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Referrence to anergy and exhaustion, MDSCs involvement in the immunosenescece
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'''Immunosenescence''' is the gradual deterioration of the [[immune system]] brought on by [[Ageing|natural age advancement]]. The [[adaptive immune system]] is affected more than the [[innate immune system]].<ref name="pmid32092501">{{cite journal | vauthors=Pangrazzi L, Weinberger B | title=T cells, aging and senescence | journal=Experimental Gerontology | volume=134 | pages=110887 | year=2020 | doi = 10.1016/j.exger.2020.110887 | pmid=32092501| s2cid=211237913 }}</ref>
'''Immunosenescence''' is the gradual deterioration of the [[immune system]] brought on by [[Ageing|natural age advancement]]. The [[adaptive immune system]] is affected more than the [[innate immune system]].<ref name="pmid32092501">{{cite journal | vauthors=Pangrazzi L, Weinberger B | title=T cells, aging and senescence | journal=Experimental Gerontology | volume=134 | pages=110887 | year=2020 | doi = 10.1016/j.exger.2020.110887 | pmid=32092501| s2cid=211237913 }}</ref> Besides anergy and exhaustion, immunosenescence belongs among the major immune system dysfunctional states. However, while cell anergy or exhaustion are reversible condition, immunosenescence is believed to be a state that can not be reversed.<ref>{{Cite journal|last=Crespo|first=Joel|last2=Sun|first2=Haoyu|last3=Welling|first3=Theodore H.|last4=Tian|first4=Zhigang|last5=Zou|first5=Weiping|date=2013-04|title=T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment|url=https://pubmed.ncbi.nlm.nih.gov/23298609/|journal=Current Opinion in Immunology|volume=25|issue=2|pages=214–221|doi=10.1016/j.coi.2012.12.003|issn=1879-0372|pmc=3636159|pmid=23298609}}</ref><ref>{{Cite journal|last=Zhang|first=Zhen|last2=Liu|first2=Shasha|last3=Zhang|first3=Bin|last4=Qiao|first4=Liang|last5=Zhang|first5=Yi|last6=Zhang|first6=Yi|date=2020|title=T Cell Dysfunction and Exhaustion in Cancer|url=https://www.frontiersin.org/articles/10.3389/fcell.2020.00017/full|journal=Frontiers in Cell and Developmental Biology|language=English|volume=8|doi=10.3389/fcell.2020.00017|issn=2296-634X}}</ref> Immunosenescence involves both the host's capacity to respond to infections and the development of long-term immune memory. This age-associated [[immune deficiency]] is found in both long- and short-living species as a function of their age relative to life expectancy rather than chronological time.<ref name="Ginaldi2001">{{cite journal|title=Immunosenescence and infectious diseases|journal=Microbes and Infection|year=2001|first=L.|last=Ginaldi |author2=M.F. Loreto |author3=M.P. Corsi |author4=M. Modesti |author5=M. de Martinis |volume=3|issue=10|pages=851–857 |doi=10.1016/S1286-4579(01)01443-5|pmid=11580980 }}</ref> It is considered a major contributory factor to the increased frequency of morbidity and mortality among the elderly.

Immunosenescence involves both the host's capacity to respond to infections and the development of long-term immune memory. This age-associated [[immune deficiency]] is found in both long- and short-living species as a function of their age relative to life expectancy rather than chronological time.<ref name="Ginaldi2001">{{cite journal|title=Immunosenescence and infectious diseases|journal=Microbes and Infection|year=2001|first=L.|last=Ginaldi |author2=M.F. Loreto |author3=M.P. Corsi |author4=M. Modesti |author5=M. de Martinis |volume=3|issue=10|pages=851–857 |doi=10.1016/S1286-4579(01)01443-5|pmid=11580980 }}</ref> It is considered a major contributory factor to the increased frequency of morbidity and mortality among the elderly.


