Chapter 31: Assessment of Immune Function

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Welcome back to the Deep Dive.

Today we are jumping straight into what is probably one of the most complex but absolutely essential fields in nursing.

Oh, absolutely.

The immune system.

The textbook.

And our mission today is really to turn that density into clear, actionable knowledge you can use at the bedside.

That's right.

The immune system is it's just notoriously challenging.

I mean, you have cells, chemicals, organs, they're all constantly moving, constantly talking to each other.

It's a huge amount of information.

It's overwhelming.

It is.

So this deep dive, we've designed to, you know, walk you through the core concepts, the anatomy, the physiology, the stages of response, and most critically, the nursing assessment you need to master.

Right.

Because our goal isn't just to read definitions from a textbook.

We want to understand the clinical significance.

Why does this matter for my patient today?

Precisely.

Let's get right into it.

The very beginning.

What even is immunity?

Okay, let's start there.

So at its core, immunity is the body's protective response.

But it's highly specific.

It's aimed at foreign agents, foreign organisms, and it's really about maintaining homeostasis.

Okay.

So it's not just about fighting germs.

It's about balance.

Exactly.

It has three vital functions.

First, defense.

That's the one we all think about.

But second is rapid response.

And third is surveillance.

It's constantly checking to make sure your own cells are behaving.

And that surveillance depends on two really key properties, doesn't it?

Yeah.

Memory and tolerance.

Absolutely critical.

Immune memory is why, you know, you get chicken pox once and you're protected for life.

Right.

And tolerance is the system's ability to recognize your own cells and leave them alone while going after everything else.

When tolerance fails, well, that's where so many diseases begin.

Okay.

So before we go any further, we have to get the language right, the clinical vocabulary.

We have to.

Let's start with the basics, the invader and the response.

The invader is the antigen.

The antigen.

So that's the protein or whatever substance that kicks the whole thing off.

That's it.

It induces the immune response.

And the mirror image of that is the antibody, the protein the body makes in response to that specific antigen.

The custom -made weapon.

The custom -made weapon.

And these antibodies have specific actions.

The textbook mentions agglutination.

Which is just a clumping effect.

Exactly.

The antibodies kind of cross -link the antigens, make them clump together, which makes them easier to deal with.

It's also used in things like blood typing.

Okay.

And then there's a word that always sounds complicated.

Opsinization.

It does, but the concept is simple.

It's basically a preparation step for cleanup.

You're making the target easier to see.

You're making it easier to grab.

The antigen antibody molecules get coated with these sticky proteins.

Think of it like trying to grab a slippery fish.

If you dip it in honey first, it's much easier to hold onto.

That honey is Opsinization.

And it

is called phagocytosis.

Literally cell eating.

Cell eating.

White blood cells, like macrophages, just ingest and destroy those coated foreign particles.

That's a great analogy.

It makes it really clear.

And what about when the body needs to destroy its own cells?

That is apoptosis.

Programmed cell death.

So this is the controlled demolition.

Perfectly put.

It's the botter's methodical way of eliminating cells that are worn out, infected, or potentially malignant.

It's a critical process.

If it fails, a cancer cell might survive if it happens too much.

You get autoimmune damage.

You get autoimmune damage.

It's all about that regulation.

Which brings us to the system level terms.

Immunoregulation, the checks and balances, and immunopathology.

The study of what happens when it all goes wrong.

And when it does go wrong, the source gives us four major categories of immune disorders.

This is straight from table 31 to 1.

It's a really good framework.

It is.

The first is autoimmunity.

This is that failure of tolerance we just talked about.

The body attacks itself.

Exactly.

The immune response gets misdirected.

Think of rheumatoid arthritis or lupus.

The body is seeing its own joints as foreign.

Okay.

The second category is an overreaction.

Hypersensitivity.

Right.

This is an inappropriate or just exaggerated response to something that should be harmless.

Allergies.

Allergies.

From hay fever all the way to life threatening anaphylaxis.

The response is just way out of proportion to the threat.

Okay.

Third,

problems with overproduction.

Gammopathies.

Yeah.

This is when you get an overproduction of immunoglobulins.

Those antibody proteins.

You see this in conditions like multiple myeloma where one specific type of plasma cell just goes into overdrive.

And the last big bucket is immune deficiencies.

And you have to distinguish the two types here.

