Hypothesis: platelet-rich plasma as an adjunct therapy for eczema targeting inflammation, skin barrier repair, and chronic recurrence

Eczema comprises a group of chronic, relapsing inflammatory skin disorders characterized by erythema, papules, vesicles, exudation, and pruritus, and includes subtypes such as atopic dermatitis (AD), contact dermatitis, nummular eczema, and asteatotic eczema [1][2][3]. The core pathological features consist of pruritus, barrier dysfunction, and immune dysregulation. Although treatment options have improved, current therapeutic strategies remain unsatisfactory: prolonged use of topical corticosteroids can cause skin atrophy, while calcineurin inhibitors such as tacrolimus show limited efficacy in certain patients [4,5]. Biologics like dupilumab and JAK inhibitors are effective for moderate-to-severe cases but present challenges including high cost, the need for injection, and potential risks of infection or malignancy [5,6].The pathogenesis of eczema arises from complex interactions among genetic susceptibility (e.g., filaggrin (FLG) mutations), impaired skin barrier function (e.g., elevated pH and microbial dysbiosis), dysregulated immune responses (including Th2/Th17 imbalance), and environmental factors [1,4,7,8]. This multifactorial complexity complicates the development of targeted therapies; biologics directed at specific pathways, such as Th2, often fail to ameliorate concurrent barrier impairment or microbial imbalance [9,10]. These limitations highlight the need for novel, safe, and multifaceted treatment strategies.Platelet-rich plasma (PRP), an autologous blood product containing concentrated platelets and bioactive molecules including platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), Epidermal Growth Factor (EGF), Insulin-like Growth Factor (IGF) and transforming growth factor-β(TGF-β), has gained attention as a potential therapeutic agent in dermatology [11].In addition, PRP also exhibits anti-apoptotic effects, immunosuppressive properties, reduction of melanin synthesis, antimicrobial activity, and antioxidant effects [11]. Clinically, PRP has been demonstrated to be effective in treating various dermatological conditions, including androgenetic alopecia (by stimulating hair follicle stem cells and reducing perifollicular inflammation) [12], alopecia areata (AA) [13] and psoriasis (through normalizing keratinocyte hyperproliferation and downregulating the pro-inflammatory interleukin (IL)-17, a Th17-related cytokine) [14].Notably, both AA and psoriasis share pathophysiological overlaps with eczema: all involve chronic immune activation (e.g., Th2/Th17 skewing), epithelial barrier disruption, and neuroimmune crosstalk [15][16][17][18]. These conserved pathways imply that the multifunctional properties of PRP, namely anti-inflammatory, barrier-repairing, and immunomodulatory effects, may similarly target core mechanisms in eczema. To our knowledge, no systematic studies have yet explored the use of PRP in eczema treatment, and available data regarding its role in the condition's complex pathophysiology remain limited. Considering the unmet clinical need and the favorable safety profile of PRP, we hypothesize that PRP could act as a novel adjuvant therapy for eczema, potentially mitigating inflammation, restoring epidermal barrier function, and reducing chronic recurrence via its pleiotropic effects. This study seeks to elucidate the mechanisms through which PRP modulates eczema, thereby providing preclinical evidence to inform future clinical trials and potentially advance toward more personalized and effective management strategies. [2]; EGF and IGF-1 stimulate keratinocyte migration and differentiation, which are essential for reassembling the stratum corneum's "brick-and-mortar" structure. EGF, in particular, activates keratinocyte differentiation markers such as FLG2 and tight junction proteins including ZO-1 and occluding, thereby reinforcing barrier integrity [28]; VEGF enhances microvascularization and improves nutrient delivery to compromised skin. PRP's regenerative potential has also been demonstrated in other inflammatory or barrier-deficient dermatoses, such as AA, where it promotes hair follicle regeneration via upregulation of follicular stem cell markers and suppression of perifollicular inflammation [29]. Although the specific manifestations of barrier