Human Physiology, 14th edition (2016)

(Tina Sui) #1

526 Chapter 15


One of the best-known examples of delayed hypersensitiv-
ity is contact dermatitis, caused by poison ivy, poison oak,
and poison sumac. The skin tests for tuberculosis—the tine test
and the Mantoux test—also rely on delayed hypersensitivity
reactions. If a person has been exposed to the tubercle bacillus
and consequently has developed T cell clones, skin reactions
appear within a few days after the tubercle antigens are rubbed
into the skin with small needles (tine test) or are injected under
the skin (Mantoux test).
In allergic contact dermatitis, a susceptible person can
develop an inflammatory skin rash in response to cosmetics,
jewelry, or other products that contact the skin. In allergic con-
tact dermatitis, small organic molecules in these products pen-
etrate into the skin and bind to self-proteins, creating a new
antigen in a process called haptenization. This new antigen can
then activate a T cell response and lead to the development of
the allergic rash.


| CHECKPOINT


  1. Explain the mechanisms that may be responsible for
    autoimmune diseases.
    12a. Distinguish between immediate and delayed
    hypersensitivity.
    12b. Describe the sequence of events by which allergens
    can produce symptoms of runny nose, skin rash, and
    asthma.


Timmy received a booster vaccine for tetanus, diph-
theria, and pertussis. This contains inactivated bacte-
rial toxins that stimulate active immunity, so that Timmy
developed clones of lymphocytes able to combat a pos-
sible future virulent infection. When Timmy was cut by
an old can in the road, it might have given him tetanus
if he hadn’t received this immunization. The cut did pro-
voke a local inflammation, where the release of histamine
and other pro-inflammatory cytokines caused blood ves-
sels to dilate, making the area red, and fluid to leak from
capillaries, making it swollen. The pain could have been
exacerbated by the cytokine prostaglandin E 2. Pus was
produced by the neutrophil release of proteases that liq-
uefy tissues and by dead neutrophils. The cleansing of
the wound and application of a bactericidal salve helped
to prevent the infection from spreading and possibly
causing a systemwide inflammation known as sepsis.
Timmy’s seasonal cough may be due to an immediate
hypersensitivity reaction that causes IgE production and
the release of histamine from mast cells and basophils.
Histamine is a major mediator of the allergic symptoms
of rhinitis, and so the antihistamine helped alleviate Tim-
my’s cough.
See the additional chapter 15 Clinical Investigation on
Rheumatoid Arthritis in the Connect site for this text.

Clinical Investigation SUMMARY

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