NatAttack3000

NatAttack3000 t1_iswpok1 wrote

It does, but GM-CSF is released to create more phagocytic cells because they are being depleted by the infection - DCs definitely die off due to increased apoptosis in sepsis (this contributes to post sepsis immunosuppression) and in severe infections like severe influenza. I suppose this is far more relevant for something relatively severe, with heavy symptoms that you take days to fight. An acute infection with little symptoms is not likely to do this, but I'm still dubious about saying you have more effective innate immunity during an acute infection given how common confections are too... Active inflammation also inhibits other immune functions like for formation of germinal centres, some t cell functions etc, so having extra neutrophils might help with some aspects but not others.

An example is BCG vaccination (a live vaccine) induces emergency granulopoiesis which confers short term protection against bacterial sepsis, so an infectious 'nudge' like thia to the immune system can help it in the short term but you don't want to whack it with a baseball bat (eg. Severe influenza).

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NatAttack3000 t1_isv6o3h wrote

That inflammation doesn't make us super immune for a time, otherwise we would be inflamed all the time. Inflammation comes at a cost - causes cell death, uses up energy. When you have an acute infection, you can deplete things like DCs and other phagocytes briefly and become somewhat immunosuppressed until they recover - this explains the very real phenomenon of secondary infections (eg. Bacterial pneumonia at the tail and of a bad influence infection). So in real terms most people ARE at higher risk of infection following an initial infection, particularly if the infection was severe

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NatAttack3000 t1_isv65oc wrote

Kids also don't have the breadth of immune memory as adults do, so your child might get sick from every new virus they encounter (or most of them) while adults have immunity from having seen that virus 10 times already in their lifetime.

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NatAttack3000 t1_isv5rju wrote

Tha adaptive immune system is highly specific, but the innate immune system plays an important role in the start of an infection. When it is busy trying to kill one thing you are at slightly higher risk of a different infection- this is largely why secondary infections are a thing.

The adaptive immune system kicks in a bit later, and is certainly more powerful, but a functional innate immune system should prevent a lot of pathogens from causing infections before the adaptive response has really had to worry about it, by phagocytosis etc. Especially if the exposure dose of virus/pathogen is fairly low.

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NatAttack3000 t1_isv5hmn wrote

No they're right. The innate immune system plays an important role in the start of an infection. When it is busy trying to kill one thing you are at slightly higher risk of a different infection- this is largely why secondary infections are a thing.

What you are speaking about is the adaptive immune system which kicks in a bit later, and is certainly more powerful, but a functional innate immune system should prevent a lot of infections before the adaptive response has really had to worry about it.

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