Options and current practice of determining ferrets paternity (Mustela putorius furo)

Paternity tests dealing with the origin of individuals within breeds. It is an important parameter for those interested in the targeted livestock and lead to the improvement of their breed. This thesis deals with paternity tests used by the animals at the current level of genetic research and their potential application in ferrets form of literary analysis. The literature review is a basic characteristic of ferrets. Furthermore, there are contained basic genetic data, including molecular taxonomy, information, testing and paternity testing paternity insight into carnivores (Carnivora). In the discussion are discussed possibilities of using this test in ferrets. In addressing the issue of the literature, I found that at present is carried out by PCR (polymerase chain reaction), which enables rapid DNA amplification. Using this method is performed comparing STR trio mother-baby-father. Preferably STR polymorphism is of good resolution, high variability and easy amplification by PCR, but the main disadvantage is the high mutation rate and limited number of markers in a single reaction (maximum 17). STR profiling results are expressed paternity index (Pi). The index is the result of paternity probability calculation that helps us express how big probability of paternity this alleged male. Equivalent expression Pi is the percentage ranging from 0% to 100%. The result is either confirming or disproving fatherhood. This problem is in ferrets yet elaborated and testing is currently not used. Within the current knowledge of the paternity test in ferrets contributed to the improvement of their breed that would reduce the risk of inbreeding, the transmission of hereditary diseases or defects in the next generation and to prevent fraudulent behavior in order to deceive the future owner

Engineered human cytokine/antibody fusion proteins expand regulatory T cells and confer autoimmune disease protection.

Low-dose human interleukin-2 (hIL-2) treatment is used clinically to treat autoimmune disorders due to the cytokine's preferential expansion of immunosuppressive regulatory T cells (Tregs). However, off-target immune cell activation and short serum half-life limit the clinical potential of IL-2 treatment. Recent work showed that complexes comprising hIL-2 and the anti-hIL-2 antibody F5111 overcome these limitations by preferentially stimulating Tregs over immune effector cells. Although promising, therapeutic translation of this approach is complicated by the need to optimize dosing ratios and by the instability of the cytokine/antibody complex. We leverage structural insights to engineer a single-chain hIL-2/F5111 antibody fusion protein, termed F5111 immunocytokine (IC), which potently and selectively activates and expands Tregs. F5111 IC confers protection in mouse models of colitis and checkpoint inhibitor-induced diabetes mellitus. These results provide a roadmap for IC design and establish a Treg-biased immunotherapy that could be clinically translated for autoimmune disease treatment

Engineered human cytokine/antibody fusion proteins expand regulatory T cells and confer autoimmune disease protection

Low-dose human interleukin-2 (hIL-2) treatment is used clinically to treat autoimmune disorders due to the cytokine's preferential expansion of immunosuppressive regulatory T cells (Tregs). However, off-target immune cell activation and short serum half-life limit the clinical potential of IL-2 treatment. Recent work showed that complexes comprising hIL-2 and the anti-hIL-2 antibody F5111 overcome these limitations by preferentially stimulating Tregs over immune effector cells. Although promising, therapeutic translation of this approach is complicated by the need to optimize dosing ratios and by the instability of the cytokine/antibody complex. We leverage structural insights to engineer a single-chain hIL-2/F5111 antibody fusion protein, termed F5111 immunocytokine (IC), which potently and selectively activates and expands Tregs. F5111 IC confers protection in mouse models of colitis and checkpoint inhibitor-induced diabetes mellitus. These results provide a roadmap for IC design and establish a Treg-biased immunotherapy that could be clinically translated for autoimmune disease treatment