TABLE 1.

Observed immune and other dysregulations (peripheral, neurological and enteric) along with the MSC potential alleviating mechanisms.

Dysregulation	Potential mechanism of MSC
Immuno-genetically determined inability to mount efficient anti-infectious responses with consequent chronic inflammation	Overall restoration/improvement of the dysimmune pathways through;
Elevated pro-inflammatory cytokine levels
Diminished anti-inflammatory cytokine levels
Altered cytokine production by monocyte after TLR-based stimulation
Altered CD8+ and CD4+ T-cell profiles	-Synthesis and releasing of anti-inflammatory cytokines and growth factors;
Altered NK cell activity
Imbalance of serum immunoglobulin due to B cell dysfunction
Peripheral and central autoimmune processes due to deregulated anti-infectious responses leading to inflammation and autoimmunity after rupture of tolerance and autoantibodies production
Altered composition of intestinal microbiota leading to increased intestinal permeability (leaking of unwanted bacteria metabolites that might harm the brain) and chronic inflammation	-Suppression of cell-mediated immune response through inhibition of proliferation of several cell subsets including T-lymphocytes and NK cells
Altered immune-related transcriptome profiles
Altered genome-wide expression profiles in lymphoblastoid cells
Elevated activation of astrocytes and microglia	Provide neuroprotection through anti-inflammatory mechanisms by inhibiting microglial activation and astrocyte proliferation
Synaptic dysfunction and neuro-structural changes	Act in the existing neural and synaptic network to restore plasticity;
	Local secretion of substances that could reduce inflammation and promote tissue repair;
	Promote neuron survival via secretion of neurotrophic factors;
	Aid in synaptogenesis and regeneration of functional neurological pathways by supplying bioactive agents that stimulate the action of intrinsic neural progenitor cells