interferons...

Started by CalculusCrazed
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CalculusCrazed

CalculusCrazed

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Why aren't interferons part of the adaptive immunity system? It seems like they adapt according to my book:

"Infection by one kind of virus actually can produce protection against infection by other kinds of viruses."

It's not really pertinent to know, just curious. Any ideas?
 
SDN is not for hwk.

Also why would something all purpose and general like interferons be part of something specific?
 
Interferons are THE crucial paracrine/endocrine signalling molecule of the innate immune system. Read some journals if your so concerned.

They upregulate general ISGs that are not specific to the infection at hand. Hence, they are innate rather then adaptive.
 
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serenade said:
SDN is not for hwk.

Also why would something all purpose and general like interferons be part of something specific?
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Lol, not "hwk." Genuine curiosity. If you don't like that, then you don't have to comment.

I don't think you understand my question. They seem to be adaptive, at least from what I can gather. That ability to adapt would, logically, place them in the adaptive immunity system in my mind. Just wondering why they are considered innate, when they do change.

But, since I should not be doing "hwk" on SDN, then I suppose I should expect no intellectually stimulating conversation with my fellow pre-meds.
 
Wow, I am just now learning about A&P. There is no need to jump down my throat here. If you didn't have anything polite to respond with, you should have ignored my post.
 
Well I'm not actually how "adaptive" interferons are. I do know that a basis for the adaptability of the immune system is the hypervariable region of antibodies produced by B cells. Essentially you have two major component to the antibody, the heavy and light chain. The heavy gene is encoded by 3 genes and the light chain 2 genes (actually two different types of light chains). I forget the exact numbers but there are many different forms of the gene that code for each individual component of a light of heavy chain (its like the V D and J segment, V would have 40, D like 6 and J like 20) and by having different combinations of different segments you create variability in the structure of the anitbody allowing it to recognize different antigens. So yea you can see there is a great variability simply from the huge different number of combinations of different chain genes. But there is also further randomization of the process (aka more adaptability) because of the way the genes that will code for the antibody are tethered together. The body uses a tamed transposable element to excise parts the regions of the genome with these chain genes to place a V D and J next to each other (light has only 2 genes, I think V and J). The process involves a double strand DNA break which to repair requires a plethora of enzymes however the process is inaccurate so that extra nucleotides can possibly be added or removed in random fashion to the region involved in the double strand DNA break.

Thus the same combination of V D and J in one cell will not be the same if the same genes are picked in another cell due to this messy repair.

That's at least part of adaptive immunity at least the part I understand. Don't know much at all about interferons but maybe someone else can help you there.
 
Also, I guess something interesting to note is the relatively recent adaptive immunity has emerged in the evolutionary timeline. I think it first appeared by in chondrichthyes. Again, it all has to do with the tamed transposable element. Our genomes are riddled with them as they usually excise themselves and reinsert in different places without discretion. However the transposable element in us codes for a analog of a transposase with the ability to excise a specific sequence of usually inverted DNA in a way that creates blunt ends (the dsDNA break) place the different V D J fragments next to each other.
 
CalculusCrazed said:
Why aren't interferons part of the adaptive immunity system? It seems like they adapt according to my book:

"Infection by one kind of virus actually can produce protection against infection by other kinds of viruses."

It's not really pertinent to know, just curious. Any ideas?
Click to expand...

Now that I've actually read your question, I'll take a swing at the answer 😛


If infection with a virus leads to a cell non-specifically releasing a number of interferons that happen to protect against a variety of viruses, there is nothing adaptive about this. If I am interpreting your question correctly, you may be confusing "a response against multiple threats" (could be innate or adaptive) with "a response tailor made to the threat at hand" (which is adaptive)
 
theWUbear said:
Now that I've actually read your question, I'll take a swing at the answer 😛


If infection with a virus leads to a cell non-specifically releasing a number of interferons that happen to protect against a variety of viruses, there is nothing adaptive about this. If I am interpreting your question correctly, you may be confusing "a response against multiple threats" (could be innate or adaptive) with "a response tailor made to the threat at hand" (which is adaptive)
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"If infection with a virus leads to a cell releasing a number of interferons," is that not a specific response? Interferons are being released due to the presence of some sort of specific antigen on the viral surface. I think a way interferons may work is that they target a part of viral surfaces that is highly conserved, so that in response to releasing against one virus it can also successfully target other viruses because the substrate or surface it is specific for is common for many viruses.
 
