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Updated: May 24, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Telomere dysfunction, autoimmunity and aging.

Philipp J Hohensinner¹, Jörg J Goronzy, Cornelia M Weyand

¹Department of Medicine: Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California and Palo Alto Department of Veterans Affairs Health Care System, Palo Alto, California, USA.

Aging and Disease

|March 8, 2012

Summary

Immune aging (immunosenescence) impairs host defense and increases inflammation. In rheumatoid arthritis, telomere shortening and DNA repair defects accelerate immune aging, impacting lymphocyte survival and disease progression.

Keywords:

Autoimmunity Diabetes Lupus Rheumatoid arthritis Sarcoidosis Shelterin Telomerase Telomere Telomere Dysfunction

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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

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Published on: May 22, 2013

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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

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Published on: April 13, 2015

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

Area of Science:

Immunology
Gerontology
Molecular Biology

Background:

Immune aging (immunosenescence) compromises host defense against infections and cancer, paradoxically increasing susceptibility to damaging inflammation.
Chronic inflammation in immune-mediated diseases acts as a stressor, accelerating immune cell aging through impacts on replication and exhaustion.
Immune cell longevity is linked to telomere integrity, influenced by cell division, oxidative stress, and DNA repair.

Purpose of the Study:

To investigate the relationship between immune aging, telomere dynamics, and DNA repair mechanisms in autoimmune diseases.
To understand how chronic inflammation in rheumatoid arthritis (RA) affects immune cell longevity and contributes to accelerated aging.

Main Methods:

Analysis of telomere length and structure in lymphocytes.
Assessment of DNA repair mechanisms, including telomerase activity and Ataxia telangiectasia mutated (ATM) kinase function.
Correlation of molecular findings with clinical parameters in patients with RA and other autoimmune diseases.

Main Results:

Telomerase deficiency in RA patients is linked to premature immune aging.
Defects in DNA repair pathways, such as ATM deficiency, shorten lymphocyte survival in RA.
Telomere length and structure exhibit distinct patterns across different autoimmune diseases, indicating varied molecular mechanisms.

Conclusions:

Accelerated immune aging in RA is associated with impaired telomere maintenance and DNA repair.
The interplay between chronic inflammation and aging processes in the immune system is complex and disease-specific.
Understanding these molecular mechanisms is crucial for developing targeted therapies for autoimmune diseases and age-related immune dysfunction.