</p><p class="MsoNormal">*By Myriams-Fotos on pixabay.com*</p><p class="MsoNormal"></p><p class="MsoNormal">
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*Lately, I haven't had much time to write for Steem, mostly because my MSc program is eating up all my time with deadlines over deadlines. One of the deadlines was for an essay on the innate and the adaptive immune system. I received it back with a decent grade (which surprised me, I didn't write an essay since school), so I thought "why not share it with Steemians?". It's on a higher level than my usual science posts, obviously. I might share my other essays too, once they're graded. Don't want to get punished for plagiarism because I put my essay online too early ...*
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<b>Introduction</b></p><p class="MsoNormal">Every organism exists in a constant fight for survival. The
most <span style="mso-no-proof:yes">apparent</span> fight may be the one
against being eaten by other organisms, but <span style="mso-no-proof:yes">many
threats are</span> not as immediately visible. Pathogens in the <span style="mso-no-proof:yes">form</span> of bacteria, viruses, or parasites are a
persistent hazard to the health of any larger organism, be it a plant or an
animal. To defend themselves, humans have developed a sophisticated immune
system, consisting of both an innate and adaptive part. The two parts, while often
being described as separate from each other, work closely together.</p>
<p class="MsoNormal"><span style="mso-no-proof:yes">The innate immune system
forms the first line of</span> defence. Barriers like the skin <span style="mso-bidi-font-family:"Times New Roman"">(Proksch et al., 2008)</span> together with the mucociliary
epithelium <span style="mso-bidi-font-family:"Times New Roman"">(Sadikot et al., 2005)</span> in the airways and acid in
the stomach <span style="mso-bidi-font-family:"Times New Roman"">(Salama et al., 2013)</span> prevent pathogens from
entering the body and infecting cells in the first place. If a pathogen manages
to breach through, it <span style="mso-no-proof:yes">is immediately met</span>
with antimicrobial proteins <span style="mso-bidi-font-family:"Times New Roman"">(Gallo and Hooper, 2012)</span>, lysozymes <span style="mso-bidi-font-family:"Times New Roman"">(Fleming, 1922; Irwin et al., 2011)</span>, and the complement system <span style="mso-bidi-font-family:"Times New Roman"">(Sarma and Ward, 2011)</span>, which are often enough <span style="mso-no-proof:yes">to kill it quickly</span>. The classical pathway of
the complement system results in a membrane attack complex (MAC), which creates
a hole in the pathogen’s membrane. <span style="mso-bidi-font-family:"Times New Roman"">(Sarma and Ward, 2011)</span></p>
<p class="MsoNormal">A survival of this immediate response <span style="mso-no-proof:yes">is followed</span> by the early innate response,
during which innate immune cells migrate to the area of infection <span style="mso-bidi-font-family:"Times New Roman"">(Jones, 2000)</span>. The cells take up pathogens
through phagocytosis, which is where their name “phagocytes” derives from, and
trigger an inflammatory response, recruiting more so-called professional
phagocytes <span style="mso-bidi-font-family:"Times New Roman"">(Rosales and Uribe-Querol, 2017)</span>. At the same <span style="mso-no-proof:yes">time,</span> a <span style="mso-no-proof:yes">particular</span>
type of phagocyte, the dendritic cells (DCs), <span style="mso-no-proof:yes">migrates</span>
into the lymphoid tissue to present the antigen derived from the invading
pathogen to the lymphocytes, which are cells of the adaptive immune system,
serving as the main link between the two systems <span style="mso-bidi-font-family:"Times New Roman"">(Banchereau and Steinman, 1998)</span>.</p>
<p class="MsoNormal">Upon coming into contact with an antigen, T lymphocytes (or
T-cells) mature into either cytotoxic T-cells (Tc cells), which proceed to kill
cells with intracellular pathogens (e.g. viruses), or T-helper cells (Th cells),
which among other things help activate B-cells <span style="mso-bidi-font-family:"Times New Roman"">(Kaech and Cui, 2012)</span>. B lymphocytes (or B-cells)
also <span style="mso-no-proof:yes">recognise</span> antigens, with each B-cell
expressing receptors that match one specific antigen. An activated B-cell can
secrete its receptors as Immunoglobulins, also called Antibodies (Abs) <span style="mso-bidi-font-family:"Times New Roman"">(Pernis et al., 1971)</span>, which then opsonise,
aggregate or neutralise pathogens <span style="mso-bidi-font-family:"Times New Roman"">(Tomasi, 1970)</span>. They can also create a link
