Untitled - D Ank Unlimited

Th1/Th2 differentiation 692 T h0 cells
T H2
B
cell
IL-4
IL-5
IL-6
IL-7
APC
T H 0
by antigen-presenting cells. Effector Th cells are designated
as Th1 or Th2 with respect to phenotype. Th1 cells
synthesize IFNγ and IL2 and are active against intracellular
bacteria and viruses. They also mediate isotype switching
to IgG1 and IgG3 in humans. Th2 cells synthesize IL4, IL5,
IL10, and IL13; combat extracellular bacteria and parasites;
and facilitate isotype switching to IgA, IgE and IgG4. Th
cells usually manifest CD4 coreceptors.
Th1/Th2 differentiation
The pathway whereby Th cells proliferate to synthesize
IFN-γ- and IL4-secreting Th0 cells that become Th1 or Th2
effector cells based on other transcription factors and cytokines.
T-bet and IL12 can induce differentiation of Th0 cells
into Th1 effector lymphocytes. GATA-3 and IL4 can induce
differentiation of Th0 cells into Th2 effector lymphocytes.
Th3 cells
CD4 + regulatory T cells that synthesize large quantities
of TGF-β.
Th17 cells
A recently discovered unique subset of CD4 T cells that
synthesize IL17 and are distinct from Th1 and Th2. Th17
cells are of central importance to the pathogenesis of
inflammatory diseases and autoimmune diseases. They
develop via cytokine signals distinct from and antagonized
by products of the Th1 and T2 lineages. IL23, TGF-β, IL6,
IL7, and their receptors are important for the development
of the Th17 lineage. Expression of RORγt transcription
factor directs Th17 differentiation. Th17 development
T c
Plasma cell
LAK
cell
NK
cell
IL-1
IL-10
Cell-mediated immunity
IgG, IgM, IgA
Humoral immunity
IFN-γ
Th0 cells.
Macrophage
ROI
RNI
IL-2
IFN-γ
T H 1
TNF-α
IL-8
PMN
leucocyte
depends on the pleiotropic cytokine TGF-β that is also
linked to regulatory T cell function. In pathogen-driven
inflammation, naïve T cells that recognize foreign antigen
may receive signals from regulatory T cells (TGF-β) to
induce Th17 development, whereas the pathogen-induced
signal that acts with TGF-β to switch the response to Th17
(IL6) also subverts T reg dominance and facilitates T reg
expansion that could block further T effector differentiation
as the inflammatory inducing pathogen is cleared.
TGF-β synthesis may initiate development of T reg that may
maintain dominant suppressive function in the absence of
pathogenic challenges but facilitate Th17 effector development
when needed. Key transcription factors include T-bet
that specifies Th1, GATA-3 that specifies Th2, and FOXp3
that specifies T reg development. IL17 cytokines are products
of two of the three arms of effector CD4 + T cell lineages:
IL17A and IL17F in Th17 and IL25 in Th2. Innate immune
cell products that control Th17 responses include new members
of the IL12 family cytokines, IL23 and IL27; and IL6,
prototype for IL12 cytokines. IL27 and SOC3 are negative
regulators for the development of Th17 cells. The Th17 lineage
is implicated in multiple auto-inflammatory disorders
and a possible role in allograft rejection.
T h0 cells
A murine and human CD4 + T cell subset based on cytokine
production and effector functions. Th0 cells synthesize multiple
cytokines. They are responsible for effects intermediate
of those of Th1 and Th2 cells, based on the cytokines