Immunosenescence is not a random deteriorative phenomenon, rather it appears to inversely repeat an evolutionary pattern and most of the parameters affected by immunosenescence appear to be under genetic control.<ref name="Franceschi1999">{{cite journal|title=Biomarkers of immunosenescence within an evolutionary perspective: the challenge of heterogeneity and the role of antigenic load|journal=Experimental Gerontology|year=1999|first=C.|last=Franceschi |author2=S. Valensin |author3=F. Fagnoni |author4=C. Barbi |author5=M. Bonafe|volume=34|issue=8|pages=911–921|doi=10.1016/S0531-5565(99)00068-6 |pmid=10673145|s2cid=32614875}}</ref> Immunosenescence can also be sometimes envisaged as the result of the continuous challenge of the unavoidable exposure to a variety of [[antigens]] such as [[viruses]] and [[bacteria]].<ref name="Franceschi2000">{{cite journal|title=Human immunosenescence: the prevailing of innate immunity, the failing of clonotypic immunity, and the filling of immunological space|journal=Vaccine|year=2000|first=C.|last=Franceschi |author2=M. Bonafè |author3=S. Valensin|volume=18|issue=16|pages=1717–1720|doi=10.1016/S0264-410X(99)00513-7|pmid=10689155 }}</ref> It has also been studied in the model marsupial, the red-tailed phascogale (''Phascogale calura'').<ref>{{cite journal|last1=Letendre|first1=C.| last2=Young|first2=L.J.|last3=Old|first3=J.M.| title=Immunosenescence in a captive semelparous marsupial, the red-tailed phascogale (Phascogale calura) |journal= BMC Zoology |date=2018|volume=3|pages=10|doi=10.1186/s40850-018-0036-3|s2cid=53496572|doi-access=free}}</ref><ref>{{cite journal|last1=Letendre|first1=C.| last2=Young|first2=L.J.|last3=Old|first3=J.M.| title=Limitations in the isolation and stimulation of splenic mononuclear cells in a dasyurid marsupial, Phascogale calura |journal= BMC Research Notes |date=2018|volume=11|pages=856|doi=10.1186/s13104-018-3824-5|doi-access=free}}</ref>
Immunosenescence is not a random deteriorative phenomenon, rather it appears to inversely repeat an evolutionary pattern and most of the parameters affected by immunosenescence appear to be under genetic control.<ref name="Franceschi1999">{{cite journal|title=Biomarkers of immunosenescence within an evolutionary perspective: the challenge of heterogeneity and the role of antigenic load|journal=Experimental Gerontology|year=1999|first=C.|last=Franceschi |author2=S. Valensin |author3=F. Fagnoni |author4=C. Barbi |author5=M. Bonafe|volume=34|issue=8|pages=911–921|doi=10.1016/S0531-5565(99)00068-6 |pmid=10673145|s2cid=32614875}}</ref> Immunosenescence can also be sometimes envisaged as the result of the continuous challenge of the unavoidable exposure to a variety of [[antigens]] such as [[viruses]] and [[bacteria]].<ref name="Franceschi2000">{{cite journal|title=Human immunosenescence: the prevailing of innate immunity, the failing of clonotypic immunity, and the filling of immunological space|journal=Vaccine|year=2000|first=C.|last=Franceschi |author2=M. Bonafè |author3=S. Valensin|volume=18|issue=16|pages=1717–1720|doi=10.1016/S0264-410X(99)00513-7|pmid=10689155 }}</ref> It has also been studied in the model marsupial, the red-tailed phascogale (''Phascogale calura'').<ref>{{cite journal|last1=Letendre|first1=C.| last2=Young|first2=L.J.