Citations 2
Thymic stromal lymphopoietin induces adipose loss through sebum hypersecretion
Choa, Ruth , Tohyama, Junichiro , Wada, Shogo , Meng, Hu , Hu, Jian , Okumura, Mariko, May, Rebecca M., Robertson, Tanner F. , Pai, Ruth-Anne Langan , Nace, Arben , Hopkins, Christian , Jacobsen, Elizabeth A. , Haldar, Malay , Behrens, Edward M. , Minn, Andy J. , Seale, Patrick , Cotsarelis, George , Li, Mingyao , Kambayashi, Taku , FitzGerald, Garret A , Behrens, Edward M , Kim, Brian , Seykora, John T , Li, Mingyao , Arany, Zoltan Pierre , Kambayashi, Taku , Jacobsen, Elizabeth A
Science | July 29, 2021 | Volume: 373 | Issue: 6554 | Pages: No page available
Sweat out the fat with TSLP! Thymic stromal lymphopoietin (TSLP) is a cytokine that can promote immune responses that characterize allergic diseases. Choa et al . found that mice engineered to produce elevated TSLP displayed selective white adipose tissue loss that protected them from obesity, insulin resistance, and steatohepatitis (see the Perspective by Schneider). Protection was not mediated by eosinophils, regulatory T cells, or innate lymphoid cells. Rather, TLSP induced the migration of conventional T cells to sebaceous glands in the skin. Once there, these T cells promoted white adipose tissue loss by the hypersecretion of sebum, a lipid-rich substance that augments the skin’s barrier function. This mechanism, which likely evolved to enhance cutaneous antimicrobial defenses, could be possibly targeted in future treatments for obesity. —STS
TLR Stimulation Modifies BLyS Receptor Expression in Follicular and Marginal Zone B Cells
Treml, Laura S., Hoek, Kristen L., Kambayashi, Taku , Bram, Richard J. , Khan, Wasif N. , Carlesso, Gianluca , Stadanlick, Jason E. , Cancro, Michael P.
The Journal of Immunology | April 18, 2014 | Volume: 178 | Issue: 12 | Pages: 7531-7539
Abstract Through their differential interactions with B lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL), the three BLyS family receptors play central roles in B cell survival and differentiation. Recent evidence indicates BLyS receptor levels shift following BCR ligation, suggesting that activation cues can alter overall BLyS receptor profiles and thus ligand sensitivity. In this study, we show that TLR stimuli also alter BLyS receptor expression, but in contrast to BCR ligation, TLR9 and TLR4 signals, preferentially increase transmembrane activator calcium modulator and cyclophilin ligand interactor (TACI) expression. Although both of these TLRs act through MyD88-dependent mechanisms to increase TACI expression, they differ in terms of their downstream mediators and the B cell subset affected. Surprisingly, only TLR4 relies on c-Rel and p50 to augment TACI expression, whereas TLR9 does not. Furthermore, although all follicular and marginal zone B cells up-regulate TACI in response to TLR9 stimulation, only marginal zone B cells and a subset of follicular B cells respond to TLR4. Finally, we find that both BLyS and APRIL enhance viability among quiescent and BCR-stimulated B cells. However, although BLyS enhances viability among TLR stimulated B cells, APRIL does not, suggesting that TACI but not BLyS receptor 3 may share survival promoting pathways with TLRs.