Page last updated: 2024-10-24

regulation of activated CD4-positive, alpha-beta T cell apoptotic process

Definition

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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Proteins (1)

ProteinDefinitionTaxonomy
Programmed cell death 1 ligand 1A programmed cell death 1 ligand 1 that is encoded in the genome of human. [PRO:WCB, UniProtKB:Q9NZQ7]Homo sapiens (human)

Compounds (4)

CompoundDefinitionClassesRoles
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
pomalidomide3-aminophthalimidoglutarimide: structure in first sourcearomatic amine;
dicarboximide;
isoindoles;
piperidones
angiogenesis inhibitor;
antineoplastic agent;
immunomodulator
apiinapiin : 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
fosbretabulinstilbenoid