|last3=Old|first3=J.M.| title=Immunosenescence in a captive semelparous marsupial, the red-tailed phascogale (Phascogale calura) |journal= BMC Zoology |date=2018|volume=3|pages=10|doi=10.1186/s40850-018-0036-3|s2cid=53496572|doi-access=free}}</ref><ref>{{cite journal|last1=Letendre|first1=C.| last2=Young|first2=L.J.|last3=Old|first3=J.M.| title=Limitations in the isolation and stimulation of splenic mononuclear cells in a dasyurid marsupial, Phascogale calura |journal= BMC Research Notes |date=2018|volume=11|pages=856|doi=10.1186/s13104-018-3824-5|doi-access=free}}</ref>
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* [[Hematopoietic stem cells]] (HSC), which provide the regulated lifelong supply of [[leukocyte]] progenitors that are in turn able to differentiate into a diversity of specialised immune cells (including [[lymphocytes]], [[Antigen-presenting cell|antigen-presenting]] [[dendritic cells]], and [[phagocytes]]) diminish in their self-renewal capacity. This is due to the accumulation of [[Oxidative stress|oxidative damage]] to [[DNA]] by aging and cellular metabolic activity<ref>
* [[Hematopoietic stem cells]] (HSC), which provide the regulated lifelong supply of [[leukocyte]] progenitors that are in turn able to differentiate into a diversity of specialised immune cells (including [[lymphocytes]], [[Antigen-presenting cell|antigen-presenting]] [[dendritic cells]], and [[phagocytes]]) diminish in their self-renewal capacity. This is due to the accumulation of [[Oxidative stress|oxidative damage]] to [[DNA]] by aging and cellular metabolic activity<ref>
High frequency electromagnetic waves such as gamma and xrays can penetrate and damage DNA. {{cite journal|title=Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells|journal=Nature|year=2004|first=K|last=Ito |author2=A. Hirao |author3=F. Arai |author4=S. Matsuoka |author5=K. Takubo |author6=I. Hamaguchi |author7=K. Nomiyama |author8=K. Hosokawa |author9=K. Sakurada |author10=N. Nakagata |author11=Y. Ikeda |author12=T. W. Mak |author13=T. Suda |volume=431|issue=7011|pages=997–1002 |doi=10.1038/nature02989|pmid=15496926 |bibcode=2004Natur.431..997I|s2cid=4370804}}</ref> and the shortening of [[telomeric]] terminals of chromosomes.
High frequency electromagnetic waves such as gamma and xrays can penetrate and damage DNA. {{cite journal|title=Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells|journal=Nature|year=2004|first=K|last=Ito |author2=A. Hirao |author3=F. Arai |author4=S. Matsuoka |author5=K. Takubo |author6=I. Hamaguchi |author7=K. Nomiyama |author8=K. Hosokawa |author9=K. Sakurada |author10=N. Nakagata |author11=Y. Ikeda |author12=T. W. Mak |author13=T. Suda |volume=431|issue=7011|pages=997–1002 |doi=10.1038/nature02989|pmid=15496926 |bibcode=2004Natur.431..997I|s2cid=4370804}}</ref> and the shortening of [[telomeric]] terminals of chromosomes.
