Current Research Into Telomeres III
excelife at earthlink.net
Wed Sep 2 01:13:17 EST 1998
In article <35ECC85A.513B at netcom.ca>, tmatth at netcom.ca says...
>> Dr R. Effros at U.C.L.A. is researching the effects of telomeric >>
shortening on the T-Cells in the immunological systems of the elderly. >>
Her observations include the dominance of senescent "memory" T-cells in >>
>To be precise, are you saying that Rita Effros has found that the
>*majority* of memory T-cells are now longer able to divide and produce
>more such T-cells? Do you have a reference for this?
The cite for this study is Am J. Hum.Gen. 62-5 May 98;(1003-1007). A better
study addressing your question would be Effros RB, Pawlee G, Immunology
Today, 1997, 18;(450-454) where she researches the Hayflick limit and immune
>> which may "prevent renewal of the T-cell pool with more functional
>>T-cells". The implications being that the restoration of replicative
>>capacity in those T-cells that are approaching senescence could have the
>>effect of restoring functioning of some parts of the immunological system
>>in the elderly.
>Or since now you say "are approaching senescence" do you mean that she
>found that the T-cells had reduced replicative ability in older people?
>(which would not necessarily be related to any telomere shortening).
Yes the "memory" T-cells showed senescent characteristics including the
inability to replicate and the short telomeres associated with senescence.
Specifically a cell surface molecule CD28 is not expressed in senescent
T-cells. One proposed function of CD28 is the induction of the enzyme
telomerase, (Weng et al. J. Exp. Med. 1996, 183:2472-2479). Lacking the
expression of telomerase the telomeres in these T-cells shortened and the
cells entered senescence.
The implications being that re-activating telomerase prior to critical
telomeric shortening can avoid senescence altogether and maintain functioning
of the immune system.
>> Rawes V, Kipling D, Kill IR and Faragher RG at The University of Brighton,
>> UK, have demonstrated results that "suggest that the process of senescence
>> is a common feature of different cell lineages but that the specific rate
>> can differ between them."
>Do they mean different "rate" or after a different number of divisions?
I'm not sure of your exact question here. They are saying that particular
cell lines replicate faster than others, lose telomeric length and enter
senescence at an earlier time. Because they are the same cell line and have
similar telomeric length, the cells enter senescence at approx. the same
>> Thus the cell lines constituting the endothelial cells
>> in the vascular system may be experiencing telomeric loss faster than
>> cell lines in the body. This may be a factor underlying age-related
>> "disease" progression in some systems of the body.
>Certainly, because division "rate" is highly different in different
>dividing systems and under different life, and health (sometimes
Absolutely! As is seen in T-cells, specifically in HIV patients, where
T-cells are forced to replicate faster to meet an infection their telomeres
shorten because the cells are replicating faster than telomerase can replace
>> Tahara H, et al, at Hiroshima University School of Medicine, Japan,
>> demonstrated that "a significant proportion of WRN, (Werner's syndrome),
>> cell strains showed drastic shortening or lengthening of telomere lengths
>> during cell passages compared with normal cell strains" This confirms
>> earlier studies that Werner's syndrome and the childhood aging disease
>> progeria result from errors in the system(s) that maintain telomeric >>
>But it doesn't say anything about whether these diseases are related to
It fully conforms to the telomeric theory of aging that suggests that if a
person were born with shortened telomeres their cells would senesce faster
and they would exhibit the signs of aging.
>Sorry, to be always playing the "skeptic", Tom.
No need to be sorry! Skepticism is one of the foundations of science. One
should always test for the null hypothesis and only by proving that wrong can
they make any claim to knowledge. The more you challenge any particular
theory the sounder the reasoning to support it has to be.
>I found your post to be most interesting, as usual.
Thank you! I do try to be informative and accurate. If I make a factual
error or mis-state the findings of some research I WANT to be told about it.
It does me absolutely no good to be operating on false assumptions. It's an
old saying that if the facts don't fit the theory then change the theory not
Thomas Mahoney, Pres.
Lifeline Laboratories, Inc.
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