IL-4 produced at the local site, the T cells differentiate into TH2 cells

IL-4, IL-5, and IL-13

IL-4 acts on B cells to stimulate class switching to IgE
IL-5 is involved in the development and activation of eosinophils
IL-13 enhances IgE production and acts on epithelial cells to stimulate mucus se
cretion
mast cell
chemokines (e.g., IL-8)

Mast cell activation leads to degranulation

TNF, IL-1, and chemokines, which promote leukocyte recruitment (typical of the l
ate-phase reaction);
IL-4, which amplifies the TH2 response

Upon activation, eosinophils liberate proteolytic enzymes as well as two unique

proteins called major basic protein and eosinophil
cationic protein, which damage tissues

Naive CD4+ T cells recognize peptides displayed by dendritic cells and secrete I
L-2
which functions as an autocrine growth factor to stimulate proliferation of the
antigenresponsive T cells

T cells to TH1 or TH17 cells is driven by the cytokines produced by APCs at the
time of T-cell activation.
APCs (dendritic cells and macrophages) produce IL-12, which induces differentiat
ion of CD4+ T cells to the TH1 subset.
IFN- produced by these effector cells promotes further TH1 development, thus ampl
ifyin the reaction.
If the APCs produce inflammatory cytokines such as IL-1, IL-6, and IL-23, these
stimulate differentiation of T cells to the TH17 subset.

TH1 cells secrete cytokines, mainly IFN-, which are responsible for many of the m
anifestations of delayed-type hypersensitivity.
IFN--activated (classically activated) macropha es are altered in several ways:
their ability to pha ocytose and kill microor anisms is markedly au mented;
they express more class II MHC molecules on the surface, thus facilitatin furth
er anti en presentation;
they secrete TNF, IL-1, and chemokines, which promote inflammation;
they produce more IL-12, thereby amplifyin the TH1 response.

Activated TH17 cells secrete IL-17, IL-22, chemokines, and several other cytokin
es.
Collectively, these cytokines recruit neutrophils and monocytes to the reaction,
thus promotin inflammation.
TH17 cells also produce IL-21, which amplifies the TH17 response.

Suppression by re ulatory T cells

immunosuppressive cytokines such as IL-10 and TGF-, which inhi
it lymphocyte acti
vation and effector functions

Anergy
Suppression
y regulatory T cells
Deletion
y apoptosis

Defective tolerance or regulation

A
normal display of self antigens
Inflammation or an initial innate immune response

SLE is an autoimmune disease involving multiple organs,

characterized
y a vast array of autoanti
odies, particularly antinuclear anti
o
dies (ANAs), in which injury is
caused mainly
y deposition of immune complexes and

inding of anti
odies to various cells and tissues.
The hallmark of SLE is the production of autoanti
odies

Antinuclear anti
odies (ANAs) can
e grouped into four categories:

(1) anti
odies to DNA
(2) anti
odies to histones
(3) anti
odies to nonhistone proteins
ound to RNA
(4) anti
odies to nucleolar antigens

Sjgren syndrome is a chronic disease characterized

y dry eyes (keratoconjunctivitis sicca) and dry mouth
(xerostomia) resulting from immunologically mediated
destruction of the lacrimal and salivary glands.

Systemic Sclerosis (Scleroderma)

(1) chronic inflammation thought to
e the result of autoimmunity
(2) widespread damage to small
lood vessels
(3) progressive interstitial and perivascular fi
rosis in the skin and multiple
organs

Profound immune deficiency, primarily affecting cellmediated immunity, is the ha

llmark of AIDS

Amyloidosis is a condition associated with a num
er of

inherited and inflammatory disorders in which extracellular deposits of fi
rilla
r proteins are responsi
le for
tissue damage and functional compromise.

The deposition of these proteins may result from:

excessive production of proteins that are prone to misfolding and aggregation;
mutations that produce proteins that cannot fold properly and tend to aggregate;
defective or incomplete proteolytic degradation of extracellular proteins.