Wednesday, June 19, 2019

Journal of Research and Review- Lupine Publishers



Therapeutic recombinant interferons and cytokines are being used to treat different diseases but these proteins can start immunogenic reactions. These reactions neutralize the effect of therapeutic proteins and make them useless. There are many factors responsible for causing and effecting immunogenicity including dosage, route of administration, genetic status, and polymorphism and Allergic responses. The body’s first immune response against recombinant therapeutic cytokines is mediated by innate system, subsequently activating the adaptive immune system. The key factors in immunogenicity are the glycosylation and aggregated structure of therapeutic protein that distinguishes the protein/cytokine from self-proteins. There are many ways to reduce immunogenicity like to decrease the number of epitopes for T-cells or by screening the history of allergies. IFNs are basically proteins in nature many of which are related both in 3D structure and amino acid sequences. Recombinant Interferons are widely used these days against viral infections and cancers. In this review the antiproliferative activity and the effects of various recombinant human interferons on the cytotoxic and cytostatic activity of natural killer cells and monocytes are discussed in detail. Many diseases are being treated with drugs having protein nature. These exogenous proteins having therapeutic role are used as a replacement therapy for self-proteins. These Protein therapeutics are checked and analyzed to maintain biosafety measures and toxicity, viral and bacterial contaminations are removed. Beyond checking these measure there is immune response to a protein drug that is called "immunogenicity" can neutralize the effect of therapeutic cytokine (Barandun and others [1]; Dasgupta and others [2]). The concept was that 'self' derived protein therapeutics like recombinant human cytokines IFNβi-3 IFNα4,5 GM-CSF6 and human anti-TNFa7,8 antibodies will not cause immunogenicity.

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