*Particularly, an increased numbers of MDSCs are observed in bone marrow, spleen and peripheral blood of aged mice. Such accumulation of MDSCs impairs senescence and results in the diminished ability of tumor cell clearance and changes in homeostasis and energetic metabolism.<ref>{{Cite journal|last=Salminen|first=Antero|last2=Kauppinen|first2=Anu|last3=Kaarniranta|first3=Kai|date=2018-10-01|title=Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence|url=https://doi.org/10.1007/s10522-018-9762-8|journal=Biogerontology|language=en|volume=19|issue=5|pages=325–339|doi=10.1007/s10522-018-9762-8|issn=1573-6768}}</ref> Moreover, the increased appearance of MDSCs within a tissue leads to the induction of IL-10 and TGFβ secretion that further promotes tumor cell expansion.<ref>{{Cite journal|last=Salminen|first=Antero|last2=Kauppinen|first2=Anu|last3=Kaarniranta|first3=Kai|date=2019-08-01|title=AMPK activation inhibits the functions of myeloid-derived suppressor cells (MDSC): impact on cancer and aging|url=https://doi.org/10.1007/s00109-019-01795-9|journal=Journal of Molecular Medicine|language=en|volume=97|issue=8|pages=1049–1064|doi=10.1007/s00109-019-01795-9|issn=1432-1440|pmc=PMC6647228|pmid=31129755}}</ref>
* There is a notable decline in the total number of [[phagocytes]] in aged hosts, coupled with an intrinsic reduction of their [[Bactericide|bactericidal]] activity.<ref>{{cite journal|title=Neutrophil ageing and immunesenescence|journal=Mech Ageing Dev|year=2001|first=J.M.|last=Lord|author2=S. Butcher |author3=V. Killampali |author4=D. Lascelles |author5=M. Salmon |volume=122|issue=14|pages=1521–1535|doi=10.1016/S0047-6374(01)00285-8|pmid=11511394 |s2cid=1898942}}</ref><ref>{{cite journal|title=Immunosenescence and macrophage functional plasticity: dysregulation of macrophage function by age-associated microenvironmental changes|journal=Immunol Rev|year=2005|first=R.D.|last=Strout|author2=J. Suttles|volume=205|pages=60–71|doi=10.1111/j.0105-2896.2005.00260.x|pmid=15882345|pmc=1201508 }}</ref>
* There is a notable decline in the total number of [[phagocytes]] in aged hosts, coupled with an intrinsic reduction of their [[Bactericide|bactericidal]] activity.<ref>{{cite journal|title=Neutrophil ageing and immunesenescence|journal=Mech Ageing Dev|year=2001|first=J.M.|last=Lord|author2=S. Butcher |author3=V. Killampali |author4=D. Lascelles |author5=M. Salmon |volume=122|issue=14|pages=1521–1535|doi=10.1016/S0047-6374(01)00285-8|pmid=11511394 |s2cid=1898942}}</ref><ref>{{cite journal|title=Immunosenescence and macrophage functional plasticity: dysregulation of macrophage function by age-associated microenvironmental changes|journal=Immunol Rev|year=2005|first=R.D.|last=Strout|author2=J. Suttles|volume=205|pages=60–71|doi=10.1111/j.0105-2896.2005.00260.x|pmid=15882345|pmc=1201508 }}</ref>
* The cytotoxicity of [[Natural killer cell|natural killer]] (NK) cells and the antigen-presenting function of dendritic cells is known to diminish with old age.<ref>{{cite journal|title=Decreased natural killer cell activity is associated with atherosclerosis in elderly humans|journal=Exp Gerontol|year=2001|first=H.|last=Bruunsgaard |author2=A. N. Pedersen |author3=M. Schroll |author4=P. Skinhoj |author5=B. K. Pedersen|volume=37|issue=1|pages=127–136|doi=10.1016/S0531-5565(01)00162-0|pmid=11738153 |s2cid=32717204}}</ref><ref name="Mocchegiani2004">{{cite journal|title=NK and NKT cell functions in immunosenescence|journal=Aging Cell|year=2004|first=E|last=Mocchegiani|author2=M. Malavolta|volume=3|issue=4|pages=177–184|doi=10.1111/j.1474-9728.2004.00107.x|pmid=15268751 |s2cid=19710282|doi-access=free}}</ref><ref>{{cite journal|title=The frail elderly: role of dendritic cells in the susceptibility of infection|journal=Mech Ageing Dev|year=2002|first=K.