Rapid Healing of Venous Ulcers and Lack of Clinical Rejection With an Allogeneic Cultured Human Skin Equivalent

Improvement in Clinical Outcomes, Physical Function, and Bodily Pain Following a 12 Week Course of Intermittent Pneumatic Compression Therapy in Patients with Chronic Venous Ulcers: Results of an Observational Longitudinal Retrospective Study

“…It is often thought that venous ulcers heal easily with standard graded compression consisting of short stretch and elastic bandages that provide 20-30 mmHg compression at the ankle. But data from randomized clinical trials have shown that less than 50% of patients with this type of compression healed within a 24 week period [11]. Greater incidence of wound closure has been demonstrated when compression is greater (30-40 mmHg) [8].…”

Fibroblasts from chronic wounds show altered TGF‐β‐signaling and decreased TGF‐β Type II Receptor expression

“…Due in part to increased emphasis on evidence-based medicine, there has been greater standardization in treatment strategies and in what constitutes effective conventional therapy Falanga, 2000). Also, a number of new therapies, including the use of recombinant growth factors (Steed, 1995;Robson et al, 1998Robson et al, , 2001Smiell et al, 1999) and bioengineered skin, (Gentzkow et al, 1996;Bowering, 1998;Falanga et al, 1998;Falanga and Sabolinski, 1999) have been tested successfully in clinical trials. However, in spite of this substantial progress in how chronic wounds are treated, there remains a great need for accelerating their healing and for preventing recurrences.…”

Intrabody-mediated phenotypic knockout of major histocompatibility complex class I expression in human and monkey cell lines and in primary human keratinocytes

“…Likewise, the use of bilayered living skin equivalent, made of type I bovine collagen and cultured allogeneic cells (keratinocytes and fibroblasts) isolated from human neonatal foreskin, although already showing clinical benefit for the treatment of several skin disorders, may also benefit from supplying MHC-deficient keratinocytes and fibroblasts to this form of tissue therapy. [74][75][76] However, these keratinocyte allografts and/or living skin equivalents will first need to be tested in vivo to determine if the MHC-deficient cells have significantly decreased immunogenicity compared with their untreated counterparts. 77 In addition to the studies described above, further manipulation of the major histocompatibility complex via the combined disruption of both class I and class II antigens could potentially permit the indefinite survival of keratinocyte allografts in patients with significant thermal injury, as class II knockout keratinocytes have been shown to be even less immunogenic than class I knockout keratinocytes, possibly as a result of the role of MHC class II antigens in the afferent arm of antigen processing, 315 in amplifying T-helper activity and ultimately in activating allospecific CTLs.…”