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The importance of antibody molecules was first recognized in the 1890s,

when it was shown that immunity to tetanus and diphtheria was caused by
antibodies against the bacterial exotoxins (1). Around the same time, it was
shown that antisera against cholera vibrios could transfer immunity to nave
animals, and also kill the bacteria in vitro (1). However, although antitoxin
antibodies rapidly found clinical application, there was little understanding
regarding the nature of the antibody molecule. Indeed, the earliest theories
suggested that the antitoxins were derived by modification of the toxin
intriguingly similar antigen incorporation theories were propounded as late
as 1930 (1).
The immune response of lymphocytes is triggered by materials called immunogens,
macromolecules capable of
triggering an adaptive immune response by inducing the formation of antibodies or
sensitized T cells in an immunocompetent host. Immunogens can then specifically react
with such antibodies or sensitized T cells. The term antigen refers to a substance that
reacts with antibody or sensitized T cells but may not be able to evoke an immune
response in the first place. Thus, all immunogens are antigens, but the converse is not
true. However, many times the terms are used synonymously, and the distinction
between them is not made. In discussing serological reactions or particular names of
substances such as blood groups, the term antigen is still more commonly used; hence
both terms are used in this chapter.

One of the most exciting areas of research focuses on how and why we respond to
particular immunogens. This
response is actually caused by a combination of factors: the nature of the immunogen
itself, genetic coding of MHC molecules that must combine with an immunogen before T
cells are able to respond, and immunogen processing and presentation. This chapter
focuses on all three areas and discusses future clinical implications of some recent