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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Current Diabetes Reviews</journal-id><journal-title-group><journal-title xml:lang="en">Current Diabetes Reviews</journal-title><trans-title-group xml:lang="ru"><trans-title>Current Diabetes Reviews</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1573-3998</issn><issn publication-format="electronic">1875-6417</issn><publisher><publisher-name xml:lang="en">Bentham Science</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">643016</article-id><article-id pub-id-type="doi">10.2174/1573399820666230831153249</article-id><article-categories><subj-group subj-group-type="toc-heading"><subject>Medicine</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Review on Monoclonal Antibodies (mAbs) as a Therapeutic Approach for Type 1 Diabetes</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Agarwal</surname><given-names>Gaurav</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Patel</surname><given-names>Mayank</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff id="aff1"><institution>Faculty of Pharmacy, Panipat Institute of Engineering and Technology Panipat, Haryana, India</institution></aff><aff id="aff2"><institution>Neuropharmacology
division, Department of Pharmacology, ISF College of Pharmacy, Moga, (Pb.) 142001, India</institution></aff><pub-date date-type="pub" iso-8601-date="2024-07-01" publication-format="electronic"><day>01</day><month>07</month><year>2024</year></pub-date><volume>20</volume><issue>7</issue><issue-title xml:lang="ru"/><history><date date-type="received" iso-8601-date="2024-12-14"><day>14</day><month>12</month><year>2024</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2024, Bentham Science Publishers</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="en">Bentham Science Publishers</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://journals.eco-vector.com/1573-3998/article/view/643016">https://journals.eco-vector.com/1573-3998/article/view/643016</self-uri><abstract xml:lang="en"><p id="idm45589409543616">Monoclonal antibodies have been successfully utilized in a variety of animal models to treat auto-immune illnesses for a long time. Immune system responses will either be less active or more active depending on how the immune system is operating abnormally. Immune system hypoactivity reduces the body's capacity to fight off various invading pathogens, whereas immune system hyperactivity causes the body to attack and kill its own tissues and cells. For maximal patient compliance, we will concentrate on a variety of antibody therapies in this study to treat Type 1 diabetes (an autoimmune condition). T cells are responsible for the auto-immune condition known as T1D, which causes irregularities in the function of β-cells in the pancreas. As a result, for the treatment and prevention of T1D, immunotherapies that selectively restore continuous beta cell-specific self-tolerance are needed. Utilizing monoclonal antibodies is one way to specifically target immune cell populations responsible for the auto-immune-driven disease (mAb). Numerous mAbs have demonstrated clinical safety and varied degrees of success in modulating autoimmunity, including T1D. A targeted cell population is exhausted by mAb treatments, regardless of antigenic specificity. One drawback of this treatment is the loss of obtained protective immunity. Immune effector cell function is regulated by nondepleting monoclonal antibodies (mAb). The antigen-focused new drug delivery system is made possible by the adaptability of mAbs. For the treatment of T1D and T cell-mediated autoimmunity, different existing and potential mAb therapy methods are described in this article.</p></abstract><kwd-group xml:lang="en"><kwd>Monoclonal antibodies</kwd><kwd>Type 1 diabetes</kwd><kwd>autoimmunity</kwd><kwd>NondepletingmAb</kwd><kwd>Immunity</kwd><kwd>effector cells.</kwd></kwd-group></article-meta></front><body></body><back><ref-list/></back></article>
