ICOSLG

Official Full Name

inducible T cell costimulator ligand

Organism

Homo sapiens

GeneID

23308

Background

Enables identical protein binding activity and receptor ligand activity. Involved in T follicular helper cell differentiation. Located in intracellular membrane-bounded organelle. Is active in plasma membrane. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

B7h; B7H2; GL50; B7-H2; B7RP1; CD275; ICOSL; LICOS; B7RP-1; ICOS-L; IMD119;

Bio Chemical Class

Immunoglobulin

Protein Sequence

MRLGSPGLLFLLFSSLRADTQEKEVRAMVGSDVELSCACPEGSRFDLNDVYVYWQTSESKTVVTYHIPQNSSLENVDSRYRNRALMSPAGMLRGDFSLRLFNVTPQDEQKFHCLVLSQSLGFQEVLSVEVTLHVAANFSVPVVSAPHSPSQDELTFTCTSINGYPRPNVYWINKTDNSLLDQALQNDTVFLNMRGLYDVVSVLRIARTPSVNIGCCIENVLLQQNLTVGSQTGNDIGERDKITENPVSTGEKNAATWSILAVLCLLVVVAVAIGWVCRDRCLQHSYAGAWAVSPETELTGHV

Open

Disease

Lupus erythematosus, Sjogren syndrome

Approved Drug

Clinical Trial Drug

2 +

Discontinued Drug

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Detailed Information

The ICOSLG gene codes for a protein that serves as a ligand for the T-cell-specific receptor ICOS. Integral to T-cell co-stimulation, this protein promotes T-cell proliferation and cytokine release. ICOSLG also promotes B-cell growth and plasma cell differentiation, thereby being rather important for adaptive immunity. The ICOS/ICOSLG pathway supports immunological memory and tissue inflammation under certain conditions, therefore contributing to both primary and secondary immune responses.

In endothelial cells, ICOSLG also promotes neutrophil transmigration in reaction to many chemoattractants, hence showing its more general function in immune control beyond T-cells. Especially, the ICOSLG gene has a paralog with CD276, indicating that further immune regulatory activities are still to be thoroughly investigated. Diseases linked to ICOSLG include immunodeficiency and dyskeratosis congenita, therefore stressing its fundamental role in immune system integrity.

ICOSLG's protein structure is an intracellular domain that modulates signaling, a transmembrane region, and an Ig-like V-type domain. Activation and survival of memory T-cells, which are essential for long-term immunological responses, are driven by the receptor-ligand interaction between ICOS and ICOSLG. Regulating immunological tolerance and managing autoimmune disorders depends on this connection especially.

The Role of ICOSLG in Disease and Therapy

The ICOS/ICOSLG signaling pathway has significant implications in a variety of immune-related conditions, including autoimmune diseases, cancer, and transplant rejection. T-cell activation during immunological responses depends on the ICOSLG-ICOS connection as a co-stimulatory pathway, especially in the late phases of immune activation and the preservation of effector functions.

Blocking the ICOS/ICOSLG pathway has shown promise as a treatment strategy in autoimmune illnesses, where too much immune activation harms tissues. Blocking this route might help to lower T-cell activation and change the immunological response, hence providing a novel therapy option for conditions including rheumatoid arthritis and lupus.

In cancer, on the other hand, the ICOS/ICOSLG pathway is essential for avoiding immune response. Tumors frequently use this route to reduce T-cell function and escape immunological annihilation. Blocking ICOS or its receptor ICOSLG might help to improve the immune response against malignancies. Research on ICOSLG antagonists is now underway to see if they may increase T-cell activity in cancer immunotherapy, hence providing promise for more powerful therapies.

Recent research on immunological checkpoint molecules has highlighted the need for ICOSLG as a therapeutic target. ICOSLG, part of the larger TNF receptor superfamily, has functional parallels with other immune co-stimulatory molecules such as CD40 and OX40, which are main targets in cancer immunotherapy. Targeting these pathways helps researchers overcome immune evasion by tumors and restore the body's capacity to combat cancer.

Furthermore, the production of regulatory T-cells, which are vital for preserving immunological tolerance and avoiding autoimmunity, is significantly influenced by ICOSLG. Therefore, altering the ICOSLG pathway could be a hopeful technique to regulate autoimmune disorders and guarantee transplant success.

Future Perspectives

The ICOS/ICOSLG signaling pathway is a key regulator of immune responses, influencing T-cell activation, memory formation, and tolerance. Its role in both promoting and regulating immune responses makes it a promising target for therapeutic intervention in a variety of diseases. By blocking or modulating ICOSLG-ICOS interaction, it may be possible to treat autoimmune diseases, enhance cancer immunotherapy, and improve transplant outcomes.

Ongoing research into the molecular mechanisms of this pathway is essential for developing more effective therapies. As we learn more about the distinct roles of ICOSLG in immune regulation, we move closer to harnessing its full potential in clinical applications. The future of immunotherapy, particularly in cancer and autoimmune diseases, may well lie in further exploration of the ICOS/ICOSLG pathway, offering hope for better, more targeted treatments.

References:

Pasero C, Truneh A, Olive D. Cosignaling molecules around LIGHT-HVEM-BTLA: from immune activation to therapeutic targeting. Curr Mol Med. 2009;9(7):911-927.
Wang S, Chen L. Co-signaling molecules of the B7-CD28 family in positive and negative regulation of T lymphocyte responses. Microbes Infect. 2004;6(8):759-766.
Roussel L, Vinh DC. ICOSL in host defense at epithelial barriers: lessons from ICOSLG deficiency. Curr Opin Immunol. 2021;72:21-26.

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