2016 Group 5 Project

From CellBiology

Mast Cell





receptors, microscopy


multifunctional purpose (don't have to go into too much detail -> more depth in following sections

Origin and Differentiation

(references to be added)




Interestingly mast cells do not differentiate in the bone marrow, their precursor cells travel to extramedullary sites with good vasculature such as connective region of the skin or mucosa of the GIT. (draw image of this process).

The migration of mast cell precursors is tissue specific. It depends on the interaction of the MCP's integrins binding to the corrsponding adhesion molecules in the mucosa called MAdCAM-1. (gurish et al 2001, pg 701 D.S.). The precursors also express chemokine receptors that may play a role in migration (abonia et al., 2005)

There are both intrinsic and extrinsic factors required for Mast cell differentiation. The following have been discovered as a result of mice carrying genetic mutations:

Extrinsic and Intrinsic factors influencing Mast Cell Development
Intrinsic Extrinsic
Fibroblast derived Growth factors on haematopoietic stem cells . There are also growth factors that inhibit mastopoesis such as thrombopoetin, which acts by down-regulating GATA1 Transcription factor MitF - Involved in c-kit expression that influences mast cell specific protease expression
IL-3 from T cells5 - Induced from T cells as a result of external stimuli. For example parasite infections. It has been shown to be responsible for Mast Cell survival, developement and maturation in vitro (Metcalf, 1986)703D.S. Transcription factors: Gata1 and Gata 1 - Expressed throughout differentiation in vitro. Mutation in GATA1 gene affects all stages of differentiation of mast cells


This is different to activation in that it's how the biogenesis of the mediators occurs, not how an antigen triggers the degranulation. pg 4 moon et al


706, de silva


to read:

<pubmed>25062998</pubmed> <pubmed>25452755</pubmed> <pubmed>12592295</pubmed>

<pubmed>22561833</pubmed> review on igE interactions: http://www.nature.com/nm/journal/v18/n5/full/nm.2755.html

<pubmed>21333342</pubmed> autophagy: http://www.sciencedirect.com/science/article/pii/S0091674910030381

<pubmed>3251560</pubmed> http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3251560/





Mast cells are sentinel cells that are found distributed within the connective tissue throughout the body and play an important role in both acute and chronic inflammation. Mast cells that are coated with IgE antibodies specific for certain environmental antigens are triggered to release histamine and other cytokines that induce early vascular changes that are hallmarks of acute inflammation. [1] The immediate responsibility of mast cells is to recognise that infection by a pathogen has occurred, which is achieved by direct recognition of the pathogen by pattern recognition receptors that are activated in response to pathogen-associated molecular patterns (PAMPs). [2] A study conducted by Supajatura et al. demonstrated that the activation of different toll-like receptors (TLR2 or TLR4) by varying PAMPs resulted in differential activation of mast cells evident in lypopolysaccharide stimulation of TLR4 resulting in cytokine release compared to peptidoglycan stimulation of TLR2 receptors resulting in both degranulation and cytokine production.[2] However, mast cells can act directly on pathogens through the production of reactive oxygen species and phagocytosis, as demonstrated by the engulfing of Fim-H expressing enterobacteria. [3]

Mast cells also play a major role in atopic diseases such as asthma, eczema, anaphylaxis and allergic rhinitis. The basis of these allergic diseases is the activation and binding of the high-affinity immunoglobulin E (IgE) receptor FceR1 to initiate receptor clustering and release of mediators, a signalling network dependent on the strength and type of stimulus. [4] Furthermore, similarly to neutrophils, mast cells have been seen to produce extracellular traps through the utilisation of the cathelicidin LL-37, histones and tryptase. [5] These three products of mast cells form the structural foundation of the extracellular traps, demonstrated to trap the bacteria S. pyogenes when in close proximity in co-culture in vitro. [5]

Parathyroid bone disease





Atopy is a common syndrome underlying eczema is characterised by high Immunoglobulin E (IgE) responsiveness. IgE is produced in response to common antigens, and is bound to the surface of mast cells, which play an essential role in atopic conditions such as eczema. [7] Mast cell chymase (MCC) in particular is involved in this condition, and is a serine protease which accumulates in the dermis of the skin. An increase in MCC promotes skin inflammation and conditions such as eczema. [7] The polymorphism of MCC is significantly associated with the occurrence of eczema, and different variations of this MCC is one source of genetic risk for the condition. [7]


Atopy: predisposition to developing IgE associated allergic diseases.

Atopic disease: a clinical condition caused by an allergy

Allergic Rhinitis: commonly known as hay fever


FceR1: high affinity Immunoglobulin E receptor

  2. 2.0 2.1 <pubmed>12021251</pubmed>
  3. <pubmed>8120397</pubmed>
  4. <pubmed>12782712</pubmed>
  5. 5.0 5.1 <pubmed>18182576</pubmed>
  6. 6.0 6.1 6.2 <pubmed>20200965</pubmed>
  7. 7.0 7.1 7.2 <pubmed>8774571</pubmed>