defects differ between eczema and AA, both conditions share a core requirement for epithelial repair-a process directly facilitated by PRP's growth factor-mediated mechanisms. This mechanistic overlap supports the rationale for using PRP to treat barrier dysfunction in eczema.Eczema pathogenesis primarily involves an imbalance in the polarization of Th2, Th17, and Th22 cells, along with dysregulated molecular cascades of associated cytokines [30][31][32][33]. Specifically, IL-4 and IL-13 secreted by Th2 cells bind directly to receptors on keratinocytes and downregulate FLG and tight junction proteins (ZO-1, occludin) via activation of the JAK/STAT6 signaling pathway, thereby compromising the epidermal "brick-and-mortar" structure and increasing TEWL. Th17-derived IL-17 activates the NF-κB pathway, inducing keratinocytes to release pro-inflammatory factors such as IL-6 and TNF-α, which intensify inflammatory infiltration. IL-22 from Th22 cells disrupts keratinocyte proliferation and differentiation balance through STAT3 signaling, resulting in skin thickening and desquamation. As a key pruritogen produced by Th2 cells, IL-31 binds the IL-31RA/OSMR heterodimeric receptor on sensory neurons and activates the JAK/JNK pathway, promoting TRPV1 ion channel phosphorylation [33]. This process initiates itch signal transmission and sustains a vicious cycle of itching, scratching, and further barrier disruption.The immunomodulatory effects of platelet-rich plasma PRP in AA and psoriasis provide molecular evidence supporting its potential intervention in the Th cell axis of eczema. In AA, a Th1/Th17-dominant condition, PRP lowers mRNA expression of Th1/Th17-related pro-inflammatory factors such as IFN-γ and IL-17 in lesions, while increasing the anti-inflammatory factor IL-10 and levels of the regulatory T-cell (Treg) marker FOXP3 [13]. This core mechanism relies on PRP-derived TGF-β1, which inhibits dendritic cell maturation and downregulates surface co-stimulatory molecules CD80/CD86, thereby reducing dendritic cell (DC) -mediated activation of pathogenic T cells [13]. Similarly, in the Th17-dominant setting of psoriasis, PRP regulates DC-T cell interactions by reducing peripheral blood Th17 cells, suppressing their secretion of IL-17, IL-22, and TNF-α, and enhancing the suppressive of cells T cells Although eczema characterized by which from the Th in alopecia areata and psoriasis, all disorders share the pathological features of pathogenic T cell activation and impaired This that PRP may balance to the axis in eczema by DC-T cell interactions and reinforcing T cell PRP may also the cycle in eczema via neuroimmune In of chronic PRP the from a pro-inflammatory to an anti-inflammatory effects has been to in and the cycle in eczema on sensory activation by we hypothesize that PRP neuroimmune it may TRPV1 ion channel activation to itch signaling, while the epidermal barrier and secretion to the chronic of eczema through pathogenesis of eczema primarily by Th2, Th17, and Th22 immune in which cytokines such as and IL-31 in promoting inflammation, pruritus, and epidermal barrier dysfunction PRP immunomodulatory effects in AA, a condition, and psoriasis, which by Th17 its potential to the Th2 axis in AA, PRP mRNA expression of the pro-inflammatory cytokines IFN-γ and IL-17 while levels of the anti-inflammatory IL-10 and the regulatory T-cell (Treg) marker FOXP3 [13]. In psoriasis, PRP dendritic cell maturation and T-cell to of IL-17, IL-22, and cytokines associated with Th17 Although eczema involves activity, psoriasis primarily and AA involves all disorders share a pathological T-cell activation with PRP's to dendritic crosstalk and in AA and psoriasis a potential to Th2 inflammation in eczema. an could the chronic cycle of eczema. PRP may neuroimmune efficacy in chronic to stem from the of neuroimmune the cycle in eczema involves signaling PRP may similarly pathways through skin by which inflammation through the secretion of and the of Although are in psoriasis or AA, the antimicrobial of and to the infection risks associated with with such as or to by PRP activates by and increasing thereby enhancing These mechanisms may the effects of on eczema characterized by the where chronic inflammation sensory further and role of PRP in inflammation and has been in conditions such as AA psoriasis and its potential to In AA, PRP hair follicle