Page 521 - Review of Medical Microbiology and Immunology ( PDFDrive )

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MHC class II mebooksfree.com
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510
PART VII Immunology
Note that the receptor on the surface of B cells (either IgM
Helper
or IgD) recognizes antigen directly without the need for
T cell
presentation by MHC proteins. Also TCR proteins are
always anchored into the outer membrane of T cells. There
C
C
CD3 proteins
is no circulating form as there is with certain antibodies
DJ
J
(e.g., monomeric IgM is in the B-cell membrane, but pen-
tameric IgM circulates in the plasma).
Effect of Superantigens on T Cells CD4 protein V V Processed antigen
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Certain proteins, particularly staphylococcal enterotoxins
Ag
and toxic shock syndrome toxin, act as “superantigens”
(Figure 58–6). In contrast to the typical (nonsuper) anti-
Antigen-presenting cell
gen, which activates one (or a few) helper T cell, superanti-
gens are “super” because they activate a large number of
Helper
helper T cells. For example, toxic shock syndrome toxin
T cell
binds directly to class II MHC proteins without internal
T-cell receptor
processing of the toxin. This complex interacts with the
C
C
variable portion of the beta chain (Vβ) of the TCR of many
3
T cells.
This activates the T cells, causing the release of IL-2
from the T cells and IL-1 and tumor necrosis factor (TNF)
MHC class II
from macrophages. These interleukins account for many of CD4 protein V J DJ V Superantigen
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the findings seen in toxin-mediated staphylococcal dis-
eases. Certain viral proteins (e.g., those of mouse mam-
mary tumor virus [a retrovirus]) also possess superantigen
activity.
Antigen-presenting cell
Features of T Cells
Top: The helper T cell is activated by the presentation of processed
T cells constitute 65% to 80% of the recirculating pool of
antigen in association with class II major histocompatibility complex
(MHC) protein to the antigen-specific portion of the T-cell receptor.
small lymphocytes. Within lymph nodes, they are located
Note that superantigen is not involved and that only one or a small
in the inner, subcortical region, not in the germinal centers.
(B cells make up most of the remainder of the pool of small
Bottom: The helper T cell is activated by the binding of superantigen
lymphocytes and are found primarily in the germinal cen-
to the Vβ portion of the T-cell receptor outside of its antigen-specific
ters of lymph nodes.) The life span of T cells is long:
site without being processed by the antigen-presenting cell. Because
months or years. They can be stimulated to divide when number of helper T cells specific for the antigen are activated.
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it bypasses the antigen-specific site, superantigen can activate many
exposed to certain mitogens (e.g., phytohemagglutinin or
helper T cells. (Used with permission from Pantaleo G et al. Mechanisms of dis-
concanavalin A [endotoxin, a lipopolysaccharide found on
ease: The immunopathogenesis of human immunodeficiency virus infection. N Engl
the surface of gram-negative bacteria, is a mitogen for B
cells but not T cells]). Most human T cells have receptors
for sheep erythrocytes on their surface and can form
“rosettes” with them; this finding serves as a means of iden-
neutrophils to the site of infection. CD8 cells protect
tifying T cells in a mixed population of cells.
against viral infection by killing virus-infected cells.
Effector Functions of T Cells
The four types of T cells (Th-1, Th-2, and Th-17 types of
Th-1 cells and macrophages are the main effectors of
CD4 cells, and CD8 cells) mediate different aspects of our
delayed hypersensitivity reactions that protect against
host defenses. Th-1 cells mediate delayed hypersensitivity Th-1 Cells
intracellular microorganisms including certain fungi
reactions against intracellular organisms. Th-2 cells medi-
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(e.g., Histoplasma and Coccidioides) and certain intracellu-
ate protection against helminths (worms). Th-17 cells pro-
lar bacteria (e.g., M. tuberculosis). The most important
tect against the spread of bacterial infections by recruiting
interleukin for these reactions is gamma interferon, but
phage migration inhibition factor (MIF) also play a role.
3
Each superantigen (e.g., the different staphylococcal enterotoxins)
Th-1 cells produce the interleukins that activate the macro-
interacts with different Vβ chains. This explains why many, but not all,
phages, and macrophages are the ultimate effectors that
helper T cells are activated by the various superantigens.
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