Page 52 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Immune Defense
The body possesses nonspecific, congenital, and The nonspecific system is rarely able, for ex-
(interlinked) specific, acquired, or adaptive im- ample, when a measles infection occurs for the
mune defenses against microorganisms (bac- first time, to single-handedly prevent the virus
teria, viruses, fungi, parasites) and against replicating and spreading in the body, i.e., ill-
macromolecules identified as being “foreign”. ness follows. The specific immune defense
Fragments of pathogens and large-molecular with killer T cells (→ B2; p. 46f. B) and immu-
foreign bodies represent antigens to which noglobulins (at first IgM, then IgG; → B5) goes
the specific defense system reacts with the ac- into action only slowly (primary response or
tivation and proliferation of monospecific T and sensitization), but then manages to neutralize
B lymphocytes (T cells and B cells). B cells dif- the pathogen, i.e., the measles infection is con-
ferentiate to plasma cells which produce anti- quered. If the infection reoccurs, antibody pro-
bodies (immunoglobulins, Ig, with the sub- duction (especially IgG) sets in abruptly (sec-
groups IgA, IgD, IgE, IgG, IgM). It is their task ondary response), the virus is eliminated
to: 1) neutralize, 2) opsonize antigens, and 3) straightaway, and a renewed infection fails to
activate the complement system (see below). occur (immunity). (A primary response with
These highly specific mechanisms of the im- ensuing immunity can also be achieved by im-
mune defense serve to recognize the particular munization with pathogen antigen [active im-
antigens whose elimination is then accom- munization]).
Blood plished in a relatively nonspecific way. In addi- solved or humoral defense substances, such
Nonspecific defense (→ A) is served by dis-
tion, the antigen (with B and T memory cells)
3 is held “in memory” (immunological memory). as lysozymes and complement factors (→ A1)
At their maturation in the thymus (T cells) as well as phagocytes, i.e., especially macro-
and bone marrow (B cells), respectively, a rep- phages (formed in tissue from immigrating
8
ertoire of > 10 different monospecific lympho- monocytes) and neutrophil leukocytes, or neu-
cyte types (each against a specific antigen) is trophils (→ A2). The latter are formed, like
formed from lymphatic precursor cells that do monocytes and eosinophil leukocytes, or eo-
not possess any antigen receptors. Such as yet sinophils, in bone marrow, pass through the
naive lymphocytes circulate through the or- body and are finally attracted by chemokines
ganism (blood and lymph → lymphatics → (chemotaxis) to sites of pathogens. There they
blood and lymph). When they discover “their” set in motion the inflammatory processes
antigen, as usually happens in lymphatic tis- through the release of mediators (→ A2, 4 and
sue, exactly this lymphocyte type proliferates p. 48ff.).
(clonal selection and proliferation), and nu- The phagocytes take up the pathogen (en-
merous monospecific daughter cells are docytosis), damage it (especially after its acti-
formed. These differentiate into armed T cells vation; see below and B6) by means of lyso-
and plasma cells, respectively, which are re- zymes, oxidants such as hydrogen peroxide
–
1
sponsible for elimination of the antigen. (H 2 O 2 ) and oxygen radicals (O 2 , OH·, O 2 ), ni-
Lymphocytes with receptors against endog- trogen monoxide (NO), etc. and “digest” the
enous tissue are prematurely eliminated in the pathogen with their lysosomal enzymes (lysis).
thymus or bone marrow after recognizing If the antigen is too large (as is the case with
their antigen. This clonal deletion thus results worms, for example) the above-mentioned de-
in (central) immunological tolerance. The im- fense substances are also exported (exocyto-
mune system learns around the time of birth sis; in this case mainly from eosinophils). Nor-
to distinguish between foreign and endoge- mally the concentration of the above-men-
nous antigens. Normally it continues to recog- tioned oxidants is held at a low level by reduc-
nize throughout life those that it came into ing enzymes, such as catalase and superoxide
contact with at this time as endogenous; all dismutase. This “reining in” is given up when
those that come later are recognized as being the phagocytes are activated: the bactericidal
42 foreign. If this distinction fails, autoimmune action of the oxidants can then take its full ef-
disease occurs (→ p. 56). fect so that the phagocytes themselves and, in
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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