regeneration by promoting and reducing perifollicular [13]. In psoriasis, PRP keratinocyte hyperproliferation and inflammation by IL-17 and eczema, PRP may IL-31 and through the of its or anti-inflammatory such as and IL-10 its factors (e.g., can and epidermal the skin characterized by resulting from factors and which further barrier dysfunction Although PRP properties, it enhances skin by stimulating keratinocyte proliferation and the of barrier the of FLG expression and a key of in eczema The efficacy of PRP has also been in other and PRP with such as has been to skin by enhancing barrier function in psoriasis, which with and and in AA, which involves the use of PRP in eczema with its mechanistic inflammatory skin Eczema pathological mechanisms with conditions such as psoriasis and AA, including immune epithelial barrier defects keratinocyte differentiation, imbalance), chronic inflammation and microbial susceptibility in in eczema primarily by to the polarization in other multifunctional which involves growth factor and antimicrobial effects, it to target pathological This supports the of PRP as a that can the of and microbial in the use of PRP in eczema with its mechanistic inflammatory skin Eczema core pathological features with conditions like psoriasis and AA, including immune epithelial barrier defects keratinocyte differentiation, imbalance), chronic inflammation and microbial susceptibility in in eczema primarily by with the polarization in psoriasis or multifunctional profile growth factor antimicrobial it to target pathological This PRP as a of the of and microbial in eczema subtypes with mechanistic in genetic epidermal barrier defects (e.g., FLG mutations), stratum and contact dermatitis involves while contact dermatitis from keratinocyte by eczema to and environmental PRP therapeutic effects in eczema in it may genetic defects by FLG via enhancing keratinocyte differentiation to barrier "brick-and-mortar" structure while chronic via for contact dermatitis, its anti-inflammatory and epidermal in contact dermatitis, PRP promotes via and barrier with anti-inflammatory factors like and for eczema, it to barrier function, with its in that PRP, as a regulatory therapy for eczema, the condition's core pathological barrier dysfunction, immune chronic inflammation, microbial and a intervention a therapeutic antimicrobial and thereby the of current and novel for personalized eczema eczema topical corticosteroids and calcineurin inhibitors such as tacrolimus inflammation, barrier integrity and can further barrier function by epidermal proliferation Similarly, biologics like of the Th2 target a immune mechanism and other pathological such as Th17 and microbial while also risks of PRP's directly to the multifactorial pathogenesis of eczema, a to therapeutic PRP its autologous and effects associated with such as to corticosteroids or therapies; its to pathological immune antimicrobial activity, and with the complex of eczema, enhancing the potential for to its safety by clinical studies in psoriasis, alopecia and other inflammatory skin with and no future trials its efficacy in chronic or eczema, PRP could from an therapy to a of eczema This a in clinical to patients more personalized and treatment the intervention for PRP in eczema, the can be a as a target the in cell such as keratinocytes PRP's barrier via growth while in like chronic eczema its of eczema including pruritus, erythema, and desquamation. immune in of immune cells PRP's suppression of Th2/Th17 pro-inflammatory cytokines and of anti-inflammatory in further its of and inflammatory by T cells and cells effects be through in by in of and inflammatory such as and TNF-α, to PRP's to and inflammation and and chronic PRP's to the by suppressing chronic inflammation and promoting be using in stratum and in via and clinical trials mechanistic efficacy using core such as the Eczema and and recurrence while also safety including and infection to PRP's and clinical The with complex pathophysiological barrier dysfunction, immune and inflammation, thereby providing for the therapeutic the to be the PRP growth factor expression in eczema promotes proliferation and Th2/Th17 cytokines and and IL-10 and TNF-α, and and and improves stratum and eczema show skin inflammation and to with epidermal and structure. The PRP group exhibits in and recurrence the mechanistic markers