Keyhole Limpet Hemocyanin; MP: Methyl Prednisolone; MTX: Methotrexate; RA: Rheumatoid Arthritis; TNF: Tumor Necrosis Factor; TNF-K: human TNF-KLH heterplex; TTg mice: human TNF Transgenic mice Abstract TNF-alpha blockade is an effective Ecdysone treatment for patients with TNF-alpha-dependent chronic inflammatory diseases such as rheumatoid arthrit Crohn disease and psoriasis. Anti-TNF-alpha Kinoid using a heterplex of human TNF-alpha and KLH is an active immunotherapy targeting TNF-alpha. Since TNF-K approach is active immunization and that targeted patients received immunosuppressant treatme we evaluate the immunosuppressive effect of some of these drugs on the generation of anti-TNF-alpha antibodies produced during TNF-K treatment.
BALB mice were injected intra-muscularly by TNF-K in IS adjuvant. Mice were also Lapatinib injected intraperitoneally with one of the following: P cyclophosphami methyl-prednisolone or methotrexate. Anti-TNF-alpha and anti-KLH antibody levels were assessed by ELISA and the anti-TNF-alpha neutralizing capacity of sera by bioassay. Our results showed that current treatments used in rheumatoid arthrit such as methyl-prednisolone and methotrexate do not significantly alter anti-TNF-alpha antibody production after TNF-K immunization. Converse the administration of cyclophosphamide mg/kg after immunization significantly reduced anti-TNF-alpha antibody titers and their neutralizing capacity. Keywords: TNF-alp immunosuppressa vaccinati antibody purchase Magnolol production . Introduction Tumor necrosis factor is a well-established therapeutic target in several chronic inflammatory diseas including rheumatoid arthriti psoriasis and Crohn disease .
In two classes of TNF blocking agents have been developed so far: a soluble TNF receptor and TNF-binding monoclonal antibodies or mAbs fragmen such as inflixim adalimum golimum or certolizumab. These biologic drugs show rapid and substantial therapeutic efficacy in most patients and in experimental models . TNF is not the onlypound involved in the pathophysiology of and better disease control is often achieved when TNF order Orotic acid antagonist therapy is associated with an immunosuppressant like methotrexate . Recent data have shown that anti-TNF treatment may counteract RA progression not only via the neutralization of soluble TN but also by the modulation of T cell homeostasis. Inde infliximab treatment induces the re-emergence of a discrete regulatory T cells subtype in RA patients and inhibits T and T accumulation in the joints .
Current TNF targeting strategies have shown several drawbacks. Fir anti-TNF agents raised some conce because of the role of TNF in controlling infections and tumors. Seco primary and secondary failures are not infrequent: in clinical trials less than of responder patients attained disease remission . The risk of anti-drug antibody producti with possible loss of efficacy and side “effec is proper to current anti-TNF agen especially monoclonal muscle contraction antibodies . Thi treatments with biologics have high costs for themunity and precludes their usage in all countries . Th there is a need to develop new drugs to neutralize TNF . A promising alternative strategy consists in active immunotherapy against TNF . anti-TNF vaccination. This techniq leads to the production.