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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Perforin and granzymes: function, dysfunction and human pathology.

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    Cytotoxic lymphocytes use perforin and granzymes to kill target cells. Recent advances clarify how these toxins work, revealing their broad roles in immunity and disease, crucial for developing new cancer immunotherapies.

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    Area of Science:

    • Immunology
    • Cellular Biology
    • Structural Biology

    Background:

    • Cytotoxic lymphocytes secrete toxins like perforin and granzymes to eliminate target cells.
    • Mechanisms of pore formation and granzyme delivery were previously unclear.
    • The perforin-granzyme pathway has significant roles in immune homeostasis and disease pathology.

    Purpose of the Study:

    • To review current understanding of perforin and granzyme biology.
    • To highlight recent advances in structural and cellular biology.
    • To discuss the pathophysiological roles and clinical implications of the perforin-granzyme pathway.

    Main Methods:

    • Review of structural biology findings.
    • Analysis of cellular biology mechanisms.
    • Discussion of clinical aspects and disease associations.

    Main Results:

    • Advances in structural and cellular biology have elucidated perforin pore formation and granzyme transfer.
    • The synergy between perforin and granzymes in target cell death is better understood.
    • A range of human diseases linked to impaired perforin delivery are being identified.

    Conclusions:

    • The perforin-granzyme pathway is critical for immune function and has broad pathophysiological relevance.
    • Understanding this pathway is key for developing novel immunotherapies, particularly for cancer.
    • Further research into perforin-granzyme biology and associated diseases holds significant clinical promise.