such as elevated IL-10 and with clinical eczema management has a intervention topical calcineurin and JAK inhibitors fail to the unmet of eczema eczema topical corticosteroids and calcineurin inhibitors such as tacrolimus inflammation, barrier integrity and can further barrier function by epidermal proliferation biologics like of the Th2 target a immune mechanism and other pathological such as Th17 and microbial while also risks of PRP's directly to the multifactorial pathogenesis of eczema, a to therapeutic has demonstrated therapeutic potential in of efficacy and safety for eczema yet mechanisms. The complex of with in (e.g., may to therapeutic often by which its Although platelets are primarily for their role in evidence their in inflammatory including inflammation have demonstrated that PRP can ameliorate in certain inflammatory skin such as psoriasis and evidence supporting the efficacy of PRP in eczema, This that PRP may core in eczema growth directly the epidermal through keratinocyte proliferation and the of anti-inflammatory that barrier key T-cell such as Th2 and Th17 and associated PRP promotes immune the of antimicrobial properties, including the of function, the cycle of infection and inflammation, thereby reducing on The to pro-inflammatory cytokines like while stimulating proliferation disrupts the cycle and chronic PRP enhances skin the by restoring barrier function and synthesis, environmental In that PRP on eczema pathophysiology via core growth factor-mediated antimicrobial activity, between anti-inflammatory and regenerative and This more with the complex and chronic of eczema may that PRP, through effective eczema thereby supporting both the and clinical of future trials its efficacy in chronic or eczema, PRP could from an therapy to a of eczema This a in clinical to patients more personalized and treatment the for PRP's role challenges be clinical mechanistic as for specific growth personalized treatment strategies to skin and safety including the risks of mechanistic studies to with clinical trials to personalized the of PRP from a to the for PRP's challenges be clinical can as topical injection, or This of the of eczema patients of PRP's potential as a treatment or in with such as JAK or topical of PRP limited by the skin of its molecular delivery has been to delivery including have been to contact and Although PRP directly to the target it risks of and eczema are often by and to as skin and antimicrobial essential PRP to of PRP both and PRP, may in bioactive and release These directly therapeutic the need for a mechanistic to the of growth factors and to strategies to skin specific growth factor with in could inform that toward also for key IL-31 and barrier defects such as filaggrin or all PRP This the rationale for PRP that are in mechanistic and are with that PRP modulates the core pathological of disruption, immune chronic inflammation, and mechanisms. These growth barrier antimicrobial of the cycle through and skin core in the limitations of suppressive which and a more for eczema the and clinical through Eczema comprises a group of chronic, relapsing inflammatory skin disorders characterized by erythema, papules, vesicles, exudation, and pruritus, and includes subtypes such as atopic dermatitis (AD), contact dermatitis, nummular eczema, and asteatotic eczema [1][2][3]. The core pathological features consist of pruritus, barrier dysfunction, and immune dysregulation. Although treatment options have improved, current therapeutic strategies remain unsatisfactory: prolonged use of topical corticosteroids can cause skin atrophy, while calcineurin inhibitors such as tacrolimus show limited efficacy in certain patients [4,5]. Biologics like dupilumab and JAK inhibitors are effective for moderate-to-severe cases but present challenges including high cost, the need for injection, and potential risks of infection or malignancy [5,6].The pathogenesis of eczema arises from complex interactions among genetic susceptibility (e.g., filaggrin (FLG) mutations), impaired skin barrier function (e.g., elevated pH and microbial dysbiosis), dysregulated immune responses (including Th2/Th17 imbalance), and environmental factors [1,4,7,8]. This multifactorial complexity complicates the development of targeted therapies; biologics directed at specific pathways, such as Th2, often fail to ameliorate concurrent