T cells: unexpected players in the bone loss induced by estrogen deficiency and in basal bone homeostasis. Export

@article{citeulike:3392076, abstract = {The bone-immune interface has become a subject of intense interest in recent years. It has long been recognized that infection, inflammation, and autoimmune disorders are associated with systemic and local bone loss. Yet, it is only recently that T lymphocytes and their products have been recognized as key regulators of osteoclast formation, life span, and activity. Similarly, sex steroids and aging have been known to regulate the immune system and T cells for decades. In spite of the abundance of clinical and physiological clues, it is only in the last few years that investigators have linked immune cells to the etiology of postmenopausal and senile osteoporosis, as well as to the bone loss caused by a variety of endocrine conditions. As surprising is new evidence showing that in contrast to their bone destructive effects under certain pathological conditions, T cells are highly protective of basal bone homeostasis, through complex regulatory effects on osteoprotegerin (OPG) production by B cells, involving CD40 to CD40 Ligand (CD40L) costimulation. This article examines the experimental evidence suggesting that estrogen prevents bone loss by regulating T cell function, and that T cell costimulation with B cells is critical for OPG production and maintenance of basal bone homeostasis.}, author = {Weitzmann, M. N. and Pacifici, R.}, citeulike-article-id = {3392076}, citeulike-linkout-0 = {http://dx.doi.org/10.1196/annals.1402.068}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18083938}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18083938}, citeulike-linkout-3 = {http://www3.interscience.wiley.com/cgi-bin/abstract/117986105/ABSTRACT}, doi = {10.1196/annals.1402.068}, issn = {0077-8923}, journal = {Annals of the New York Academy of Sciences}, keywords = {bone, deficiency, estrogen, immunology, loss, superlist, t-cell, thelist}, month = {November}, pages = {360--375}, posted-at = {2008-10-10 01:50:51}, priority = {2}, title = {T cells: unexpected players in the bone loss induced by estrogen deficiency and in basal bone homeostasis.}, url = {http://dx.doi.org/10.1196/annals.1402.068}, volume = {1116}, year = {2007} }

TY - JOUR ID - citeulike:3392076 L3 - citeulike-article-id:3392076 N2 - The bone-immune interface has become a subject of intense interest in recent years. It has long been recognized that infection, inflammation, and autoimmune disorders are associated with systemic and local bone loss. Yet, it is only recently that T lymphocytes and their products have been recognized as key regulators of osteoclast formation, life span, and activity. Similarly, sex steroids and aging have been known to regulate the immune system and T cells for decades. In spite of the abundance of clinical and physiological clues, it is only in the last few years that investigators have linked immune cells to the etiology of postmenopausal and senile osteoporosis, as well as to the bone loss caused by a variety of endocrine conditions. As surprising is new evidence showing that in contrast to their bone destructive effects under certain pathological conditions, T cells are highly protective of basal bone homeostasis, through complex regulatory effects on osteoprotegerin (OPG) production by B cells, involving CD40 to CD40 Ligand (CD40L) costimulation. This article examines the experimental evidence suggesting that estrogen prevents bone loss by regulating T cell function, and that T cell costimulation with B cells is critical for OPG production and maintenance of basal bone homeostasis. JF - Annals of the New York Academy of Sciences SN - 0077-8923 EP - 375 TI - T cells: unexpected players in the bone loss induced by estrogen deficiency and in basal bone homeostasis. VL - 1116 SP - 360 KW - bone KW - deficiency KW - estrogen KW - immunology KW - loss KW - superlist KW - t-cell KW - thelist AU - Weitzmann, MN AU - Pacifici, R PY - 2007/11// UR - http://dx.doi.org/10.1196/annals.1402.068 ER -