Another study:

Here's your answer. Macrophages produce non-specific immune response. Meaning they don't have the role of identifying and producing antibodies against P.acne or any other pathogen. That's done by B cells and T cells and its called specific immune response. But unfortunately B cells and T cells don't play a role here (as far as we know).

That's actually not true. T cells are extensively involved in acne and thus the proliferation/induction of macraphages. That's why acne's considered a DTH response...

Then I take it back. What's the specific role of T cells in P.acne response and where can I read the related literature/studies?

Confused. Do you want to know how the body responds to p.acnes or how p. acnes contributes to the development of acne...since p. acnes does not cause acne?

This might help:




More info:
http://www.acne.org/messageboard/acne-from...es-t199729.html

here is something that could add to this thread, what do you guys think??

http://www.physorg.com/news112424870.html

http://www.attitudefactor.com/immune.htm

After reading the study, I'm confused at the original post. The study does say that B cells do not respond in normal acne cases, only during severe acne. We also know that B cells are responsible for producing antibodies. So why should one expect that antibodies would be produced against P.acne in normal acne cases?

OK...you're confusing me

What I don't get is why we need a vaccine against p. acnes when we already produce antibodies against p. acnes (plenty of studies shows this)......and p. acnes doesn't CAUSE acne.

I guess...in severe cases....like nodulocystic acne, p. acnes is trapped and builds up within this particular pore. This is further irritating, thus the antibodies come out....too simplistic?

However...antibodies can also be present due to other antigenic triggers such as pore clogging ingredients, irritating skin care ingredients, herbs, foods, etc.

I sort of get what he means. You can have both memory B-cells and memory T-cells. When we talk about acne as a DTH, we are speaking of a T-cell mediated response. Basically, you have a feedback loop in which T cells activate macrophages upon exposure to the antigen. Macrophages can then activate the T cells. This chronic activation will lead to inflammation, because lots of inflammatory mediators are released. So when the OP wrote about developing "antibodies," he wasn't completely correct--only the most severe cases have antibodies involved....

double post

hey hey hey,

been reading the literature sweetjade posted which is informtive and has cleared some of my misconceptions.

my immunology is a bit sketchy its been a while since i've used it. macrophages are always first at a site of infection not always the first for immune response but contributes to the immune response but causing a chain reaction ultimatly if needed, B cells for antibdies and memory cells.

when a spot forms the number of p. acne in the follicle is abnormal, this causes waste products to accumulate in the follicle. i suspect the first stages of the immune response occures but its this response that causes acne.

if i understand correctly inflammation occures, the site becomes red and heavily dilated because of the body redirecting resources to fight the infection. the body does not know if this invasion is by a simple organism or something more serious one. during the next couple of days, the bacteria dies probably through phagocytosis in relation to john1234's comment, it most probably be a t-cell mediated response, antibodies i don't believe assists much, possibly neutralizing toxins produced or improving phagocytosis (or in cystic or severe acne where the bacteria has grown beyound the follicle and erupted in the hypodermis and getting close to the blood supply thus causing a harsher response?). anyway; ultimatly puss forms at the site due to bacteria destruction and bacteria replication; samaging surrounding cells. at the end of the infection all the bacteria would have been killed and the body begins the repair stage.

p. acne is part of the natural human flora. we have many other organisms. they are hamless and helps the body but when they appear in unsual places or when their number get to high, the body will defend itself causing adverse physiological and biological reactions.

Because your body doesn't see the p. acne as an actual threat, hence is why it doesn't get eaten by the macrophages. The acne bacteria are normal, and everyone has it. It's not foreign to our body. This is just a rough guess, I might be way off but that's my 2 cents.

So let me get this straight, hormones and other factors onset a inflammatory response, but we are not exactly sure how?

Could someone put this all into perspective for me. I get that the bacteria does not play a part and that something is causing the body to inflict an inflammatory response, I just don't get why or where the hormones come in.

Well, to start off, there are several factors involved in acne formation: hyperkeratinization, sebum (over)production, presence/activity of P. acnes bacteria, and inflammation. Hyperkeratinization is abnormal shedding of skin cells within the follicles, which creates plugs... these "plugged follicles" are called microcomedones... if there is some drainage (of sebum and the other contents), it will become an open comedo, or blackhead. If there is no drainage, it will become a closed comedo, or whitehead, which can become an inflamed lesion, such as a pustule or cyst. So, microcomedones are the precursors to all acne lesions.

The big question, is what causes these factors in the first place, namely, what triggers the formation of microcomedones? The info found earlier in this post is about research involved with the answer to this question. I’ll just sum it all up for you, which will hopefully help you put it into perspective.

Basically, it appears that in most cases, hereditary differences in our skin’s innate immune system make us more likely to produce an immune response to certain internal or external stimuli. The immune response changes the cycle of the sebaceous follicle, increasing the proliferation of skin cells within the follicle… and because of the other substances within the follicles (e.g. keratin, sebum), plugs form (microcomedones), and normal drainage can no longer occur.

The stimuli discussed as the probable triggers of this initial immune response are a combination of androgens, certain hormone receptors, certain regulatory neuropeptides/ cytokines, deficiency in certain anti-oxidants, and certain environmental factors (specifically, stress response or topical stress, diets containing pro-inflammatory substances, and smoking).

A further immune response can result due to chemical changes which occur to the obstructed comedo as it progresses, which is where P. acnes can be involved. At this point, pustules or other inflamed lesions are formed.

This post has been edited by theComfyCat: Oct 1 2009, 03:47 PM