barrier impairment or microbial imbalance [9,10]. These limitations highlight the need for novel, safe, and multifaceted treatment strategies.Platelet-rich plasma (PRP), an autologous blood product containing concentrated platelets and bioactive molecules including platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), Epidermal Growth Factor (EGF), Insulin-like Growth Factor (IGF) and transforming growth factor-β(TGF-β), has gained attention as a potential therapeutic agent in dermatology [11].In addition, PRP also exhibits anti-apoptotic effects, immunosuppressive properties, reduction of melanin synthesis, antimicrobial activity, and antioxidant effects PRP has been demonstrated to be effective in treating various dermatological conditions, including androgenetic alopecia (by stimulating hair follicle stem cells and reducing perifollicular inflammation) [12], alopecia areata (AA) [13] and psoriasis (through normalizing keratinocyte hyperproliferation and downregulating the pro-inflammatory interleukin (IL)-17, a Th17-related cytokine) [14].Notably, both AA and psoriasis share pathophysiological overlaps with eczema: all involve chronic immune activation (e.g., Th2/Th17 skewing), epithelial barrier disruption, and neuroimmune crosstalk [15][16][17][18]. These conserved pathways imply that the multifunctional properties of PRP, namely anti-inflammatory, barrier-repairing, and immunomodulatory effects, may similarly target core mechanisms in eczema. To our knowledge, no systematic studies have yet explored the use of PRP in eczema treatment, and available data regarding its role in the condition's complex pathophysiology remain limited. Considering the unmet clinical need and the favorable safety profile of PRP, we hypothesize that PRP could act as a novel adjuvant therapy for eczema, potentially mitigating inflammation, restoring epidermal barrier function, and reducing chronic recurrence via its pleiotropic effects. This study seeks to elucidate the mechanisms through which PRP modulates eczema, thereby providing preclinical evidence to inform future clinical trials and potentially advance toward more personalized and effective management hypothesize that PRP, as a novel adjuvant therapy for eczema, may management through regulatory mechanisms by inflammation, restoring epidermal barrier function, and reducing chronic recurrence via its pleiotropic effects This between PRP and skin by core with growth as EGF, and skin regeneration and These factors stimulate keratinocyte and all essential for barrier in eczema. studies that PRP the antioxidant of keratinocytes and modulates melanin a potential role in skin inflammation and may ameliorate immune in eczema by T cytokines [13]. has also demonstrated effects in neuroimmune interactions in eczema, PRP may through or infection in skin and PRP may through antimicrobial or by enhancing thereby reducing in PRP release bioactive molecules that inflammation, and immune responses These mechanisms may also in chronic skin the of effects of PRP its to barrier function may thereby the of the rationale for using PRP as an therapy in eczema in its regulatory which target core pathological inflammation, epidermal barrier dysfunction, and chronic To we the therapeutic overlap of PRP inflammatory skin such as AA and psoriasis, on mechanistic to its potential for of eczema epidermal barrier dysfunction, characterized by filaggrin (FLG) impaired stratum and dysregulated with bioactive growth PRP directly pathological and proliferation and synthesis, thereby restoring junction integrity [2]; EGF and IGF-1 stimulate keratinocyte migration and differentiation, which are essential for reassembling the stratum corneum's "brick-and-mortar" structure. EGF, in particular, activates keratinocyte differentiation markers such as FLG2 and tight junction proteins including ZO-1 and occluding, thereby reinforcing barrier integrity [28]; VEGF enhances microvascularization and improves nutrient delivery to compromised regenerative potential has also been demonstrated in other inflammatory or barrier-deficient dermatoses, such as AA, where it promotes hair follicle regeneration via upregulation of follicular stem cell markers and suppression of perifollicular inflammation [29]. Although the specific manifestations of barrier defects differ between eczema and AA, both conditions share a core requirement for