.

bioRxiv · Jul 1, 2021Immunology

Dysregulation of PAX5 causes uncommitted B cell development and tumorigenesis in mice

B. Boast, K. Helian, D. Andrews, X. Li, V. Cho, A. Closa, H. J. Sutton, J. H. Reed, H. Bergmann, C. M. Roots, M. Yabas, N. Barthel, S. A. Omari, C. Young, L. A. Miosge, , A. Enders

Reduced PAX5 function in mice leads to uncommitted B cell development and B-ALL with secondary mutations in Jak3 and Ptpn11.

bioRxiv · Jan 29, 2021 · PreprintImmunology