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Supplement to

The Art of Getting Well

Immune System Protection from Foreign Invaders

Anthony di Fabio

M.Blount Foundation for Eradication of Rheumatoid Disease

AKA The Arthritis Trust of America

7376 Walker Road, Fairview, Tn 37062

Throughout 4.5 billion years our cellular and multi-cellular

ancestors struggled to survive, creatively developing and utilizing

a marvelously complex immune system. Throughout these aeons it

has been eat or be eaten.

Our bodies utilize an extremely diverse army of cells and other

molecules designed especially to protect us from the strategies of

all of those would-be eaters. (See Diagram I.) These finely tuned

protective cells also work well as a team.

Researchers continue to uncover new and amazingly complex

ways whereby protection from “outsiders” has developed. What is

already known may sound complex, but please have patience.

There’s a point of great understanding in what follows.

There’s an “innate” immune protective system. We’re born

with the ability to recognize certain microbes on sight, so to speak,

and we can then destroy them.

There is an “adaptive” immune protective system. The “re-

ceptors” (as a lock is to a key) activated in the adaptive immune

response are formed by piecing together gene segments, like piec-

ing together a jigsaw puzzle. The available pieces are used by each

cell in a different way to make a unique receptor, enabling cells to

collectively recognize infectious organisms confronted during our

lifetimes.

The end-point target of all immune processes is to destroy or

otherwise protect from an “antigen,” usually a foreign molecule

from a microorganism.

The end-object of vaccinations is to confront the immune sys-

tem with an antigen forcing the immune system to adapt to the

foreign invader; that is, the immune system must learn to identify

the invader and to retain the memory of this knowledge for the

purpose of destroying the invader now and in the future.

One major end-result of such vaccinations is to develop a sig-

nal to specialized blood components, called “complement” (an en-

zyme substance) which is used to overwhelm and to destroy for-

eign invaders. (See Diagram II.)

Specialized “antigen-presenting” cells, such as macrophages,

roam throughout our bodies literally ingesting the antigens (invad-

ers) and fragmenting them. These fragments are called “antigenic

peptides.”

Pieces of these peptides are layered on the surface of the cell

called “major histocompatibility complex” (MHC). This joining

produces a peptide-MHC combination.

Other specialized white cells called “T lymphocytes” have re-

ceptor cells that “recognize” different peptide-MHC. (The desig-

nation “T” means cells from the thymus gland.)

The T cells that are activated by that “recognition” begin to

divide, and they also secrete a substance called “lymphokines.”

Lymphokines are chemical signals that mobilize other components

of the immune system.

One set of those cells that responds to the lymphokine signals

are the “B-lymphocytes” each of which also have receptor mol-

ecules of a single specificity on their surface. (See Diagram III.)

(The designation “B” means cells from bone marrow.)

However, unlike the receptors of T cells, those of B cells can

recognize parts of antigens that are free in solution without the

MHC molecules attached.

When the B-lymphocytes are activated, they divide and dif-

ferentiate into plasma cells that secrete “antibody” proteins, water

soluble forms of their receptors.

These antibodies bind to whatever antigens they find, neutral-

izing them or precipitating their destruction by enzymes derived

from the molecule called “complement.” Complement is a blood

protein which can destroy pathogens on first encounter.

Complement activity -- the end point of adaptive immuniza-

tion, to develop a “complement” to antibodies -- can be triggered

in three ways. (See Diagram IV.)

(1) One type of complement called C3 can bind to any pro-

tein. Once bound to the microbe the C3 molecule causes other

complement molecules to bind to the bacterium. This is called the

“complement cascade.” Their joint action overwhelms the bacte-

rium. Our body’s cells are protected from C3 by proteins that inac-

tivate this molecule.

(2) Antibodies produced as a result of infection can also acti-

vate complement. After detecting an infection, a macrophage se-

cretes a substance called “interleukin-6.” As it’s carried through

the blood stream, interleukin-6 reaches the liver, causing the secre-

tion of a “mannose-binding protein.” (Mannose is a sugar formed

by the oxidation of manitol.) Mannose-binding protein binds to

the capsule of a bacterium, and this protein then triggers the comple-

ment cascade, thus overwhelming the bacterium.

(3) Antibodies produced as a result of infection also activate

complement. B cells are activated if they bind to the bacterium and

are stimulated by a so-called helper T cell. The binding stimulates

the B cell to proliferate and to secrete antibodies. The antibodies

bind to the bacterium and activate complement protein called C1Q,

which activates other complement molecules -- the “complement

cascade” -- thus overwhelming and killing the bacterium.

To make a rather long, complex story short, the many ma-

jor immune defensive mechanisms we’ve inherited usually re-

sults in producing a complement cascade, which, working to-

gether with antibodies, overwhelms an invading organism.