epithelial repair-a process directly facilitated by PRP's growth factor-mediated mechanistic overlap supports the rationale for using PRP to treat barrier dysfunction in eczema.Eczema pathogenesis primarily involves an imbalance in the polarization of Th2, Th17, and Th22 cells, along with dysregulated molecular cascades of associated cytokines [30][31][32][33]. Specifically, IL-4 and IL-13 secreted by Th2 cells bind directly to receptors on keratinocytes and downregulate FLG and tight junction proteins (ZO-1, occludin) via activation of the JAK/STAT6 signaling pathway, thereby compromising the epidermal "brick-and-mortar" structure and increasing TEWL. Th17-derived IL-17 activates the NF-κB pathway, inducing keratinocytes to release pro-inflammatory factors such as IL-6 and TNF-α, which intensify inflammatory infiltration. IL-22 from Th22 cells disrupts keratinocyte proliferation and differentiation balance through STAT3 signaling, resulting in skin thickening and desquamation. As a key pruritogen produced by Th2 cells, IL-31 binds the IL-31RA/OSMR heterodimeric receptor on sensory neurons and activates the JAK/JNK pathway, promoting TRPV1 ion channel phosphorylation [33]. This process initiates itch signal transmission and sustains a vicious cycle of itching, scratching, and further barrier disruption.The immunomodulatory effects of platelet-rich plasma PRP in AA and psoriasis provide molecular evidence supporting its potential intervention in the Th cell axis of eczema. In AA, a Th1/Th17-dominant condition, PRP lowers mRNA expression of Th1/Th17-related pro-inflammatory factors such as IFN-γ and IL-17 in lesions, while increasing the anti-inflammatory factor IL-10 and levels of the regulatory T-cell (Treg) marker FOXP3 [13]. This core mechanism relies on PRP-derived TGF-β1, which inhibits dendritic cell maturation and downregulates surface co-stimulatory molecules CD80/CD86, thereby reducing dendritic cell (DC) -mediated activation of pathogenic T cells [13]. Similarly, in the Th17-dominant setting of psoriasis, PRP regulates DC-T cell interactions by reducing peripheral blood Th17 cells, suppressing their secretion of IL-17, IL-22, and TNF-α, and enhancing the suppressive of cells T cells Although eczema characterized by which from the Th in alopecia areata and psoriasis, all disorders share the pathological features of pathogenic T cell activation and impaired This that PRP may balance to the axis in eczema by DC-T cell interactions and reinforcing T cell PRP may also the cycle in eczema via neuroimmune In of chronic PRP the from a pro-inflammatory to an anti-inflammatory effects has been to in and the cycle in eczema on sensory activation by we hypothesize that PRP neuroimmune it may TRPV1 ion channel activation to itch signaling, while the epidermal barrier and secretion to the chronic of eczema through skin by which inflammation through the secretion of and the of Although are in psoriasis or AA, the antimicrobial of and to the infection risks associated with with such as or to by PRP activates by and increasing thereby enhancing These mechanisms may the effects of on eczema characterized by the where chronic inflammation sensory further and The role of PRP in inflammation and has been in conditions such as AA psoriasis and its potential to In AA, PRP hair follicle regeneration by promoting and reducing perifollicular [13]. In psoriasis, PRP keratinocyte hyperproliferation and inflammation by IL-17 and eczema, PRP may IL-31 and through the of its or anti-inflammatory such as and IL-10 its factors (e.g., can and epidermal the skin characterized by resulting from factors and which further barrier dysfunction Although PRP properties, it enhances skin by stimulating keratinocyte proliferation and the of barrier the of FLG expression and a key of in eczema The efficacy of PRP has also been in other and PRP with such as has been to skin by enhancing barrier function in psoriasis, which with and and in AA, which involves the use of PRP in eczema with its mechanistic inflammatory skin Eczema core pathological features with conditions like psoriasis and AA, including immune epithelial barrier defects keratinocyte differentiation, imbalance), chronic inflammation and microbial susceptibility in in eczema primarily by with the polarization in psoriasis or multifunctional profile growth factor antimicrobial it to target