Figure legends
Figure 1. Mast cell activation pathways and release of
mediators. Mast cells are endowed with a palette of receptors that can
recognize endogenous and exogenous products and release different sets
of mediators dependent on the receptor involved. Upon recognition mast
cells react by releasing mediators through one or several pathways: 1)
degranulation and release of granules containing e.g., histamine,
heparin, proteases and cytokines; 2) release of newly synthesized lipid
mediators such as PGD2, LTC4/D4/E4, TXA2 and 15-HETE; 3) release of de
novo synthesized cytokines, chemokines, growth factors and interferons;
4) release of extracellular vesicles, e.g., exosomes, containing miRNA,
mRNA and proteins.
Figure 2. Models representing mast cell differentiation in
hematopoiesis. (A) The tree-like model represents hematopoiesis as a
strict series of branching events, in which cell lineage potential is
lost at defined checkpoints along differentiation from hematopoietic
stem cells to lineage-committed cells. The position of the mast cell
branch in this model is controversial. (B) The hematopoietic landscape
model represents a continuum of single differentiating progenitors, in
which there are multiple paths from hematopoietic stem cells to each
lineage’s entry point. Ba, basophil; Eo, eosinophil; Ery, erythrocyte,
Gr, granulocyte, HSC, hematopoietic stem cell; Ly, lymphocyte; MC, mast
cell; MK, megakaryocyte; Mo, monocyte, Neu, neutrophil.
Figure 3. Fate decisions in the life of the mast cell. Mast
cell progenitors (MCp) in the bone marrow (1) are entering the blood
stream and are recruited into the tissue (2). During this process the
cells have to avoid premature degranulation (2). In the tissue (3) MCs
can degranulate in three possible modes, either by full exocytosis,
compound exocytosis or by kiss-and-run exocytosis.
Figure 4: MC-targeted treatments under development. Examples of
treatments currently under development that target mast cell mediators,
mast cell activating signals / receptors or their signaling molecules,
inhibitory receptors, or mast cell depletion.