|last=Uyemura|author2=S. C. Castle |author3=T. Makinodan |volume=123|issue=8|pages=955–962|doi=10.1016/S0047-6374(02)00033-7|pmid=12044944 |s2cid=11558962}}</ref><ref>{{Cite journal|last1=Sanchez-Correa|first1=Beatriz|last2=Campos|first2=Carmen|last3=Pera|first3=Alejandra|last4=Bergua|first4=Juan M.|last5=Arcos|first5=Maria Jose|last6=Bañas|first6=Helena|last7=Casado|first7=Javier G.|last8=Morgado|first8=Sara|last9=Duran|first9=Esther|last10=Solana|first10=Rafael|last11=Tarazona|first11=Raquel|date=2016-04-01|title=Natural killer cell immunosenescence in acute myeloid leukaemia patients: new targets for immunotherapeutic strategies?|journal=Cancer Immunology, Immunotherapy|language=en|volume=65|issue=4|pages=453–463|doi=10.1007/s00262-015-1720-6|pmid=26059279|s2cid=20498123|issn=1432-0851}}</ref> The age-associated impairment of dendritic [[antigen-presenting cell]]s (APCs) has profound implications as this translates into a deficiency in [[cell-mediated immunity]] and thus, the inability for effector [[T-lymphocytes]] to modulate an [[adaptive immune response]] (see below).
* The cytotoxicity of [[Natural killer cell|natural killer]] (NK) cells and the antigen-presenting function of dendritic cells is known to diminish with old age.<ref>{{cite journal|title=Decreased natural killer cell activity is associated with atherosclerosis in elderly humans|journal=Exp Gerontol|year=2001|first=H.|last=Bruunsgaard |author2=A. N. Pedersen |author3=M. Schroll |author4=P. Skinhoj |author5=B. K. Pedersen|volume=37|issue=1|pages=127–136|doi=10.1016/S0531-5565(01)00162-0|pmid=11738153 |s2cid=32717204}}</ref><ref name="Mocchegiani2004">{{cite journal|title=NK and NKT cell functions in immunosenescence|journal=Aging Cell|year=2004|first=E|last=Mocchegiani|author2=M. Malavolta|volume=3|issue=4|pages=177–184|doi=10.1111/j.1474-9728.2004.00107.x|pmid=15268751 |s2cid=19710282|doi-access=free}}</ref><ref>{{cite journal|title=The frail elderly: role of dendritic cells in the susceptibility of infection|journal=Mech Ageing Dev|year=2002|first=K.|last=Uyemura|author2=S. C. Castle |author3=T. Makinodan |volume=123|issue=8|pages=955–962|doi=10.1016/S0047-6374(02)00033-7|pmid=12044944 |s2cid=11558962}}</ref><ref>{{Cite journal|last1=Sanchez-Correa|first1=Beatriz|last2=Campos|first2=Carmen|last3=Pera|first3=Alejandra|last4=Bergua|first4=Juan M.|last5=Arcos|first5=Maria Jose|last6=Bañas|first6=Helena|last7=Casado|first7=Javier G.|last8=Morgado|first8=Sara|last9=Duran|first9=Esther|last10=Solana|first10=Rafael|last11=Tarazona|first11=Raquel|date=2016-04-01|title=Natural killer cell immunosenescence in acute myeloid leukaemia patients: new targets for immunotherapeutic strategies?|journal=Cancer Immunology, Immunotherapy|language=en|volume=65|issue=4|pages=453–463|doi=10.1007/s00262-015-1720-6|pmid=26059279|s2cid=20498123|issn=1432-0851}}</ref> The age-associated impairment of dendritic [[antigen-presenting cell]]s (APCs) has profound implications as this translates into a deficiency in [[cell-mediated immunity]] and thus, the inability for effector [[T-lymphocytes]] to modulate an [[adaptive immune response]] (see below).

