Autoimmunity to protective molecules (Re: What if......)

[Guest guest]

>> Here's the main problem raised by that view. Why aren't there more

known symptom-causing autoreactivities in the classical infectious

diseases (especially chronic ones)?

> I was under the impression that there were already plenty of them. It's

> been widely reported that the 1918 flu was so lethal mainly because it

> overstimulated the immune system (thus, also, leading to its higher

> lethality in the young and healthy). Many common symptoms (e.g. fever)

> are consequences of immune system activation. But perhaps you are

> defining autoreactivity narrowly, so that these sorts of things don't

> qualify?

I'm defining autoreactivity not as reactivity beyond the host's best

interest, but as reactivity against host molecules. So the 1918 flu

doesn't qualify if its virulence is mainly due to reaction to viral

molecules (I don't know if that's so).

> In any case, it's not a very profitable activity to investigate

> autoreactivity in diseases long known to be caused by infections.

Indeed. Whether the 1918 flu features serious harmful autoreactivity,

no one may even know. It's apparently not a terribly well-resolved

question for many mycobacterioses or infections generally. It's a

subject that in addition to usually being secondary in practical

importance, as you say, can also be hell to investigate. Even

investigating autoreactivities in the first place can be difficult (T

cells are stickier to investigate than antibodies), but showing

whether they are harmful or not is often far harder.

> > [...] We know that stress

> >state bacteria are hard to kill and can be culture-negative, but they

> >also tend to be small (perhaps to increase their surface area : volume

> >ratio for better nutriment uptake).

> ...or perhaps for the same reason you'd get smaller if _you_ were

> starved.

One can watch the numbers go up, though (despite total energy

starvation), as the cell sizes shrink. Some also say it could

additionally be a dispersal mechanism. If a cell in a starvation

environment divides into 25 ultramicrocells, that's 24 more chances to

colonize a more fun environment. It's good business all around.

[Guest guest]

On Mon, Jul 09, 2007 at 10:01:17PM -0000, wrote:

>

>>> Here's the main problem raised by that view. Why aren't there more

>>>known symptom-causing autoreactivities in the classical infectious

>>>diseases (especially chronic ones)?

>

>> I was under the impression that there were already plenty of them. It's

>> been widely reported that the 1918 flu was so lethal mainly because it

>> overstimulated the immune system (thus, also, leading to its higher

>> lethality in the young and healthy). Many common symptoms (e.g. fever)

>> are consequences of immune system activation. But perhaps you are

>> defining autoreactivity narrowly, so that these sorts of things don't

>> qualify?

>

>I'm defining autoreactivity not as reactivity beyond the host's best

>interest, but as reactivity against host molecules. So the 1918 flu

>doesn't qualify if its virulence is mainly due to reaction to viral

>molecules (I don't know if that's so).

In that case, let me go back to that quote from the book you cited

a while ago ( " The Mystery of Autoimmune Diseases " , by T. E. W. Feltkamp,

in _The Decade of Autoimmunity_, by Y. Shoenfeld (editor)):

Everyone is autoimmunopotent. This means that everyone has not

only autoreactive B cells waiting for help of proper T cells, but

is in fact producing many anti-self antibodies. A glance at a

Western blot, showing your own serum full of distinct antibodies

reacting with your own cytoplasmic and nuclear antigens, is

revealing. Serologists working in routine laboratories were

already aware of this phenomenon for a long time. They decided

not to report the presence of autoantibodies, such as rheumatoid

factors, to clinicians, unless the titre is above the level which

is present in 95% of the population. Thus, the presence of

autoantibodies is a completely normal phenomenon, unless the

titres are so high that they sre only found in 5% of the local

population. The adjective " local " is of utmost importance. In

" underdeveloped " areas of the world, for instance, the immune

system is far more active. This results in far higher levels of

autoantibodies in the normal local population.

Notice especially the last two sentences.

[Guest guest]

On Mon, Jul 09, 2007 at 08:43:42PM -0400, Norman Yarvin wrote:

>On Mon, Jul 09, 2007 at 10:01:17PM -0000, wrote:

>>

>>>> Here's the main problem raised by that view. Why aren't there more

>>>>known symptom-causing autoreactivities in the classical infectious

>>>>diseases (especially chronic ones)?

>>

>>> I was under the impression that there were already plenty of them. It's

>>> been widely reported that the 1918 flu was so lethal mainly because it

>>> overstimulated the immune system (thus, also, leading to its higher

>>> lethality in the young and healthy). Many common symptoms (e.g. fever)

>>> are consequences of immune system activation. But perhaps you are

>>> defining autoreactivity narrowly, so that these sorts of things don't

>>> qualify?

>>

>>I'm defining autoreactivity not as reactivity beyond the host's best

>>interest, but as reactivity against host molecules. So the 1918 flu

>>doesn't qualify if its virulence is mainly due to reaction to viral

>>molecules (I don't know if that's so).

>

>In that case, let me go back to that quote from the book you cited

>a while ago ( " The Mystery of Autoimmune Diseases " , by T. E. W. Feltkamp,

>in _The Decade of Autoimmunity_, by Y. Shoenfeld (editor)):

>

> Everyone is autoimmunopotent. This means that everyone has not

> only autoreactive B cells waiting for help of proper T cells, but

> is in fact producing many anti-self antibodies. A glance at a

> Western blot, showing your own serum full of distinct antibodies

> reacting with your own cytoplasmic and nuclear antigens, is

> revealing. Serologists working in routine laboratories were

> already aware of this phenomenon for a long time. They decided

> not to report the presence of autoantibodies, such as rheumatoid

> factors, to clinicians, unless the titre is above the level which

> is present in 95% of the population. Thus, the presence of

> autoantibodies is a completely normal phenomenon, unless the

> titres are so high that they sre only found in 5% of the local

> population. The adjective " local " is of utmost importance. In

> " underdeveloped " areas of the world, for instance, the immune

> system is far more active. This results in far higher levels of

> autoantibodies in the normal local population.

>

>Notice especially the last two sentences.

On second thought, I guess you'll object that those higher levels of

antibodies aren't noted as producing symptoms. Still, with there being

lots of autoantibodies, and lots of extra symptoms, it'd be surprising if

the two had absolutely nothing to do with each other.