Aging and disease

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01 June 2011. VOL 2, ISSUE 6 Previous Issue Next Issue

Is Immune Aging a Cause of Disease among the Elderly, or is it a Passive Indicator of General Decline of Physiologic Function?
Abbe N. Vallejo

2011, 2 (6): 444-448

PDF (385KB)
NF-κB in Aging and Disease
Jeremy S. Tilstra, Cheryl L. Clauson, Laura J. Niedernhofer, Paul D. Robbins

2011, 2 (6): 449-465

PDF (1175KB)
Frailty, Inflammation, and Immunity
Huifen Li, Bhavish Manwani, Sean X. Leng

2011, 2 (6): 466-473

PDF (390KB)
Interferon-gamma – Inducible Inflammation: Contribution to Aging and Aging-Associated Psychiatric Disorders
Gregory Oxenkrug

2011, 2 (6): 474-486

PDF (582KB)
Dysregulated Inflammation as a Risk Factor for Pneumonia in the Elderly
Angela R. Boyd, Carlos J. Orihuela

2011, 2 (6): 487-500

PDF (605KB)
Effects of Aging on Inflammation and Hemostasis through the Continuum of Critical Illness
Sachin S Kale, Sachin Yende

2011, 2 (6): 501-511

PDF (600KB)
Immunity, Cancer and Aging: Lessons from Mouse Models
Cheryl E. Myers, Noweeda N. Mirza, Joseph Lustgarten

2011, 2 (6): 512-523

PDF (426KB)
Telomere Dysfunction, Autoimmunity and Aging
Philipp J. Hohensinner, Jörg J. Goronzy, Cornelia M. Weyand

2011, 2 (6): 524-537

PDF (696KB)
Down Syndrome: Is It Really Characterized by Precocious Immunosenescence?
Maaike AA. Kusters, Ruud HJ. Verstegen, Esther de Vries

2011, 2 (6): 538-545

PDF (423KB)

Cover Illustration

01 June 2011. Vol.2 No.6
Immune aging is associated with loss of critical immune functions, such as host protection from infection and malignancy. Unexpectedly, immunosenescence also renders the host susceptible to inflammation, which may translate into tissue-damaging disease as the senescent immune system loses its ability to maximize inflammatory protection while minimizing inflammatory injury. On the other hand, chronic inflammation associated with immune-mediated disease represents a profound stress factor for the immune system, affecting cellular turn-over, replication and exhaustion. Immune cell longevity is tightly connected to the functional integrity of telomeres which are regulated by cell multiplication, exposure to oxidative stress and DNA repair mechanisms. Lymphocytes are amongst the few cell types that can actively elongate telomeres through the action of telomerase. In patients with the autoimmune disease rheumatoid arthritis (RA), telomerase deficiency is associated with prematurity of immune aging. Patients with RA have other defects in DNA repair mechanisms, including the kinase Ataxia telangiectasia mutated (ATM), critically involved in the repair of DNA double strand breaks. ATM deficiency in RA shortens lymphocyte survival. Dynamics of telomeric length and structure are beginning to be understood and have distinct patterns in different autoimmune diseases, suggesting a multitude of molecular mechanisms defining the interface between chronic immune stimulation and progressive aging of the immune system.

[Detail]

Cover Illustration

Immune aging is associated with loss of critical immune functions, such as host protection from infection and malignancy. Unexpectedly, immunosenescence also renders the host susceptible to inflammation, which may translate into tissue-damaging disease as the senescent immune system loses its ability to maximize inflammatory protection while minimizing inflammatory injury. On the other hand, chronic inflammation associated with immune-mediated disease represents a profound stress factor for the immune system, affecting cellular turn-over, replication and exhaustion. Immune cell longevity is tightly connected to the functional integrity of telomeres which are regulated by cell multiplication, exposure to oxidative stress and DNA repair mechanisms. Lymphocytes are amongst the few cell types that can actively elongate telomeres through the action of telomerase. In patients with the autoimmune disease rheumatoid arthritis (RA), telomerase deficiency is associated with prematurity of immune aging. Patients with RA have other defects in DNA repair mechanisms, including the kinase Ataxia telangiectasia mutated (ATM), critically involved in the repair of DNA double strand breaks. ATM deficiency in RA shortens lymphocyte survival. Dynamics of telomeric length and structure are beginning to be understood and have distinct patterns in different autoimmune diseases, suggesting a multitude of molecular mechanisms defining the interface between chronic immune stimulation and progressive aging of the immune system.