pathological This PRP as a of the of and microbial in eczema subtypes with mechanistic in genetic epidermal barrier defects (e.g., FLG mutations), stratum and contact dermatitis involves while contact dermatitis from keratinocyte by eczema to and environmental PRP therapeutic effects in eczema in it may genetic defects by FLG via enhancing keratinocyte differentiation to barrier "brick-and-mortar" structure while chronic via for contact dermatitis, its anti-inflammatory and epidermal in contact dermatitis, PRP promotes via and barrier with anti-inflammatory factors like and for eczema, it to barrier function, with its in the intervention for PRP in eczema, the can be a as a target the in cell such as keratinocytes PRP's barrier via growth while in like chronic eczema its of eczema including pruritus, erythema, and desquamation. immune in of immune cells PRP's suppression of Th2/Th17 pro-inflammatory cytokines and of anti-inflammatory in further its of and inflammatory by T cells and cells effects be through in by in of and inflammatory such as and TNF-α, to PRP's to and inflammation and and chronic PRP's to the by suppressing chronic inflammation and promoting be using in stratum and in via and clinical trials mechanistic efficacy using core such as the Eczema and and recurrence while also safety including and infection to PRP's and clinical The with complex pathophysiological barrier dysfunction, immune and inflammation, thereby providing for the therapeutic the to be the PRP growth factor expression in eczema promotes proliferation and Th2/Th17 cytokines and and IL-10 and TNF-α, and and and improves stratum and eczema show skin inflammation and to with epidermal and The PRP group exhibits in and recurrence the mechanistic markers such as elevated IL-10 and with clinical eczema management has a intervention topical calcineurin and JAK inhibitors fail to the unmet of eczema eczema topical corticosteroids and calcineurin inhibitors such as tacrolimus inflammation, barrier integrity and can further barrier function by epidermal proliferation biologics like of the Th2 target immune mechanism and other pathological such as Th17 and microbial while also risks of PRP's directly to the multifactorial pathogenesis of eczema, a to therapeutic Although platelets are primarily for their role in evidence their in inflammatory including inflammation have demonstrated that PRP can ameliorate in certain inflammatory skin such as psoriasis and This that PRP may core in eczema growth directly the epidermal through keratinocyte proliferation and the of anti-inflammatory that barrier key T-cell such as Th2 and Th17 and associated PRP promotes immune the of antimicrobial properties, including the of function, the cycle of infection and inflammation, thereby reducing on The to pro-inflammatory cytokines like while stimulating proliferation disrupts the cycle and chronic PRP enhances skin the by restoring barrier function and synthesis, environmental In that PRP on eczema pathophysiology via core growth factor-mediated antimicrobial activity, between anti-inflammatory and regenerative and This more with the complex and chronic of eczema may that PRP, through effective eczema thereby supporting both the and clinical of future trials its efficacy in chronic or eczema, PRP could from an therapy to a of eczema This a in clinical to patients more personalized and treatment the for PRP's challenges be clinical can as topical injection, or This of the of eczema patients of PRP's potential as a treatment or in with such as JAK or topical of PRP limited by the skin of its molecular delivery has been to delivery including have been to contact and Although PRP directly to the target it risks of and eczema are often by and to as skin and antimicrobial essential PRP to of PRP both and PRP, may in bioactive and release These directly therapeutic the need for a mechanistic to the of growth factors and to strategies to skin specific growth factor with in could inform that toward also for key IL-31 and barrier defects such as filaggrin or all PRP This the rationale for PRP that are in mechanistic and are with that PRP modulates the core pathological of disruption, immune chronic inflammation, and mechanisms. These growth barrier antimicrobial of the cycle through and skin core in the limitations of suppressive which and a more for eczema the and clinical through