In article <880mvg$u0d$1 at nnrp1.deja.com>, Jamie Cunliffe
<URL:mailto:cunlij at my-deja.com> wrote:
> In article <ant101644b49Pk=+ at mrc7acorn1.path.cam.ac.uk>,
> Mike Clark <mrc7 at cam.ac.uk> wrote:
>>> The trouble is that if you try to force immune recognition to fit a neat
>> 25 word or less summary your bound to get it wrong. Any immune system
>> that declared to the environment how it worked in very simple and easy
>> to follow unwavering rules is doomed. A degree of unpredictability in
>> immune response is almost certainly an asset to survival of a species.
>> Mike
>> There's a lot of meat to reply to here! Not least in expanding on your
> second and third sentences. That is the subject of a maturing file. But
> let's stick with "bound to get it wrong". Do you want to wager on that?
> Ok, I won't argue that you won't find detail that is wrong. But I will
> wager
>> a) The conventional view is fatally flawed.
> b) The system is a morphostatic not an enemy hunting system.
We are not necessarily talking about how it evolved but about how the
immune system is used by higher organisms now.
If I have immunoglobulins with specificity for a pathogen and then when the
pathogen enters the body the antibodies form an immune complex with the
pathogen where is the disorder that the antibodies recognise?
>> >
> > What bugs me is just how slavishly some people will adhere to simple
> > ideas even in the face of overwhelming contradictory evidence!
>> Please tabulate so that I can address.
>>>>> They conveniently forget that you can tolerise a mouse with human IgG in
>> deaggrated form but if you aggregate it or put it into adjuvant the
>> same protein sequence becomes highly immunogenic. The mouses immune
>> system is not 'responding' to the sequence difference of the human IgG
>> but to other properties of the administered preparation.
>> Once again (see reply to Ian) aggregated proteins are typical of
> intracellular disorder or sick self cells. If you had to guess what
> typifies sick or spilt cells you'd probably come up with this list.
>> Aggregated proteins
> Lots of HSPs
> Inside out membranes
> Organelles membranes
> Mitochondrial membranes
> Nuclear membranes
> ECF DNA
> Spilt Il-1 (why don't apoptosing cells - with lots of intracellular Il-
> 1 - stimulate inflammation and immune responses?)
> Eicosanoids released in response to membrane damage
> I bet you could add a lot of candidates yourself if you have really
> understood what I am saying.
Yes but aggregated antibodies are not typical of intracellular disorder
they are typical of immune complexes with pathogens!
Aggregated antibodies activate complement and bind to low affinity FcR as
to immune complexes. I'm not discussing how the system evolved just how it
works now.
[snip]
>> Jamie
Mike Clark, <URL:http://www.path.cam.ac.uk/~mrc7/>
--
o/ \\ // || ,_ o M.R. Clark, PhD. Division of Immunology
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