back to the innate immune system to activate the classical pathway of the
complement system, resulting in a MAC <span style="mso-bidi-font-family:"Times New Roman"">(Ochsenbein and Zinkernagel,
2000)</span>,
or facilitate the death of the pathogen via <span style="mso-no-proof:yes">antibody-dependent</span>
<span style="mso-no-proof:yes">cell mediated</span> cytotoxicity (ADCC). ADCC
is the result of a natural killer (NK) cell, which is part of the innate immune
system, recognising the pathogen-bound antibody and promptly killing the cell <span style="mso-bidi-font-family:"Times New Roman"">(Leibson, 1997)</span>. </p>
<p class="MsoNormal">Looking at these two crucial parts of the immune system that
work very closely together, the question arises if one displays any advantages
over the <span style="mso-no-proof:yes">other</span> and if one can <span style="mso-no-proof:yes">be regarded</span> as “better”.</p>
<p class="MsoNormal"><b>Discussion</b></p>
<p class="MsoNormal">With the overarching goal of the immune system being to keep
the body alive, healthy, and free of pathogens, an evaluation of the innate and
adaptive systems must focus on which one has the highest impact on this goal. Which
do humans need more to survive?</p>
<p class="MsoNormal"> </p>
<p class="MsoNormal"><b><i>Innate immunity: Protection from the beginning</i></b></p>
<p class="MsoNormal">The innate immune system, as the name already suggests, is
the one we are born <span style="mso-no-proof:yes">with</span>. It develops
during gestation and functions even without previous exposure to pathogens <span style="mso-bidi-font-family:"Times New Roman"">(Ygberg and Nilsson, 2012)</span>. <span style="mso-no-proof:
yes">And</span> while breastfed babies receive antibodies through the <span style="mso-no-proof:yes">milk</span> their mothers produce <span style="mso-bidi-font-family:"Times New Roman"">(Butler, 1979)</span>, innate immunity is the <span style="mso-no-proof:yes">central</span> defence against pathogens a new-born
child has. </p>
<p class="MsoNormal">While the adaptive immune system does exist at birth too, research
shows that the high amount of T and B lymphocytes present at birth exhibit only
a very low level of functionality <span style="mso-bidi-font-family:"Times New Roman"">(Ygberg and Nilsson, 2012)</span>. Only over time does this
part slowly learn to <span style="mso-no-proof:yes">recognise</span> pathogens <span style="mso-no-proof:yes">and</span> it typically takes 1.5 to 2 years until a
child can produce antibodies to bacterial capsular polysaccharides <span style="mso-bidi-font-family:"Times New Roman"">(Rijkers et al., 1998)</span>.</p>
<p class="MsoNormal"><span style="mso-no-proof:yes">Considering the discrepancy
in the speed of development</span>, adaptive immunity appears to be severely
lacking.</p>
<p class="MsoNormal"> </p>
<p class="MsoNormal"><b style="mso-bidi-font-weight:normal"><i style="mso-bidi-font-style:
normal">Specific recognition of the pathogens that slip through</i></b></p>
<p class="MsoNormal">Once, <span style="mso-no-proof:yes">however,</span> the
adaptive immune system is fully matured, it can fight pathogens that managed to
escape the innate one. If <span style="mso-no-proof:yes">a virus has
successfully infected a cell</span>, the innate immune system tends to be
unable to recognise this, as long as the virus doesn’t cause the cell to go
into apoptosis <span style="mso-bidi-font-family:"Times New Roman"">(Arandjelovic and Ravichandran,
2015)</span>
or stops the expression of the <span style="mso-no-proof:yes">major</span> <span class="e24kjd">histocompatibility </span>complex class I (MHC I), the latter
being a “kill signal” for NK cells <span style="mso-bidi-font-family:"Times New Roman"">(Anfossi et al., 2006)</span>. This is where Tc cells step
in: They recognize viral proteins produced inside the cell and presented
through the MHC I <span style="mso-bidi-font-family:"Times New Roman"">(Monaco, 1992)</span> and react with the release of
perforin, granzyme, and granulysin, which has a cytotoxic effect on the
infected cell <span style="mso-bidi-font-family:"Times New Roman"">(Krensky and
Clayberger, 2005; Thiery and Lieberman, 2014).</span></p>
<p class="MsoNormal">If the pathogen that evaded the innate immunity is not a
virus, Th and B-cells work together to get rid of it. When an antigen-specific
Th cell comes in contact with a B-cell specific for the same antigen, the
B-cell differentiates into either an antibody-producing plasma <span style="mso-no-proof:yes">cell</span> or a memory B-cell <span style="mso-bidi-font-family:"Times New Roman"">(Lanzavecchia, 1985; Parker,
1993)</span>.
