Tumor necrosis factor superfamily in innate immunity and inflammation.

Autor: Šedý J; Laboratory of Molecular Immunology, Infectious and Inflammatory Disease Center, Sanford Burnham Medical Research Institute, La Jolla, California 92037., Bekiaris V; Laboratory of Molecular Immunology, Infectious and Inflammatory Disease Center, Sanford Burnham Medical Research Institute, La Jolla, California 92037., Ware CF; Laboratory of Molecular Immunology, Infectious and Inflammatory Disease Center, Sanford Burnham Medical Research Institute, La Jolla, California 92037.
Jazyk: angličtina
Zdroj: Cold Spring Harbor perspectives in biology [Cold Spring Harb Perspect Biol] 2014 Dec 18; Vol. 7 (4), pp. a016279. Date of Electronic Publication: 2014 Dec 18.
DOI: 10.1101/cshperspect.a016279
Abstrakt: The tumor necrosis factor superfamily (TNFSF) and its corresponding receptor superfamily (TNFRSF) form communication pathways required for developmental, homeostatic, and stimulus-responsive processes in vivo. Although this receptor-ligand system operates between many different cell types and organ systems, many of these proteins play specific roles in immune system function. The TNFSF and TNFRSF proteins lymphotoxins, LIGHT (homologous to lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for herpes virus entry mediator [HVEM], a receptor expressed by T lymphocytes), lymphotoxin-β receptor (LT-βR), and HVEM are used by embryonic and adult innate lymphocytes to promote the development and homeostasis of lymphoid organs. Lymphotoxin-expressing innate-acting B cells construct microenvironments in lymphoid organs that restrict pathogen spread and initiate interferon defenses. Recent results illustrate how the communication networks formed among these cytokines and the coreceptors B and T lymphocyte attenuator (BTLA) and CD160 both inhibit and activate innate lymphoid cells (ILCs), innate γδ T cells, and natural killer (NK) cells. Understanding the role of TNFSF/TNFRSF and interacting proteins in innate cells will likely reveal avenues for future therapeutics for human disease.
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Databáze: MEDLINE