Rednawz said:
"If infection with a virus leads to a cell releasing a number of interferons," is that not a specific response? Interferons are being released due to the presence of some sort of specific antigen on the viral surface.I think a way interferons may work is that they target a part of viral surfaces that is highly conserved, so that in response to releasing against one virus it can also successfully target other viruses because the substrate or surface it is specific for is common for many viruses.
Click to expand...

You are thinking of antibodies, which are part of adaptive immunity. Interferons have the same action at the same site no matter what the infection is, and that same action happens to be effective against multiple viruses.
 
DrYoda said:
You are thinking of antibodies, which are part of adaptive immunity. Interferons have the same action at the same site no matter what the infection is, and that same action happens to be effective against multiple viruses.
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That's exactly what I mean by saying interferons target high conserved regions.
 
theWUbear said:
Now that I've actually read your question, I'll take a swing at the answer 😛


If infection with a virus leads to a cell non-specifically releasing a number of interferons that happen to protect against a variety of viruses, there is nothing adaptive about this. If I am interpreting your question correctly, you may be confusing "a response against multiple threats" (could be innate or adaptive) with "a response tailor made to the threat at hand" (which is adaptive)
Click to expand...

So essentially, it is not adapting, just able to protect against many different things. I guess the book confused me in that, I took it as if there was some sort of genetic change that made it more potent over other viruses.
 
What would you say the types of substrates are for the anti-viral gene products?!
 
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Where do I ever say interferons are adaptive? They are specific yes, adaptive no. Complement (I'm guessing you refer to proper substrate binding, and not the way its used in genetics) is specific binding.
 
theWUbear said:
reading comprehension, serenade

that's highlighted for you trigger happy mods as well. you wouldn't dare close this thread in forum #11 (allo)
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Heh, I guess I'll have to apologize for the heuristic analysis. Anyways... everyone knows that the most important information is in the first sentence :laugh:.
 
DrYoda said:
The point here is it's a general anti-infectious effect that is not adaptive. Complement is effective against various infections but that doesn't make it part of adaptive immunity.
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Yep. Nothing adaptive there. No recombination, no somatic hypermutation, no memory. The complement system and the interferon response are all coded in your raw genes and they recognize patterns on viruses/their peptides.
 
Interferons are produced by a number of cells, mostly innate but also by adaptive cells. You can expect early on in infection that NK cells and macrophages produce interferon. Middle stage of infection, interferon can be secreted by CD4+ T cells, specifically Th1 cells. This inflammatory response is usually in reaction to intracellular pathogens.

Upon reinfection, these same CD4+ T cells can produce interferon at an earlier time point during the infection. This is because of the development of memory T cells.
 
Rednawz said:
Where do I ever say interferons are adaptive? They are specific yes, adaptive no. Complement (I'm guessing you refer to proper substrate binding, and not the way its used in genetics) is specific binding.
Click to expand...

Complement is not specific, it binds to your own cells all the time. However, not enough can bind at one time to cause perforation or phagocytosis.
 
serenade said:
SDN is not for hwk.
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And since when is SDN not for Hawks?

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It's important to understand that there are many different interferons whose production is stimulated by various things. Most of the receptors that signal for interferon production are stimulated by general viral or bacterial products. For instance, during viral infection, often dsRNA is produced as an intermediate in replication. Both cytosolic and cell surface receptors can recognize this dsRNA in a SEQUENCE INDEPENDENT manner, such as RIG-I or TLR-3, leading to not only an upregulation or Interferon Stimulated Genes (ISGs) but also the production of the proteins in the pathway, including RIG-I or TLR-3. In this way, the cell becomes hypersensitive to further infection for a short period of time. In this way you can see how IFN-s may seem adaptive, when in reality they are non-specifically acting on general products of viral infection.
 
Here is a great review of interferon signaling:

http://www.ncbi.nlm.nih.gov/pubmed/16681834

It's important to remember that the innate immune system is most clearly distinguished from the adaptive system in that it functions through the distinction between self and non-self. The body has developed various receptors that recognize broad patterns associated with pathogenic material, called pathogen-associated molecular patterns (PAMPs). The body's pattern recognition receptors (PRRs) then become activated and induce the appropriate response. Receptors that probe for specific patterns associated with viral nucleic acid tend to activate a cascade of signaling which induces the transcription of interferons.
 
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