You have primary immune deficiencies.

The ones you're born with.

Right.

Congenital or inherited.

The system just never developed correctly.

And then you have secondary immune deficiencies.

The ones you acquire later.

Exactly.

Caused by something external that interferes with a system that was previously working fine.

This could be an illness like HIV or what we see all the time in the hospital.

Immunosuppressive medications.

So understanding that distinction is key for your nursing care.

It dictates everything, especially your infection control priorities.

Okay.

So that's the foundation.

Now let's get into the architecture.

If immunity is an army, where are the barracks, the training grounds, the bases?

A great way to think about it.

The anatomy is everything.

And we have to start at the production center.

The bone marrow.

Ground zero.

It is ground zero.

It's the source of all your white blood cells, your leukocytes.

They all come from stem cells in the marrow.

And these stem cells can become anything.

They're pluripotent.

Exactly.

They differentiate down different pathways to become your B cells, which make antibodies, and your T cells, the direct attackers, if the bone marrow factory is compromised.

Say from chemotherapy.

The entire defense system just collapses.

That's why bone marrow function is such a critical nursing assessment.

Okay.

So the cells are produced.

Where do they go for training and deployment?

That's the lymphoid tissues.

Right.

These are your filtering and proliferation hubs.

Let's start with the spleen.

The spleen is like a huge blood filter.

It's got red pulp, which cleans out old red blood cells, but its white pulp is packed with lymphocytes.

It's a major surveillance outpost.

Which is why if a patient has their spleen removed.

They're at a huge risk for certain bacterial infections,

specifically encapsulated bacteria.

It's a critical clinical point.

They lose that filtering capacity.

Got it.

And then the lymph nodes,

they're everywhere.

And they are phenomenal.

Their main job is to filter the lymph fluid before it gets back into the bloodstream.

They trap invaders.

Okay.

But their second job is to be the proliferation centers.

When an antigen shows up, the B and T cells in that node start multiplying like crazy.

And clinically.

That's the swollen gland you feel in your neck when you have a sore throat.

That's exactly it.

That's lymphadenopathy.

You are literally feeling the army being built.

Okay.

So we have the architecture.

Now for the function.

The source splits this into the two pillars.

Natural and acquired immunity.

We need to really understand the difference here.

Okay.

So natural immunity.

This is also called innate immunity.

It's what you're born with.

It's your first line of defense.

Broad spectrum.

Generic is a perfect word.

It's rapid, but it doesn't have a memory.

It sees a bad guy.

It attacks.

It doesn't remember the bad guy's face for next time.

It uses cells like monocytes, macrophages, and natural killer cells.

Okay.

The immediate responders.

Immediate responders.

And they set the stage for the which is acquired immunity.

This is the one that develops after you're born.

Right.

You get it from being exposed to an antigen, either by getting sick or by getting a vaccine.

And the key features here are specificity and memory.

It's tailored protection.

It is.

It's slower to get going the first time, but it provides durable, specific protection for the long haul.

And we can break that down even further into how you get it right.

Active versus passive.

We can.

Active acquired immunity is when your own body does the work.

So you get a vaccine, your body makes the antibodies and the memory cells.

Exactly.

And that's why it's usually long lasting years or even a lifetime.

Okay.

In contrast, passive acquired immunity is temporary.

You're getting the protection from an outside source.

Like a baby getting antibodies from mom through the placenta.

That's the classic example.

Or getting an injection of immune globulin after you've been exposed to something.

It's a

protection fades.

Okay.

That makes sense.

So an invasion happens.

The natural barriers are breached.

The body has three main ways to respond.

Right.

Three responses that work together.

The very first one is the phagocytic immune response.

The cleanup crew.

The cleanup crew and the first attackers.

Your white blood cells, especially macrophages, rush in, find the foreign particles and just eat them.

They also clean up any of your own dead cells.

So after that initial rush, you get the more specific weapons.

The second line is the humoral immune response.

This is your B cell response.

Humoral means related to the body fluids.

So B cells turn into plasma cells.

The antibody factory.

The antibody factories.

And they pump huge amounts of these customized antibodies into your blood and tissues to find and neutralize the invaders.

Okay.

And then the third line, the ground troops,

the cellular immune response.

This is your T cells.

They become cytotoxic or killer T cells.

And unlike antibodies, which kind of tag things for destruction,

T cells attack directly.