While plasma cells proliferate, a process called clonal expansion, and produces
antigen-specific antibodies<span style="mso-spacerun:yes"> </span><span style="mso-bidi-font-family:"Times New Roman"">(Lane et al., 1981)</span>, the memory B-cells migrate
into the bone marrow where they store the antigen information in case of a
reinfection and can survive for a long time <span style="mso-bidi-font-family:"Times New Roman"">(Manz et al., 1998; Slifka and
Ahmed, 1998)</span>.</p>
<p class="MsoNormal">The memory and antigen-specificity are what the innate
immune system is lacking, and what makes the adaptive immune system so <span style="mso-no-proof:yes">valuable</span>.</p>
<p class="MsoNormal"> </p>
<p class="MsoNormal"><b style="mso-bidi-font-weight:normal"><i style="mso-bidi-font-style:
normal"><span style="mso-ansi-language:EN-US" lang="EN-US">Less specific antigen
recognition has its strengths </span></i></b></p>
<p class="MsoNormal"><span style="mso-no-proof:yes">It is possible for B-cells to
differentiate</span> into plasma cells without Th cell stimulation, but only if
the antigen possesses a highly repetitive structure, usually due to
polysaccharides on its surface. Antigens of this kind are called
“thymus-independent” <span style="mso-bidi-font-family:"Times New Roman"">(Stein, 1992)</span>. The problem with this
pathway is the lack of “isotope switching”, a process required to create
different types of antibodies. Thymus-independent differentiation only yields
IgM antibodies that are excellent at activating the complement <span style="mso-no-proof:yes">system</span> but <span style="mso-no-proof:yes">are
not</span> as effective in opsonisation, neutralisation, agglutination, or the
facilitation of ADCC <span style="mso-bidi-font-family:"Times New Roman"">(Forthal, 2014)</span>. <span style="mso-no-proof:
yes">Th</span> cell cytokines <span style="mso-no-proof:yes">are required</span>
for a switch to IgG, IgE, or IgA antibodies, all of them possessing different
characteristics necessary for <span style="mso-no-proof:yes">an effective</span>
immune response <span style="mso-bidi-font-family:"Times New Roman"">(Coffman et al., 1993)</span>. </p>
<p class="MsoNormal"><span style="mso-no-proof:yes">However,</span> this is not
the only weakness of the B-cell’s need for collaboration with an
antigen-specific Th cell. IgM antibodies might seem like a decent defence, but
as mentioned in the introduction, bacterial capsular polysaccharides <span style="mso-no-proof:yes">are not recognised</span> by young children’s adaptive
immune systems. <span style="mso-no-proof:yes">This</span> lack of recognition means
that not only does the less-specific antigen recognition by B-cells result in
antibodies with low functional variety<span style="mso-no-proof:yes">; it</span>
<span style="mso-no-proof:yes">does not</span> even necessarily function during
early human life.</p>
<p class="MsoNormal">Innate immune cells, on the other hand, are less specific in
recognising pathogens, but the broad spectrum of pathogen-associated molecular
patterns (PAMPs) detected via pattern-recognition receptors (PRR) like the
toll-like receptors (TLR) is often more than sufficient to trigger an
inflammation response that can successfully fight pathogens <span style="mso-bidi-font-family:"Times New Roman"">(Bianchi, 2007)</span>. <span style="mso-no-proof:
yes">In fact,</span> <span style="mso-no-proof:yes">it is likely that that at
least 98% of pathogens can</span> be fought off by the innate immune system
alone, without requiring additional help from adaptive immune cells <span style="mso-bidi-font-family:"Times New Roman"">(Jones, 2000)</span>. </p>
<p class="MsoNormal">A lower specificity also has the advantage of being faster,
while the innate system can react immediately or within a few hours, adaptive
immunity can take days to become fully functional <span style="mso-bidi-font-family:"Times New Roman"">(Borghesi and Milcarek, 2007)</span>. By the time T and B-cells
have reached the point of being able <span style="mso-no-proof:yes">to fight
the infection adequately</span>, the innate immune system might have already
taken care of it.</p>
<p class="MsoNormal"> </p>
<p class="MsoNormal"><b style="mso-bidi-font-weight:normal"><i style="mso-bidi-font-style:
normal">Innate and adaptive immunity cannot be <span style="mso-no-proof:yes">clearly</span>
separated</i></b></p>
<p class="MsoNormal">Looking at the weaknesses of both innate and adaptive
immunity possess; it becomes apparent that they tend to complement each other.
