Target type: biologicalprocess
Any process that modulates the frequency, rate or extent of activated CD4-positive, alpha-beta T cell apoptotic process. [GO_REF:0000058, GOC:TermGenie, PMID:24187568]
The regulation of activated CD4-positive, alpha-beta T cell apoptotic process is a complex and tightly controlled mechanism that ensures the appropriate elimination of these immune cells once their function is complete or they become potentially harmful. This process involves a delicate balance of pro- and anti-apoptotic signals, orchestrated by a multitude of molecular pathways.
**Induction of Apoptosis:**
* **Activation-induced cell death (AICD):** Activated CD4+ T cells express high levels of Fas (CD95) and its ligand (FasL), leading to the formation of the death-inducing signaling complex (DISC). This complex activates caspase-8, initiating the apoptotic cascade.
* **T cell receptor (TCR) signaling:** Continuous or excessive TCR stimulation can trigger apoptosis. This involves signaling pathways like the mitogen-activated protein kinase (MAPK) cascade, which can induce pro-apoptotic proteins like Bim and Bax.
* **Cytokine deprivation:** The absence of essential growth factors, such as interleukin-2 (IL-2), can lead to apoptosis by inhibiting anti-apoptotic pathways and promoting the expression of pro-apoptotic proteins.
* **DNA damage:** Exposure to genotoxic agents or other forms of DNA damage can activate the p53 pathway, leading to the induction of apoptosis.
**Regulation of Apoptosis:**
* **Anti-apoptotic signaling:** CD4+ T cells express various anti-apoptotic proteins, such as Bcl-2, Bcl-xL, and Mcl-1, which inhibit the activation of caspases and prevent apoptosis. These proteins are often upregulated by survival signals, such as IL-2.
* **Immune checkpoints:** Regulatory T cells (Tregs) express inhibitory molecules like CTLA-4 and PD-1, which can dampen the immune response and prevent excessive T cell activation and apoptosis.
* **Metabolic reprogramming:** Activated CD4+ T cells undergo metabolic reprogramming, relying heavily on glycolysis. Disruptions in this metabolic switch can contribute to apoptosis.
**Consequences of Dysregulation:**
* **Autoimmune diseases:** Defects in apoptotic pathways can lead to the accumulation of autoreactive T cells, resulting in autoimmune disorders.
* **Cancer:** Aberrant regulation of apoptosis can allow cancer cells to escape immune surveillance and promote tumor growth.
* **Infections:** Impaired apoptosis can compromise the ability of the immune system to effectively eliminate pathogens.
In summary, the regulation of activated CD4+ T cell apoptosis is a critical aspect of immune homeostasis. This process is tightly controlled by a complex interplay of pro- and anti-apoptotic signals, ensuring the appropriate elimination of these cells while maintaining immune function.'
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Protein | Definition | Taxonomy |
---|---|---|
Programmed cell death 1 ligand 1 | A programmed cell death 1 ligand 1 that is encoded in the genome of human. [PRO:WCB, UniProtKB:Q9NZQ7] | Homo sapiens (human) |
Compound | Definition | Classes | Roles |
---|---|---|---|
sesamin | (+)-sesamin : A lignan that consists of tetrahydro-1H,3H-furo[3,4-c]furan substituted by 1,3-benzodioxole groups at positions 1 and 4 (the 1S,3aR,4S,6aR stereoisomer). Isolated from Cinnamomum camphora, it exhibits cytotoxic activity. | benzodioxoles; furofuran; lignan | antineoplastic agent; neuroprotective agent; plant metabolite |
pomalidomide | 3-aminophthalimidoglutarimide: structure in first source | aromatic amine; dicarboximide; isoindoles; piperidones | angiogenesis inhibitor; antineoplastic agent; immunomodulator |
apiin | apiin : A beta-D-glucoside having a beta-D-apiosyl residue at the 2-position and a 5,4'-dihydroxyflavon-7-yl moiety at the anomeric position. apiin: structure | beta-D-glucoside; dihydroxyflavone; glycosyloxyflavone | EC 3.2.1.18 (exo-alpha-sialidase) inhibitor; plant metabolite |
fosbretabulin | stilbenoid |