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  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher">BJCR</journal-id>
      <journal-title-group>
        <journal-title xml:lang="en">British Journal of Contemporary Research</journal-title>
        <abbrev-journal-title xml:lang="en">BJCR</abbrev-journal-title>
      </journal-title-group>
      <issn>2979-8582</issn>
      <publisher>
        <publisher-name>Bexford Publishing Ltd</publisher-name>
        <publisher-loc><uri>https://bexfordpublishing.co.uk</uri></publisher-loc>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">BEX_SEP_26_013</article-id>
      <article-id pub-id-type="doi">10.67693/BJCR-CWLLXLWQ</article-id>
      <article-categories>
        <subj-group xml:lang="en" subj-group-type="heading">
          <subject>Review Article</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title xml:lang="en">CAR-T Cell Therapy: Structure, Mechanism of Action, Adverse Effects, and Current Challenges</article-title>
      </title-group>
      <contrib-group content-type="author">
      <contrib corresp="yes">
        <name-alternatives>
          <name name-style="western" specific-use="primary">
            <given-names>Dr. Krishna Kumar Prajapati</given-names>
          </name>
        </name-alternatives>
        <email>krishnaprajapati90@hotmail.com</email>
        <bio xml:lang="en"><p>Department of Zoology Marwar Business School, Naseerabad Gorakhpur, UP, India</p></bio>
      </contrib>
      </contrib-group>
      <pub-date date-type="pub" publication-format="epub">
        <day>10</day>
        <month>10</month>
        <year>2026</year>
      </pub-date>
      <volume>1</volume>
      <issue>5</issue>
      
      
      <pub-history>
        <event event-type="received">
          <event-desc>Received: <date date-type="received">
            <day>02</day>
            <month>09</month>
            <year>2026</year>
          </date></event-desc>
        </event>
        
        <event event-type="accepted">
          <event-desc>Accepted: <date date-type="accepted">
            <day>10</day>
            <month>09</month>
            <year>2026</year>
          </date></event-desc>
        </event>
      </pub-history>
      <permissions>
        <copyright-statement>Copyright (c) 2026 Dr. Krishna Kumar Prajapati</copyright-statement>
        <copyright-year>2026</copyright-year>
        <license xlink:href="https://creativecommons.org/licenses/by/4.0">
          <license-p>This work is licensed under a Creative Commons Attribution 4.0 International License.</license-p>
        </license>
      </permissions>
      <abstract><p>The Chimeric antigen receptor T-cells are genetically modified T-cells which are used to as powerful therapeutic treatment of patients with chemotherapy-refractory/relapsed blood cancers, acute lymphoblastic leukemia, diffuse large B-cell lymphoma, follicular lymphoma and other types of cancers. In CAR-T cell therapy, the T-cells are collected from the tumor patients and prepared the CAR-T cells lies in appropriate T-cells genetically processed in laboratory conditions. By helping the CRISPR/Cas9 technique used instead of retroviral vectors to integrate the CAR gene into specific sites in the genome of T-cells. CAR-T cells are special genetical modified T-cells which wears chimeric antigen receptor (CAR) protein on its cell membrane. The composition of these CAR protein consists of three parts such as recognition region which consist a single chain antibody domain. These domains are responsible for recognition and binding to specific antigen present on cancerous cell. The middle parts of these antibody is embedded in membrane and third parts are internal signaling region. The single chain variant antibody (ScFv) recognition domains which have properties anti-tumor effects through the secretion of inflammatory cytokinese.g., IL-2, IFN-γ, and TNF-α, cytolytic effector function via perforin and granzyme. TNF-related apoptosis-inducing ligand, which binds to death receptors such as DR4 and DR5 on tumor cell surface to activate graft-versus tumor effect. Also, tumor cell apoptosis can be initiated via the activation of caspase-8 and the formation of death-inducing signaling complex (DISC) leading to cell death mediated by mature caspase-3 subsequent cleavage of over 500 cellular substrates as a result of Fas and Fas ligand (FasL) pathway activation.</p></abstract>
    </article-meta>
  </front>
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