While the adaptive immune system <span style="mso-no-proof:yes">would not</span>
be able to function without antigen presentation by innate <span style="mso-no-proof:yes">antigen-presenting</span> cells, it also feeds back
into processes of the innate one. B-cells producing IgM antibodies as a
reaction to thymus-independent antigens is one example, the fact that the
adaptive immune system can suppress over the top innate responses is another <span style="mso-bidi-font-family:"Times New Roman"">(Palm and Medzhitov, 2007)</span>.</p>
<p class="MsoNormal">Beyond that, the difference between the innate and adaptive
immune system <span style="mso-no-proof:yes">is not</span> even that clear-cut.
B-cells have been shown to not only produce <span style="mso-no-proof:yes">antibodies</span>
but also play a role in early inflammatory cytokine response during bacterial
sepsis <span style="mso-bidi-font-family:"Times New Roman"">(Kelly-Scumpia et al., 2011)</span>, <span style="mso-no-proof:
yes">even though</span> the early inflammatory response <span style="mso-no-proof:
yes">is</span> typically associated with the innate immune system only. NK
cells, typically counted to the innate immune system, develop from the
lymphocyte lineage instead of being a granulocyte like the other innate immune
cells <span style="mso-bidi-font-family:"Times New Roman"">(Lanier et al., 1992)</span>, which is why some consider
them innate-like T lymphocytes instead <span style="mso-bidi-font-family:"Times New Roman"">(Van Kaer, 2007)</span>. They also appear to be able
to develop <span style="mso-no-proof:yes">memory</span>, an ability they share
with B-cells <span style="mso-bidi-font-family:"Times New Roman"">(Sun and Lanier, 2009)</span>.</p>
<p class="MsoNormal"> </p>
<p class="MsoNormal"><b>Concluding remarks</b></p>
<p class="MsoNormal"><span style="mso-bidi-font-weight:bold">The human immune
system is complex<span style="mso-no-proof:yes">; even</span> <span style="mso-no-proof:yes">now,</span> we <span style="mso-no-proof:yes">do not</span>
know all the details about how it works. <span style="mso-no-proof:yes">One apparent
fact</span> is that innate and adaptive immunity both have strengths and
weaknesses, but the way they work together makes it possible to fight of
threats that either alone might miss.</span></p>
<p class="MsoNormal"><span style="mso-bidi-font-weight:bold">While innate
immunity is what infants have to rely on in their first years, works
considerably faster than adaptive immunity, can react to a broad range of
pathogens thanks to its low specificity, and <span style="mso-no-proof:yes">is
required</span> for the adaptive immune system to function, it could not fulfil
its purpose by itself. Even during gestation the foetus profits from the
mother’s adaptive immunity through antibodies passed on through the placenta
and that process continues during breastfeeding, <span style="mso-no-proof:
yes">providing protection</span> against pathogens that are not taken care of
by innate immunity.</span></p>
<p class="MsoNormal"><span style="mso-bidi-font-weight:bold">In older children
and adults, the innate immune system still <span style="mso-no-proof:yes">does
not</span> operate in a vacuum and relies on interactions with the lymphocytes
of the adaptive immune system, specifically for cases when it fails. As <span style="mso-no-proof:yes">effective</span> as innate immune cells might be, they
are not able to protect the body from everything, and if the adaptive immune
system <span style="mso-no-proof:yes">were</span> not there to provide a second
line of defence, the result would be an untimely death.</span></p>
<p class="MsoNormal"><span style="mso-bidi-font-weight:bold">That the adaptive
immune system is dependent on the innate immune system has also been explained
in detail, which leads to the conclusion that it <span style="mso-no-proof:
yes">cannot</span> <span style="mso-no-proof:yes">be determined</span> which
part of the immune system is “better” – as they are both equally <span style="mso-no-proof:yes">crucial</span> for human survival.</span></p>
<p class="MsoNormal"><span style="mso-bidi-font-weight:bold"> </span></p>
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