From:  Revisiting immunotherapeutic strategies for the management of atopic dermatitis
 

MSC-based therapies in mouse models of AD

MSC sourceAD modelMouse strainRouteMechanisms of actionReferences
hBM-MSCsOvalbumin-induced ADBALB/c or C3H/HeNIVSuppression of T cells function via NO and suppression of B-cell function via class switch recombination[40]
hUCB-MSCsDermatophagoides farinae-induced ADNc/NgaSCInhibition of mast cells degranulation through PGE2 and TGF-β1[41]
hAD-MSCsDermatophagoides farinae-induced ADNc/NgaIVB-cell suppression via cyclooxygenase 2 regulation[42]
hAD-MSCsDinitrochlorobenzene-induced ADBALB/cIVRegulation of MIP-2 and miR-122a-SOCS1 expression, as well as Th1/Th2 responses[43]
hSOD3-MSCsOvalbumin-induced ADBALB/cSCSuppression of response elicited by keratinocytes, mast cells, neutrophils, dendritic cells, and T cells through multiple mechanisms[44]
hUCB-MSCsDermatophagoides farinae-induced ADNc/NgaSCPre-conditioning of MSC with mast cells granules optimizes suppression of mast and B cells[45]
hUCB-MSCsDermatophagoides farinae-induced ADBALB/cSCControl of both eosinophil-associated Th2 immunity and neutrophil-related Th17[46]
Primed T-MSCsDNFB-induced ADC57BL/6JSCRegulation of B cell-mediated inflammatory responses, which are dependent on CD40 expression on primed T-MSCs mediated through the non-canonical NF-κB pathway[47]
HA-SH/hAD-MSCs (3D-Hydrogel)1-chloro-DNCB-induced ADBALB/cSCImmunomodulatory action on immune cells via downregulation of major inflammatory cytokines (IL-13, CCL11, and CCL24), reduced epidermal thickness, and mast cell penetration[48]
hAD-MFSCEDermatophagoides farinae-induced ADNC/NgaTopicalDecrease of IgE and inflammatory cytokines levels. Inhibition of epidermal thickness, mast cell infiltration, and expression of expression of IL-4, IL-10, IFN-γ, TNF-α, activation-regulated chemokines[49]
hAD-MSCsOvalbumin-induced ADBALB/cSCDecrease of serum IgE levels, and mast cells infiltration skin lesions. Suppression of Th17 cells proliferation and proinflammatory cytokines (IL-17A and RORγT) expression. Upregulation of PD-L1, TGF-β and PGE2 levels[50]
hUCB-MSCs1-chloro-DNCB-induced ADBALB/cSC + IVAnti-inflammatory and Immunomodulatory function resulting in amelioration of skin lesions, through inhibition of JAK-STAT pathway and different cytokines (IL-4, IL-13, IL-17, and IgE) receptors[51]
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CCL11: eotaxin 1; CCL24: eotaxin 2; DNCB: 2,4-dinitrobenzene; DNFB: 2,4-dinitrofluorobenzene; IL: interleukin; IV: intravenous; MIP-2: macrophage inflammatory protein 2; NF-κB: nuclear factor kappa B; PGE2: prostaglandin E2; SC: subcutaneous; TGF-β1: transforming growth factor beta 1