Hand to hand combat.

It is.

They find an infected cell, bind to it, and basically punch holes in its membrane until it bursts.

Wow.

Now before all of that specific stuff happens, there's that initial reaction we all recognize.

Inflammation.

Yes.

The inflammatory response is a huge part of natural immunity.

It's triggered by any injury.

Chemicals like histamine are released and the whole point is to wall off the area and call in those first responder phagocytes.

And this works alongside the physical barriers like skin and mucus membranes.

And the chemical barriers.

Things like stomach acid or enzymes in your tears and a really important one called interferon, which is specifically used to fight viruses.

Okay.

So let's put it all together.

The source uses figure 31 to 5 to show the four stages of the immune response.

This is like the timeline of the whole battle.

It is.

And understanding this timeline helps you predict what you'll see in your patient.

It starts with stage one recognition.

The alarm goes off.

The alarm goes off.

Your lymphocytes are constantly patrolling looking for anything that's not self.

Macrophages help process and show these antigens to the lymphocytes.

The system recognizes these things called PMPs.

Pathogen associated molecular patterns.

Right.

They're like microbial barcodes.

The system sees a barcode that doesn't belong and it signals danger.

And that signal triggers stage two proliferation.

The alarm is confirmed.

So now you build the army.

The lymphocytes that recognize the threat travel to the nearest lymph node and tell the B and T cells there to start dividing rapidly.

Which is again why we feel those swollen lymph nodes.

That's the army being built.

You are palpating the proliferation stage.

You've built the numbers.

Now stage three response.

The army gets its orders.

Right.

The new cells differentiate.

Gee cells become plasma cells and start making antibodies.

That's the humoral response.

T cells become killer T cells.

That's the cellular response.

And most infections use both.

Right.

But one is usually in the lead.

One usually dominates.

For a virus like mono, the T cell response is huge.

For a bacterial infection, the antibody response might be more prominent.

And finally, the attack itself.

Stage four effector.

This is it.

The weapons connect with the target.

The antibody latches onto the bacteria or the T cell latches onto the infected cell.

And that connection triggers destruction.

Usually with help from complement and macrophages.

The invader is neutralized or destroyed.

OK.

Let's go deeper into those two big responses.

Starting with the humoral immune response.

The antibody factory.

So it all starts at the B cell recognizing a specific antigen.

When that happens, it differentiates into two crucial types of cells.

First, the plasma cell uses short lived factories.

Exactly.

They're built for one purpose.

Turn out massive amounts of antibodies right now.

But the second type of cell is just as important.

The memory cells.

And this is the whole basis for vaccination.

This is it.

The memory cells stick around for years, sometimes a lifetime, holding the blueprint for that specific antibody.

So if you ever see that antigen again, the response is immediate and massive, immediate, massive, and much more effective.

OK, let's look at the antibody itself.

These are proteins called immunoglobulins or egg.

The structure is key, right?

The Y shape.

That Y shape is everything.

The tips of the Y are the antigen binding sites.

That's what makes it specific.

The lock and key fit.

And once it binds, it can trigger agglutination, opsonization, and it can activate the complement system.

OK, now for nurses, chart 31 -2, the five classes of immunoglobulins, is absolutely core knowledge.

Non -negotiable.

You have to know these.

Let's start with the big one, IgG.

OK, IgG.

It's about 75 % of your total.

It's the workhorse for fighting bloodborne and tissue infections.

But the most important clinical fact about IgG is that it's the only one that crosses the placenta.

So this is how mom gives the baby passive immunity.

Exactly.

It protects that newborn for the first few months of life.

It's critical.

OK, next up, IgA.

IgA is about 15%.

And for IgA, think secretions.

It's found in saliva, tears, breast milk, and all the mucous membranes.

It's the guardian of your internal surfaces, like your gut and your respiratory tract.

The first line of defense at the entry point.

Precisely.

Next, IgM.

About 10%.

IgM is the first responder, right?

It's the first one on the scene.

It's the first IG produced when you have a new infection.

So if you see high levels of IgM in a patient's blood work, it usually means they have an acute active infection happening right now.

That's a huge clinical clue.

OK, what about IgD?

It's a tiny amount.

Very small, 0 .2%.

Its role isn't totally clear, but it seems to be involved in helping B cells differentiate.

