The Role of Fibroblasts in Tissue Engineering and Regeneration

T. Wong; J.A. McGrath; H. Navsaria

Disclosures

The British Journal of Dermatology. 2007;156(6):1149-1155. 

In This Article

Allogeneic vs. Autologous Fibroblasts

Fibroblasts used in tissue engineering may be allogeneic or autologous. In contrast to allogeneic cells, autologous fibroblasts carry no risk of rejection or risk of cross-infection. However, there is often a delay in culturing autologous cells in order to obtain sufficient cell numbers, whereas allogeneic cells are cryopreserved and therefore readily available.[8,9] For permanent engraftment, autologous fibroblasts are necessary. However, allogeneic fibroblasts have been used as a biological dressing or for preconditioning of the wound bed prior to application of a permanent graft, especially when wounds are very large. In addition, using autologous fibroblasts in dermal substitutes has led to better restoration of dermal skin and minimal scar formation compared with allogeneic dermal substitutes.[10,11]

There have also been a number of studies investigating the immunological impact of allogeneic cells on the recipient. One study looked at the persistence of allogeneic fibroblasts in an acute wound (porcine model) and found that after 1 week, allogeneic fibroblasts were not detectable by polymerase chain reaction.[12] Apligraf® (Novartis, Basel, Switzerland) is a living skin substitute composed of allogeneic keratinocytes and allogeneic fibroblasts and its application in acute human wounds showed that these were not detectable beyond 6 weeks.[13] It has therefore been suggested that allogeneic cells are eventually silently replaced by host cells. In addition, large trials involving grafting of allogeneic skin equivalents onto venous ulcers did not reveal evidence of rejection clinically or immunologically in the patients.[14] There was no demonstration of induction of antibodies specific for human leukocyte class I antigens expressed on allogeneic cells and no proliferation of T cells in patients after exposure to the antigens. One of the reasons for the perceived lack of acute rejection in immunocompetent hosts is that dermal fibroblasts lack major histocompatibility complex class II antigens necessary for antigen presentation.[15] It has also been proposed that as keratinocytes and fibroblasts are cultured in vitro, the antigen-presenting cells such as Langerhans cells, are gradually lost following serial passages and are therefore no longer present in cultured skin substitutes; hence, they do not stimulate an acute rejection process.[16]

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