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World J Biol Chem. May 26, 2017; 8(2): 129-137
Published online May 26, 2017. doi: 10.4331/wjbc.v8.i2.129
Immunological aspects of age-related diseases
Ken-ichi Isobe, Naomi Nishio, Tadao Hasegawa
Ken-ichi Isobe, Department of Food Science and Nutrition, Nagoya Woman’s University, Mizuho-ku, Nagoya 467-8610, Japan
Naomi Nishio, Tadao Hasegawa, Department of Bacteriology, Nagoya City University Graduate School of Medical Sciences, Mizuho-ku, Nagoya 466-8550, Japan
Author contributions: All the authors contributed to this manuscript.
Conflict-of-interest statement: There are no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Ken-ichi Isobe, MD, PhD, Professor, Department of Food Science and Nutrition, Nagoya Woman’s University, 3-40 Shioji-cho, Mizuho-ku, Nagoya 467-8610, Japan. isobe@nagoya-wu.ac.jp
Telephone: +81-52-8529425 Fax: +81-52-8527470
Received: August 22, 2016
Peer-review started: August 24, 2016
First decision: November 19, 2016
Revised: March 2, 2017
Accepted: March 14, 2017
Article in press: March 15, 2017
Published online: May 26, 2017
Processing time: 268 Days and 15.7 Hours
Abstract

The proportion of elderly people rises in the developed countries. The increased susceptibility of the elderly to infectious diseases is caused by immune dysfunction, especially T cell functional decline. Age-related hematopoietic stem cells deviate from lymphoid lineage to myeloid lineage. Thymus shrinks early in life, which is followed by the decline of naïve T cells. T-cell receptor repertoire diversity declines by aging, which is caused by cytomegalovirus-driven T cell clonal expansion. Functional decline of B cell induces antibody affinity declines by aging. Many effector functions including phagocytosis of myeloid cells are down regulated by aging. The studies of aging of myeloid cells have some controversial results. Although M1 macrophages have been shown to be replaced by anti-inflammatory (M2) macrophages by advanced age, many human studies showed that pro-inflammatory cytokines are elevated in older human. To solve this discrepancy here we divide age-related pathological changes into two categories. One is an aging of immune cell itself. Second is involvement of immune cells to age-related pathological changes. Cellular senescence and damaged cells in aged tissue recruit pro-inflammatory M1 macrophages, which produce pro-inflammatory cytokines and proceed to age-related diseases. Underlying biochemical and metabolic studies will open nutritional treatment.

Keywords: Elderly people; Damage associated molecular patterns; Immune dysfunction; Lymphoid lineage; Myeloid lineage; Shrinkage of thymus; Cytomegalovirus; Age-related tissue damage; Cellular senescence; Pro-inflammatory

Core tip: The authors divide immune cells, which are involved in age-related pathological changes, into two categories. First category is aging of immune cell-itself, which include age-related myeloid lineage deviation of hematopoietic stem cells, the shrinkage of thymus followed by the decline of naïve T cells, the cytomegalovirus infection-mediated decline of T-cell receptor repertoire diversity and functional decline of myeloid cells. Second category is the involvement of immune cells to age-related pathological changes. Age-related tissue damage and cellular senescence activate pro-inflammatory (M1) macrophages, which induce many age-related diseases. Biochemical works are needed to further elucidate age-related immune changes.