Not a major player clinically for us day to day.

And then the one we all know from allergies, IgE.

IgE.

The tiniest fraction, but it causes the biggest trouble.

It's the one involved in allergic and hypersensitivity reactions.

It binds to mass cells, and when it sees this allergen, it triggers that massive release of histamine.

Anaphylaxis.

Anaphylaxis, asthma, hives.

That's IgE.

It's also involved in fighting off parasitic infections.

Now, the whole system depends on that perfect lock and key fit.

But what happens when the fit is core?

This idea of cross reactivity.

This is where things can go terribly wrong.

Cross reactivity is when an antibody made against a foreign invader is

similar enough that it accidentally recognizes and attacks one of your own body's cells.

And the classic example of this is rheumatic fever.

It is.

The body makes antibodies to fight off a strep throat infection.

But tragically, a protein on the strep bacteria looks very similar to a protein found in human heart valves.

So the antibodies kill the strep.

And then they turn around and start attacking the heart.

It's called molecular mimicry, and it can cause permanent damage.

It's a devastating case of mistaken identity.

Okay, let's pivot to the other arm of the response.

The cellular immune response.

The T cells.

The direct attackers.

So T cells are born in the bone marrow, like B cells, but they travel to the thymus gland to mature.

That's where they get their T.

They're educated there to tell the difference between self and non -self.

And there are different types of T cells.

Table 31 to 3 breaks them down.

Let's start with the most important the helper T cells or CD4 plus gig.

The helper T cells are the generals.

They are the central commanders of the entire adaptive immune response.

When they get activated, they start secreting massive amounts of cytokines.

And we need to pause here.

Cytokines aren't antibodies, but they are the language of the immune system.

They are the command signals.

Absolutely.

These cytokines from the helper T cell will activate B cells.

They'll activate the killer T cells.

They'll call in macrophages.

The helper T cell decides what kind of battle it's going to be.

Which is why the CD4 count is so critical in monitoring HIV.

The virus takes out the general.

It takes out the general and the whole army falls into disarray.

Okay, then we have the assassins.

Yeah.

The cytotoxic T cells, CD8 plus.

Or killer T cells.

These are the direct attackers we talked about.

They hunt down your own body cells that have been infected with a virus or have become cancerous and they destroy them directly.

And they're the primary culprit in graft rejection, right?

They are.

They see that new kidney or liver as foreign and they are programmed to attack and destroy it.

So if you have killers, you must need a way to call them off.

That's the suppressor T cells.

Exactly.

They're the breaks.

Once the infection is cleared, the suppressor T cells step in and tell everyone to stand down.

They prevent the response from going on for too long and causing damage.

Okay.

We also have some other lymphocytes mentioned.

Null lymphocytes and natural killer cells.

Right.

Null cells help destroy antigens that are already coated with antibodies.

But the natural killer cells, or NK cells, are really interesting.

They're part of the innate system, but they are expert assassins of tumor cells and virally infected cells.

They're your first line of cancer surveillance.

Wow.

Okay, one last piece to this puzzle.

The amplification system that works with everything.

The complement system.

Yes, you can't forget complement.

It's a series of about 25 proteins just floating inactive in your blood, mostly made by the liver.

And without it, antibodies alone aren't always enough.

Often not enough.

Compliment is the ultimate amplifier.

Its three main jobs are defense against bacteria, bridging the innate and acquired systems, and cleaning up immune complexes.

And it works like a cascade, like dominoes falling.

A classic cascade.

One protein activates the next, which activates the next.

And this chain reaction leads to chemotaxis, calling more cells in, and ultimately the formation of something called the membrane attack complex.

Which does what it sounds like it does.

It punches a hole right through the membrane of the target cell, causing it to explode.

And this can be triggered in a few different ways, which shows how integrated it is.

Right.

The classic pathway is triggered by antibodies, so that's the adaptive system.

But the lectin and alternative pathways can be triggered directly by microbes, so that's part of the innate system.

It connects everything.

And the clinical tie -in here for chronic disease is huge.

It is.

In diseases like lupus, this complement cascade is just constantly inappropriately activated, and that runaway inflammation causes massive damage to tissues like the kidneys.

Okay, that's a lot of pathophysiology.

Let's shift to how we intervene.

Medical treatments, specifically immunomodulators.

Right.

These are biologic response modifiers.

