Humoral
·
Antibodies
·
Complement
cascade
·
Opsonins
Cellular
·
Macrophages
·
Granulocytes
·
B-lymphocytes
·
T-cells
·
Natural
killer cells
·
Memory
cells
·
Intercellular
messenger chemicals (lymphokines)
Cellular Response
Several groups
of cells are involved in a cellular response to ‘invasion’:
1.
Phagocytes
of various types, that is, cells that eat bacterial and viral particles and
other debris. Principal among these are the macrophages – wandering scavengers
found in all parts of the body and particularly geared to respond to immune
system signals.
2.
T-lymphocytes,
which have a complex role. Two main types of T-cells are recognized: so-called helper T-cells and suppressor
T-cells. Helper cells work with macrophages to generate the immune
responses and elicit antibodies that partly paralyze the invader and so help
the macrophages lock on to the enemy cells or particles. Suppressor T-cells come into play towards the
end of an infection to bring a halt to this process. They effectively terminate
the battle with the invaders. Balance between the two types of T-cell helps to
keep the reactions orderly and stop them getting too fierce or going on too long.
3.
B-lymphocytes,
which secrete the anti-bodies
4.
Natural
killer (NK) cells. As their name implies, they are destroyers – but in a
regulated, specific way. They are taught to recognize sick body cells, such as
cancerous tissues or cells invaded by viruses, and to puncture and destroy
these cells, thus releasing their contents which can then be attacked by
antibodies and cleaned up by the macrophages.
Basic immune
response
Mounting An Immune
Response
When an
infective organism invades the tissues, a precise series of events are set up
to limit spread of the foreigner and ultimately to destroy it. First a
macrophage will encounter the intruder. It engulfs it and then ‘displays’ its
characteristic proteins on the surface of the cell as a kind of “flag” or gotcha
trophy. We call this chemical flag the
antigen,
since it generates the rest of the
reaction.
By means of
chemical language (a sort of local hormone called a lymphokine), the macrophage
attracts nearby T-helper lymphocytes. They ‘read’ the antigenic matter and go
off to program B-cells to produce antibodies to this pattern. The
antibody is our own, the good guys’
response, to lock onto antigen carriers and cripple them.
T-helpers also
secrete other lymphokines, which attracts further
T-cells, killer cells and boosts the function of the B-cells, resulting in more
antibodies against the invader.
Eventually,
the enemy is overwhelmed by force majeur.
Two further
steps are important. One is the introduction of memory T-cells. This really is
the essence of lasting immunity; the cells learn to ‘remember’ the particular
antigen involved. When a subsequent infection takes place, they can almost
instantly mount the antibody response, without going through the above steps,
because they remember the antigen and already have the antibodies ‘on tap’.
Finally, there
must be some way of switching off the reaction. This is where the T-suppressor
lymphocytes come in. They scale down the whole process and limit further
response. Nature doesn’t want this destructive process to go on any longer than
necessary.
It is a clever and spectacularly successful system,
the detailed complexity of which surpasses our full understanding so far. The
main drawback is that the body has to meet the foreign protein (antigen) before
it can mobilize its counter-attack (the antibody). In other words, we must be
invaded before we can fight back. This may not matter much with an illness like
German measles or chicken-pox, but it is a serious inadequacy when it comes to
potentially fatal diseases such as smallpox and diphtheria. Basically, those
who survive such dangerous infections do so because their immune systems work
very fast and start to produce antibodies in the nick of time, just before
death supervenes. Those with a slower immune response are not so lucky and will
die.
Or at least they used to. Now we can use vaccination
to prevent such deaths. We introduce an artificial infection, commonly done by
injecting a dead or weakened virus which does not harm the patient, but teaches
his or her body to recognize the virus protein and make antibodies. Thus when
the real invaders come along the body is ready and can start its
counter-offensive by mobilizing antibodies within hours, instead of days, and
so beat off the attack.
The frightening new disease AIDS (Acquired Immune
Deficiency Syndrome) destroys T-lymphocytes and B-lymphocytes so that the body
cannot make enough antibodies. The victim, therefore, dies of simple everyday
infections which can no longer be resisted in the way in which a healthy
individual routinely shrugs them off. Ironically, of course, it means also that
the body is hampered in its ability to round on the AIDS virus and so this is a
particularly grim infection. The search for a vaccine seems very bleak.
Other Cells which may be involved
The
eosinophil is a cell mobilized especially against
parasites and allergens. The monocyte is a
short-lived circulating phagocyte that differentiates into the
macrophage, a cell that may live from months
to several years. The macrophages (literally “great gobbler” cells) are the sweep clean army of
the immune system, engulfing bacteria, viruses, circulating cell debris and
aggregations of immune complexes.
These cells
tend to reside in various organ systems, where they selectively differentiate
according to the needs of their host organ. For example, macrophages in the
liver are celled
Küpffer’s cells, and those in the lung are
termed alveolar macrophages. The
macrophage, like other phagocytes, depends on the generation of free radicals
such as peroxide to destroy its target matter.
Mast cells are involved in the histamine response
(redness, swelling and itching) that characterizes allergic reactions, such as
dermatitis.
Complement
The complement
system is another immune response highway which helps to amplify the efficacy
of immune reactions. “Complement” is actually a group of active enzymes which work
in a cascade or tumbledown effect; the release of one triggers the next and so
on, in sequential fashion. They are generally identified in the laboratory as
C1 to C9.
The antigen-antibody complex combines
with C1, which in turn acts on C2 and C4. This acts on C3 and son on, in what
is called a cascade effect, each step leading to the next. The resultant enzymes act on the invader in a
variety of ways and also participate in a local tissue reaction, familiar to us
as inflammation. Although this is unpleasant and can be painful, it does serve
a purpose in containing the attack.