Lymphotoxin alpha

LTA
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesLTA, LT, TNFB, TNFSF1, Lymphotoxin alpha, TNLG1E
External IDsOMIM: 153440; MGI: 104797; HomoloGene: 497; GeneCards: LTA; OMA:LTA - orthologs
Orthologs
SpeciesHumanMouse
Entrez

4049

16992

Ensembl

ENSMUSG00000024402

UniProt

P01374

P09225

RefSeq (mRNA)

NM_000595
NM_001159740

NM_010735

RefSeq (protein)

NP_000586
NP_001153212

NP_034865

Location (UCSC)Chr 6: 31.57 – 31.57 MbChr 17: 35.42 – 35.42 Mb
PubMed search
Wikidata
View/Edit HumanView/Edit Mouse

Lymphotoxin-alpha (LT-α) formerly known as tumor necrosis factor-beta (TNF-β) is a protein that in humans is encoded by the LTA gene. Belonging to the hematopoietic cell line, LT-α exhibits anti-proliferative activity and causes the cellular destruction of tumor cell lines. As a cytotoxic protein, LT-α performs a variety of important roles in immune regulation depending on the form that it is secreted as. Unlike other members of the TNF superfamily, LT-α is only found as a soluble homotrimer, when found at the cell surface it is found only as a heterotrimer with LTβ.

LT-α has a significant impact on the maintenance of the immune system including the development of secondary lymphoid organs. Absence of LT-α leads to the disruption of gastrointestinal development, prevents Peyer's patch development, and results in a disorganized spleen.

As a signaling molecule, LT-α is involved in the regulation of cell survival, proliferation, differentiation, and apoptosis. LT-α plays an important role in innate immune regulation and its presence has been shown to prevent tumor growth and destroy cancerous cell lines. In contrast, unregulated expression of LT-α can result in a constantly active signaling pathway, thus leading to uncontrolled cellular growth and creation of tumors. Hence depending on the context, LT-α may function to prevent growth of cancer cells or facilitate the development of tumors. Furthermore, LT-α effects depend on the type of organ it acts upon, type of cancer cells, cellular environment, gender, and time of effect during an immune response.