We use them when the body's own response is either too weak or too strong.

One major category is interferons.

These are proteins our body makes naturally to fight viruses.

They are, and we can give them as a drug.

They don't kill the virus directly, but they kind of warn the neighboring cells to put up their defenses.

They also boost the activity of NK cells and macrophages.

We use them for things like hepatitis C and MS.

Okay.

Another big category, especially oncology, are the colony stimulating factors.

CSFs.

CSFs are growth factors for your bone marrow.

After a round of chemotherapy wipes out a patient's white blood cells, we can give them a CSF to tell the bone marrow to ramp up production of neutrophils, for example.

So it pulls them out of that dangerous neutropenic state faster.

Much faster.

It's a critical supportive care measure.

And then we get to the really targeted therapies.

Monoclonal antibodies.

Moabs.

This is a huge leap forward.

These are lab -made synthetic antibodies.

They are designed to target one very specific antigen.

So instead of chemotherapy, which is like a carpet bomb.

These are the smart bombs.

Exactly.

A Moab can be designed to only target a protein that's on the surface of a cancer cell, blocking the signals that cell needs to grow and sparing the healthy cells around it.

And beyond these specific drugs, the source points to some really revolutionary advances.

It does.

Genetic engineering is one.

We can now manufacture immune proteins in the lab.

And even more advanced is gene therapy, where we try to fix a defective gene in a patient, like in a child born with SCID.

And the use of stem cells.

Right.

A stem cell transplant can essentially reset a person's entire immune system.

It's standard of care for some primary immunodeficiencies.

And it's being explored for severe autoimmune diseases.

And of course, the huge field of cancer and immunotherapy.

This is the future.

Things like checkpoint inhibitors.

They're drugs that basically take the breaks off the patient's own immune system, allowing their T cells to see and attack the cancer that was hiding from them.

It's incredibly powerful.

But also carries risks of overstimulating the system.

Absolutely.

It can cause autoimmune -like side effects that nurses have to be really skilled at managing.

Which is the perfect transition to the nurse's primary role in all of this.

Assessment.

None of this matters if we can't assess our patients properly.

It all starts with a thorough health history and physical exam.

You have to identify every single factor that could be compromising that patient's defense.

And there are some variables we might not always think about, like gender.

Right.

Why are so many autoimmune diseases more common in women?

Well, it seems to be linked to sex hormones.

Estrogen can enhance the immune response, while androgens can be suppressive.

Fascinating.

And then there's the unavoidable factor.

Aging.

Gerontologic considerations or immunosenescence.

This is so, so important.

As we age, our immune system naturally declines.

The thymus shrinks, the bone marrow doesn't work as well, our lymphocytes get sluggish.

And table 31 -4 outlines the consequences.

What are the big takeaways for nurses?

The biggest one is that an older adult might not mount a classic response to infection.

They might have a raging pneumonia and have a normal temperature.

So a fever is not a reliable sign.

Not at all.

You have to look for the subtle signs.

New confusion, a change in functional status, weakness.

Those might be your only clues.

They also have a decreased response to vaccines.

It's a state of increased vulnerability across the board.

And another area the nurse can directly impact is nutrition.

Oh, it's a critical determinant.

You cannot build an army without supplies.

Deficiencies in protein, in zinc, in other micronutrients, they directly lead to a weakened immune response.

So a nutritional assessment is not just a nice to have.

It's a core part of an immune assessment.

It's a priority.

You have to assess their caloric intake, their protein status.

Poor nutrition equals poor immune function.

Period.

We also need to assess immunization status.

Right.

And not just for kids, for adults too.

Are they up to date on their flu shot, their pneumococcal vaccine, their shingles vaccine, their Tdap?

It's a key part of health maintenance and infection prevention.

Okay.

When we're taking a history of infections and allergies,

what are the red flags for immune problems?

You're looking for patterns, recurrent infections,

fevers that have no clear cause, a history of TB exposure,

recent travel to areas with endemic diseases, a history of STIs.

All of these should raise your suspicion.

And for allergies, documentation is everything.

It has to be exhaustive.

What's the allergen?

What's the specific reaction?

And it has to be flagged in the EHR.

A mistake here can be fatal.

Let's talk about how other diseases impact immunity, like autoimmune and neoplastic diseases.

Right.

With cancer, it's a double -lammy.