Revision as of 19:38, 30 June 2021

Immunosenescence is the gradual deterioration of the immune system brought on by natural age advancement. The adaptive immune system is affected more than the innate immune system.[1] Besides anergy and exhaustion, immunosenescence belongs among the major immune system dysfunctional states. However, while cell anergy or exhaustion are reversible condition, immunosenescence is believed to be a state that can not be reversed.[2][3] Immunosenescence involves both the host's capacity to respond to infections and the development of long-term immune memory. This age-associated immune deficiency is found in both long- and short-living species as a function of their age relative to life expectancy rather than chronological time.[4] It is considered a major contributory factor to the increased frequency of morbidity and mortality among the elderly.

Immunosenescence is not a random deteriorative phenomenon, rather it appears to inversely repeat an evolutionary pattern and most of the parameters affected by immunosenescence appear to be under genetic control.[5] Immunosenescence can also be sometimes envisaged as the result of the continuous challenge of the unavoidable exposure to a variety of antigens such as viruses and bacteria.[6] It has also been studied in the model marsupial, the red-tailed phascogale (Phascogale calura).[7][8]

Overview of the age-associated decline in immune function

Immunosenescence is a multifactorial condition leading to many pathologically significant health problems in the aged population. Some of the age-dependent biological changes that contribute to the onset of immunosenescence are listed below:

As age advances, there is decline in both the production of new naive lymphocytes and the functional competence of memory cell populations. This has been implicated in the increasing frequency and severity of diseases such as cancer, chronic inflammatory disorders, breakthrough infections and autoimmunity.[20][21] A problem of infections in the elderly is that they frequently present with non-specific signs and symptoms, and clues of focal infection are often absent or obscured by underlying chronic conditions.[4] Ultimately, this provides problems in diagnosis and, subsequently, treatment.

In addition to changes in immune responses, the beneficial effects of inflammation devoted to the neutralisation of dangerous and harmful agents early in life and in adulthood become detrimental late in life in a period largely not foreseen by evolution, according to the antagonistic pleiotropy theory of aging.[22] It should be further noted that changes in the lymphoid compartment is not solely responsible for the malfunctioning of the immune system in the elderly. Although myeloid cell production does not seem to decline with age, macrophages become dysregulated as a consequence of environmental changes.[23]

T-cell functional dysregulation as a biomarker for immunosenescence

The functional capacity of T-cells is most influenced by the effects of aging. In fact, age-related alterations are evident in all stages of T-cell development, making them a significant factor in the development of immunosenescence.[24] After birth, the decline of T-cell function begins with the progressive involution of the thymus, which is the organ essential for T-cell maturation following the migration of precursor cells from the bone marrow. This age-associated decrease of thymic epithelial volume results in a reduction/exhaustion on the number of thymocytes (i.e. pre-mature T-cells), thus reducing output of peripheral naïve T-cells.[25][26] Once matured and circulating throughout the peripheral system, T-cells still undergo deleterious age-dependent changes. Together with the age-related thymic involution, and the consequent age-related decrease of thymic output of new T cells, this situation leaves the body practically devoid of virgin T cells, which makes the body more prone to a variety of infectious and non-infectious diseases.[6]

By age 40, an estimated 50% to 85% of adults have contracted human cytomegalovirus (HCMV), which is believed to be a major cause of immunosenescence,[1] although this is controversial.[27] Despite the fact that an average of 10% (and up to 50%) of the CD4 and CD8 memory T cells of HCMV-infected persons may be CMV-specific, these persons do not have a higher fatality rate resulting from other infections.[27]

T-cell components associated with immunosenescence include:

