TNF receptor 2 pathway: drug target for autoimmune diseases
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Updated: Jun 12, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
Published on: June 6, 2025
Denise Faustman1, Miriam Davis
1Immunobiology Laboratory, Room 3602, Building 149, Massachusetts General Hospital and Harvard Medical School, 13th Street, Charlestown, Massachusetts 02129, USA. faustman@helix.mgh.harvard.edu
Abstract:
Although drug development has advanced for autoimmune diseases, many current therapies are hampered by adverse effects and the frequent destruction or inactivation of healthy cells in addition to pathological cells. Targeted autoimmune therapies capable of eradicating the rare autoreactive immune cells that are responsible for the attack on the body's own cells are yet to be identified. This Review presents a new emerging approach aimed at selectively destroying autoreactive immune cells by specific activation of tumour necrosis factor receptor 2 (TNFR2), which is found on autoreactive and normal T lymphocytes, with the potential of avoiding or reducing the toxicity observed with existing therapies.
Insights
New therapies for autoimmune diseases aim to selectively destroy harmful T lymphocytes. Activating tumour necrosis factor receptor 2 (TNFR2) offers a targeted approach, potentially reducing side effects of current treatments.
Area of Science:
- Immunology
- Autoimmune Diseases
- Drug Development
Background:
- Current autoimmune disease therapies often cause adverse effects by damaging healthy cells alongside pathological ones.
- Existing treatments lack targeted strategies to eliminate specific autoreactive immune cells responsible for autoimmune attacks.
- The need for safer, more effective treatments for autoimmune conditions is critical.
Purpose of the Study:
- To introduce a novel therapeutic strategy for autoimmune diseases.
- To explore the selective destruction of autoreactive immune cells via targeted approaches.
- To evaluate the potential of tumour necrosis factor receptor 2 (TNFR2) activation in autoimmune therapy.
Main Methods:
- Review of emerging research on targeted autoimmune therapies.
- Analysis of TNFR2 expression on autoreactive and normal T lymphocytes.
- Investigation of TNFR2-specific activation as a therapeutic mechanism.
Main Results:
- TNFR2 is expressed on both autoreactive and normal T lymphocytes.
- Selective activation of TNFR2 presents a potential method for targeting autoreactive cells.
- This approach may lead to reduced toxicity compared to current therapies.
Conclusions:
- Targeted activation of TNFR2 is a promising strategy for autoimmune disease treatment.
- This approach holds the potential to improve safety and efficacy by sparing healthy cells.
- Further research into TNFR2-mediated therapies could revolutionize autoimmune disease management.
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