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“Lymphocyte survival” refers broadly to the set of cellular processes and extracellular signals that maintain the viability and function of immune system cells known as lymphocytes—including T cells, B cells, and natural killer cells. This involves multiple surface receptors transmitting pro-survival signals through distinct intracellular cascades—most notably those promoting anti-apoptotic protein expression/function or activating metabolic pathways like PI3K/Akt—to prevent mitochondrial release of apoptogenic factors such as cytochrome c[1]. Proper regulation ensures effective immune responses while preventing pathological accumulation or loss of these critical immune effectors[2][4]. Dysregulation contributes significantly to diseases ranging from immunodeficiencies and autoimmunity to hematologic cancers[5].
Drugs targeting molecules involved in lymphocyte survival act via: - Induction or inhibition of apoptotic pathways. - Modulation of pro-survival signaling cascades such as PI3K/Akt. - Regulation of anti-apoptotic protein expression/function.
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