Feinberg
Northwestern Medicine | Northwestern University | Faculty Profiles

News Center

  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
    • Podcast
  • Press Release
  • Media Coverage
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Menu
  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
    • Podcast
  • Press Release
  • Media Coverage
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Home » Mitochondria Could Boost Immunotherapy Effectiveness
Scientific Advances

Mitochondria Could Boost Immunotherapy Effectiveness

By Will DossApr 22, 2021
Share
Facebook Twitter Email
Chyung-Ru Wang, PhD, professor of Microbiology-Immunology, was senior author of the study published in PNAS.

Boosting mitochondrial function in a subpopulation of T cells could make cancer immunotherapy more effective, according to a recent study published in the Proceedings of the National Academy of the Sciences (PNAS).

Those cells, known as CD1d-restricted natural killer T (NKT) cells, are much more reliant on mitochondrial metabolism during development when compared with conventional CD4+ T cells. That makes those cells an attractive target for boosting immune function in cancer immunotherapy, according to Chyung-Ru Wang, PhD, professor of Microbiology-Immunology and senior author of the study, whose findings shed light on possible routes scientists could take to increase their population.

“If we can manipulate these cells, we might be able to make this cell live longer in an immunotherapy context,” said Wang, who is also a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

Conventional T cells are the body’s main line of defense against viruses and bacteria. On the other hand, NKT cells are less numerous, but produce far more inflammatory cytokines compared to conventional T cells. This places them in a unique position between the innate or immediate immune response and the adaptive immune response, according to Wang.

“Within hours, the innate immune response begins, but the adaptive response can take more than a week to establish,” Wang said. “By producing cytokines and activating other immune cells, these NKT cells can produce a response in about a day.”

Wang and her collaborators wanted to examine any differences in T cell development that lead to disparate outcomes among the two groups of T cells.

Studying mice without mitochondria complex III in T cells, the investigators found that while conventional T cells were still present, the population of NKT cells was greatly reduced because NKT cells require stronger signaling from T cell receptors for their development and intact mitochondrial activity for their survival.

This may be a homeostatic mechanism to prevent over-activation of the immune system, according to Wang.

“If these cells never died, they could generate too much immune response,” Wang said. “This signaling and metabolic requirement means they die more easily.”

However, in a cancer immunotherapy context, keeping these cells alive could be very beneficial. Conventional T cells have thousands of antigen targets, owing to the evolutionary arms race between pathogens and the human immune system.

While this is positive for fighting off infections, this means finding one antigen target that activates these T cells across many patients with cancer is highly unlikely — the variability from person to person is just too high.

However, NKT cells target lipids, which are largely the same from pathogen to pathogen — meaning a one-size-fits-all approach may be possible. Armed with these findings, Wang said she believes that boosting mitochondrial function may be one way to sustain these cells over the course of immunotherapy, strengthening immune response and the subsequent cancer-killing ability of the treatment.

“Enhancing mitochondrial function in this type of cells could be the key to making them live longer during immunotherapy,” Wang said.

Navdeep Chandel, PhD, the David W. Cugell, MD, Professor of Medicine in the Division of Pulmonary and Critical Care, a professor of Biochemistry and Molecular Genetics and a member of the Lurie Cancer Center, was a co-author of the study.

This work was supported by NIH Grants R01 AI43407 and R01 AI057460.

Cancer Microbiology Research
Share. Facebook Twitter Email

Related Posts

Dissolving Implantable Device Relieves Pain Without Drugs

Jun 30, 2022

Fathers’ Presence During Childhood Predicts Adult Testosterone Levels

Jun 29, 2022

Epigenetic Biomarkers Predict CVD Risk

Jun 28, 2022

Comments are closed.

Latest News

Physician Assistant Students Embrace ‘Shades of Purple’

Jul 1, 2022

Dissolving Implantable Device Relieves Pain Without Drugs

Jun 30, 2022

Fathers’ Presence During Childhood Predicts Adult Testosterone Levels

Jun 29, 2022

Epigenetic Biomarkers Predict CVD Risk

Jun 28, 2022

Student Spearheads Ukraine Aid Efforts

Jun 27, 2022
  • News Center Home
  • Categories
  • Press Release
  • Media Coverage
  • Editor’s Picks
  • News Archives
  • About Us
Flickr Photos
20220617_NM_0434
20220617_NM_0858
20220617_NM_0643
20220617_NM_0835
20220617_NM_0544
20220617_NM_0450
20220617_NM_0790
20220617_NM_0811
20220617_NM_0851
20220617_NM_0696
20220617_NM_0779
20220617_NM_0838

Northwestern University logo

Northwestern University Feinberg School of Medicine

RSS Facebook Twitter LinkedIn Flickr YouTube Instagram
Copyright © 2022 Northwestern University
  • Contact Northwestern University
  • Disclaimer
  • Campus Emergency Information
  • Policy Statements

Type above and press Enter to search. Press Esc to cancel.