The disease itself can suppress the immune system.

And then the treatments we use, chemotherapy, radiation, they suppress it even further.

So we're constantly walking a tightrope.

Constantly.

And for existing autoimmune diseases, you need to know their baseline, their medications, and their history of flare -ups.

What about more common things like chronic illness and surgery?

Absolutely.

Uncontrolled diabetes, for example, is terrible for immune function.

The high blood sugar impairs white blood cell activity.

Renal disease is another one.

Even something acute like a stroke can cause a temporary state of immunosuppression.

Which is why stroke -associated pneumonia is so common.

And so deadly.

Meticulous infection control for post -stroke patients is a must.

And then, of course, medications.

Table 31 -5 is a huge safety alert.

Every nurse needs to be familiar with that list.

The big ones are corticosteroids, like prednisone.

They are miraculous anti -inflammatories, but they work by wiping out your lymphocytes.

Cytotoxic chemo drugs are another.

You have to be watching that patient's CBC like a hawk.

You also mentioned transfusions and lifestyle factors.

Right.

A history of transfusions is important.

And lifestyle.

Smoking, excessive alcohol, poor diet.

All of these things chip away at your immune defenses.

Even extreme exercise can be a stressor that temporarily suppresses the system.

This leads us to a really modern concept.

Psychoneuroimmunology.

The mind -body connection.

This isn't theoretical anymore.

We know there's a physical, bi -directional pathway.

Your immune cells have receptors for stress hormones.

Chronic stress, depression, anxiety.

They have a measurable negative impact on immune function.

And conversely, positive strategies can help.

They can.

The research in chart 31 -5 shows that things like mindfulness -based stress reduction can actually lower inflammatory cytokines in the body.

So assessing a patient's stress level and coping is a legitimate part of an immune assessment.

So after that exhaustive history,

we get to the hands -on part.

The physical assessment checklist from chart 31 -3.

Right.

It has to be head to toe.

You start with inspection, look at the skin, the mucous membranes.

Are there any rashes, lesions that won't heal?

Check their temperature.

And then palpation of the lymph nodes.

Carefully palpate the cervical, axillary, and inguinal nodes.

You feeling for size, tenderness, consistency?

Are they tender, suggesting infection?

Or are they hard, fixed, and non -tender, which is more concerning for malignancy?

And what about the other systems?

You're looking for clues everywhere.

Swollen, tender joints in the musculoskeletal system, crackles in the lungs, an enlarged liver or spleen in the abdomen, cognitive changes in the neuro exam.

The immune system touches every part of the body, so your assessment has to as well.

Okay.

So assessment is done.

We move to diagnostic evaluation.

The tests in chart 31 -6.

Right.

The tests help us confirm what we suspect.

We can do tests for humoral immunity counting B cells, measuring antibody levels.

And for cellular immunity.

We can do a total lymphocyte count.

And more specifically, we can count the subsets.

The CD4 and CD8 counts.

The ratio between those two cells tells us a lot.

Now, during this whole diagnostic workup, what is the key nursing management priority?

Honestly,

it's managing the psychological burden.

This is a terrifying time for patients.

They're waiting for results that could change their entire life.

So our role is counselor and educator.

Counselor, educator, and supporter.

We have to explain the tests, manage their anxiety, and empower them with information.

It's a profoundly important part of our role.

You know, everything we've covered, from that first recognition of a microbe to the complexity of T cells,

it's just so vast.

But it's the foundation for expert clinical judgment.

It really is.

The immune system forces you to be a holistic nurse.

You have to think about physiology, aging, nutrition, pharmacology, psychology, all at the same time for every patient.

So the big takeaways are really understanding the difference between the humoral and cellular responses, knowing those four stages of defense,

and being able to spot all those external factors, the drugs, the diet, the stress that can weaken a patient's defenses.

I think so.

And looking forward, as we use more and more of these advanced immunotherapies, the nurse's role is changing dramatically.

We're shifting from just being managers of infection to becoming managers of immune modulation.

Our focus is going to be less on treating the bug and more on recognizing and managing the complex, often paradoxical side effects of tweaking the body's own powerful defense system.

That's a huge shift from infection fighter to immune modulator manager.

That really is the future of nursing care.

Thank you for joining us for this deep dive into immune function.

We hope this has given you a clear roadmap to use in your practice.