Implants immune response

The islet cells transplanted into humans are obtained from pancreatic tissue of deceased human donors (Figure 8.9). Implantation of these cells in recipients displaying a competent immune system would, at best, be of transient therapeutic benefit. The ensuing immune response would quickly destroy the foreign cells. Studies conducted thus far in humans have utilized diabetic patients who have received kidney transplants, as these are already subject to immunosuppressive therapy. However, a major stumbling block to the widespread adoption of this therapeutic approach is, predictably, the requirement to induce concurrent immune suppression. 

Any material proposed for implantation, whether for cell transplantation or some other application, must be biocompatible i.e. it must not provoke an adverse response from the host s immune system. If this goal is not met the implant may be rejected. To this end it is important that the material be easily sterilized either by exposure to high temperatures, ethylene oxide vapor, or gamma radiation. A suitable material must therefore remain unaffected by one of these three techniques. However, biocompatibility is not simply a question of sterility. The chemistry, structure, and physical form of a material are all important factors which determine its biocompatibility. Although our understanding of the human immune system is advancing rapidly, it is not yet possible to predict the immune response to a new material. This can only be determined by in vivo experiments. 

Another study in Fischer rats demonstrated that MSCs do not elicit an immune response after transplantation in immunocompetent recipients. Syngeneic Fischer MSCs or allogeneic ACI MSCs were implanted via an osteoconductive matrix into the bilateral femoral gap of Fischer rats who were then sacrificed at 3, 6 and 12 weeks post-implantation (n = 4 per time point). Histological analysis showed there was no difference between the syngeneic or allogeneic implants. Allogeneic implants did not induce significant inflammatory cell infiltration or stimulate alloreactive T-cell responses [656702]. 

Allogeneic rat mesenchymal stem cells do not elicit an immune response after implantation in immunocompetent recipients Archambault, M.P., McIntosh, K.R., Duty, A., Peter, S.J. (2000). Blood, 96 11 Abs 3295. 

For any implanted device that is intended for long-term use, collagen encapsulation of the device will occur due to the immune response to the device.60 Collagen deposition typically begins at roughly 5-7 days postimplantation and takes up to a month to reach completion. In terms of calibration of the microdialysis probe, this layer of material will provide additional mass transport resistance and could be denoted as a trauma layer. 

The influence of NO in thrombogenesis, bacterial infection, angiogenesis, and the immune response suggest that its active release into the tissue surrounding a sensor may minimize the FBR. Sensor coatings that release NO could reduce the occurrence and severity of bacterial infection, minimize inflammation and collagen capsule formation, and promote the formation of new blood vessels, all of which would create a more favorable implant environment. Since NO is reactive (i.e., has a short half-life), the effects of NO would remain localized to the area from which it is released. 

The results by Hetrick et al.32 support the use of NO-release coatings for developing more tissue-compatible sensors. However, the impact of NO on the biocompatibility at a NO-releasing implant is a multifaceted question that is still not fully understood. Further study into the mechanisms by which NO decreases tissue encapsulation and chronic immune response while increasing angiogenesis will aid in optimization of the NO release properties (e.g., flux, concentration, and duration) of an implant coating for sensor applications. 

For short-term applications, the host reaction to the foreign material should reach steady state rapidly and resist fouling during the duration of use. For long-term implantations, the steady-state immune response must be limited to minimal fibrous... 

The presence of an implant almost always energizes the body s immune system, which sends out white hlood cells to destroy the "foreign invader" (the implant). Even if a hiocompatihle material is used for the implant, inflammation caused hy the surgical procedure used in its insertion may also cause an immune response. Although the immune system s macrophages are generally unable to eliminate the implant itself, they may cause scar tissue to form around the implant. The scar tissue often prevents the restoration of normal tissue at the site of the implant, which can prompt an early failure of the implant itself. 

Of all forms of skin grafting, autografting is by far the most likely to be successful. In other forms of grafting, a patient is likely to suffer not only from infections developing from the loss of skin, hut also from immune responses as his or her body begins to reject the "foreign" implant, the skin from some nonself source. 

However, to make such a therapy reality, concerns over cell viability inside the implantable device have to be adequately addressed. The implant s polymer composition and morphology would have to be optimized in order to maximize the life-span of the cells and to minimize host immune responses. The vascularization of the implant would be another determinant that plays an important role regarding cell viability because it enables the implant to receive nutrients necessary for their survival, to eliminate metabolic by-products and to provide the systemic entrance of therapeutic proteins. 

In addition to a deep knowledge of immune response mechanisms, a rehable designing of implants needs to consider also timescale of the immune response. Indeed, there are three major timescales of the immune response hyperacute, acute, and chronic. While hyperacute response, typically connected to innate immunity, develops on the timescale of seconds to minutes, acute response is humoral mediated and occurs on the order of weeks, its intensity and appearance being highly dependent on whether exposure to antigen is the first exposure or a repeated exposure. Finally, chronic response is cell mediated and occurs in the order of months to years. 

Altered immune response Implantation of prosthetic materials... 

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