References

  1. ^ a b Pangrazzi L, Weinberger B (2020). "T cells, aging and senescence". Experimental Gerontology. 134: 110887. doi:10.1016/j.exger.2020.110887. PMID 32092501. S2CID 211237913.
  2. ^ Crespo, Joel; Sun, Haoyu; Welling, Theodore H.; Tian, Zhigang; Zou, Weiping (2013-04). "T cell anergy, exhaustion, senescence, and stemness in the tumor microenvironment". Current Opinion in Immunology. 25 (2): 214–221. doi:10.1016/j.coi.2012.12.003. ISSN 1879-0372. PMC 3636159. PMID 23298609. {{cite journal}}: Check date values in: |date= (help)
  3. ^ Zhang, Zhen; Liu, Shasha; Zhang, Bin; Qiao, Liang; Zhang, Yi; Zhang, Yi (2020). "T Cell Dysfunction and Exhaustion in Cancer". Frontiers in Cell and Developmental Biology. 8. doi:10.3389/fcell.2020.00017. ISSN 2296-634X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ a b Ginaldi, L.; M.F. Loreto; M.P. Corsi; M. Modesti; M. de Martinis (2001). "Immunosenescence and infectious diseases". Microbes and Infection. 3 (10): 851–857. doi:10.1016/S1286-4579(01)01443-5. PMID 11580980.
  5. ^ a b Franceschi, C.; S. Valensin; F. Fagnoni; C. Barbi; M. Bonafe (1999). "Biomarkers of immunosenescence within an evolutionary perspective: the challenge of heterogeneity and the role of antigenic load". Experimental Gerontology. 34 (8): 911–921. doi:10.1016/S0531-5565(99)00068-6. PMID 10673145. S2CID 32614875.
  6. ^ a b Franceschi, C.; M. Bonafè; S. Valensin (2000). "Human immunosenescence: the prevailing of innate immunity, the failing of clonotypic immunity, and the filling of immunological space". Vaccine. 18 (16): 1717–1720. doi:10.1016/S0264-410X(99)00513-7. PMID 10689155.
  7. ^ Letendre, C.; Young, L.J.; Old, J.M. (2018). "Immunosenescence in a captive semelparous marsupial, the red-tailed phascogale (Phascogale calura)". BMC Zoology. 3: 10. doi:10.1186/s40850-018-0036-3. S2CID 53496572.
  8. ^ Letendre, C.; Young, L.J.; Old, J.M. (2018). "Limitations in the isolation and stimulation of splenic mononuclear cells in a dasyurid marsupial, Phascogale calura". BMC Research Notes. 11: 856. doi:10.1186/s13104-018-3824-5.
  9. ^ High frequency electromagnetic waves such as gamma and xrays can penetrate and damage DNA. Ito, K; A. Hirao; F. Arai; S. Matsuoka; K. Takubo; I. Hamaguchi; K. Nomiyama; K. Hosokawa; K. Sakurada; N. Nakagata; Y. Ikeda; T. W. Mak; T. Suda (2004). "Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells". Nature. 431 (7011): 997–1002. Bibcode:2004Natur.431..997I. doi:10.1038/nature02989. PMID 15496926. S2CID 4370804.
  10. ^ Salminen, Antero; Kauppinen, Anu; Kaarniranta, Kai (2018-10-01). "Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence". Biogerontology. 19 (5): 325–339. doi:10.1007/s10522-018-9762-8. ISSN 1573-6768.
  11. ^ Salminen, Antero; Kauppinen, Anu; Kaarniranta, Kai (2019-08-01). "AMPK activation inhibits the functions of myeloid-derived suppressor cells (MDSC): impact on cancer and aging". Journal of Molecular Medicine. 97 (8): 1049–1064. doi:10.1007/s00109-019-01795-9. ISSN 1432-1440. PMC 6647228. PMID 31129755.{{cite journal}}: CS1 maint: PMC format (link)
  12. ^ Lord, J.M.; S. Butcher; V. Killampali; D. Lascelles; M. Salmon (2001). "Neutrophil ageing and immunesenescence". Mech Ageing Dev. 122 (14): 1521–1535. doi:10.1016/S0047-6374(01)00285-8. PMID 11511394. S2CID 1898942.
  13. ^ Strout, R.D.; J. Suttles (2005). "Immunosenescence and macrophage functional plasticity: dysregulation of macrophage function by age-associated microenvironmental changes". Immunol Rev. 205: 60–71. doi:10.1111/j.0105-2896.2005.00260.x. PMC 1201508. PMID 15882345.
  14. ^ Bruunsgaard, H.; A. N. Pedersen; M. Schroll; P. Skinhoj; B. K. Pedersen (2001). "Decreased natural killer cell activity is associated with atherosclerosis in elderly humans". Exp Gerontol. 37 (1): 127–136. doi:10.1016/S0531-5565(01)00162-0. PMID 11738153. S2CID 32717204.
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  16. ^ Uyemura, K.; S. C. Castle; T. Makinodan (2002). "The frail elderly: role of dendritic cells in the susceptibility of infection". Mech Ageing Dev. 123 (8): 955–962. doi:10.1016/S0047-6374(02)00033-7. PMID 12044944. S2CID 11558962.
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