Featured Publications

Sharma P, Guo A, Poudel S, Boada-Romero E, Verbist KC, Palacios G, Immadisetty K, Chen MJ, Haydar D, Mishra A, Peng J, Babu MM, Krenciute G, Glazer ES, Green DR
Nat Immunol. 
2025 Aug;
26
(8):
1384-1396. 
doi: 10.1038/s41590-025-02223-6. 
Epub 2025 Jul 23.
Aug 1, 2025

In this study, Sharma et al. demonstrate that reduced methionine availability early during T cell activation drives CD8 T cells towards exhaustion in both infection and tumor models in mice. These effects were attributed to reduced methylation of an arginine residue in the K+ channel KCa3.1 and its increased activity, resulting in enhanced calcium influx and NFAT1 activation. Methylation of Arg350 weakens the interaction of KCa3.1 with calmodulin and may represent a mechanism to prevent T cell hyperactivation. -HW

Li B, Elsten-Brown J, Li M, Zhu E, Li Z, Chen Y, Kang E, Ma F, Chiang J, Li YR, Zhu Y, Huang J, Fung A, Scarborough Q, Cadd R, Zhou JJ, Chin AI, Pellegrini M, Yang L
Cell. 
2025 Jul 10;
188
(14):
3823-3842.e21. 
doi: 10.1016/j.cell.2025.04.032. 
Epub 2025 May 21.
Jul 10, 2025

In this study, Li et al. report that that serotonin transporter (SERT) inhibits CD8 T cell antitumor immunity by depleting intratumoral serotonin. SERT-blocking SSRI antidepressants enhance CD8 T cell function and synergize with anti-PD-1 therapy, suggesting SSRIs as potential cancer immunotherapeutics. –HYC/ZQ

Choi SH, Santin A, Myers JT, Kim BG, Eid S, Tomchuck SL, Kingsley DT, Huang AY
J Leukoc Biol. 
2025 Mar 14;
117
(3):
doi: 10.1093/jleuko/qiae242. 
Mar 14, 2025

The study shows that the mechanosensitive ion channel Piezo1 acts as a negative regulator of group 2 innate lymphoid cells (ILC2s) and their role in airway hyperreactivity (AHR) in allergic asthma. Whereas deletion of Piezo1 augments ILC2 activity and AHR, agonist mediated Piezo1 activation suppresses ILC2-driven AHR suggesting that Piezo1 agonists could have therapeutic potential in asthma. –WAC

Zhong L, Wang YH, Kahlfuss S, Jishage M, McDermott M, Yang J, Tao AY, Hu K, Noyer L, Raphael D, Patel D, Knight TE, Chitlur M, Machaca K, Feske S
Nat Immunol. 
2025 Mar;
26
(3):
484-496. 
doi: 10.1038/s41590-025-02089-8. 
Epub 2025 Feb 21.
Mar 1, 2025

Zhong et al. report that store-operated Ca2+ entry (SOCE) activated by STIM1 and mediated by ORAI channels is required for the differentiation of Th1 cells, which are crucial for immunity against intracellular pathogens. SOCE synergizes with IFN-γ induced STAT1 signaling to promote expression of the Th1 transcription factor T-bet. Loss of STIM1 impairs Th1 differentiation, particularly when the cytokine IL-12 is absent. As many viruses do not induce IL-12 production and IL-12 production is low in infants, these findings highlight the importance of SOCE in early life immune responses. –HYC/SF

Doyle CA, Busey GW, Iobst WH, Kiessling V, Renken C, Doppalapudi H, Stremska ME, Manjegowda MC, Arish M, Wang W, Naphade S, Kennedy J, Bloyet LM, Thompson CE, Rothlauf PW, Stipes EJ, Whelan SPJ, Tamm LK, Kreutzberger AJB, Sun J, Desai BN
Nat Commun. 
2024 Oct 1;
15
(1):
8479. 
doi: 10.1038/s41467-024-52773-w. 
Epub 2024 Oct 1.
Oct 1, 2024

Doyle et al. demonstrate that TRPM7 ion channel activity is essential for acidification of virus-containing endosomes by providing a cationic countercurrent that enables sustained V-ATPase proton pumping, with loss or pharmacological inhibition of TRPM7 preventing infection by pH-dependent enveloped viruses (Lassa, LCMV, Ebola, SARS-CoV-2, influenza) but not pH-independent viruses (VSV, rabies). This positions TRPM7 as a potential broad-spectrum antiviral target, as its channel activity specifically regulates the acidification of virus-laden endosomes without affecting general endosomal function, and pharmacological inhibition protected mice from influenza infection in vivo. –BD

Samper N, Hardardottir L, Depierreux DM, Song SC, Nakazawa A, Gando I, Nakamura TY, Sharkey AM, Nowosad CR, Feske S, Colucci F, Coetzee WA
Front Immunol. 
2024;
15
1490250. 
doi: 10.3389/fimmu.2024.1490250. 
Epub 2024 Dec 2.
Jan 1, 2024

This study shows that the Kir6.1 subunit of a type of ATP-sensitive potassium (KATP) channels is highly expressed in murine NK cells and that NK cells express a current sensitive to a Kir6.1 blocker. NK cell specific knockout of Kcnj8 (encoding Kir6.1) attenuates NK cell maturation, but has no effect on NK cell degranulation, IFN-γ release and tumor cell killing. –WAC

Liu B, Carlson RJ, Pires IS, Gentili M, Feng E, Hellier Q, Schwartz MA, Blainey PC, Irvine DJ, Hacohen N
Science. 
2023 Aug 4;
381
(6657):
508-514. 
doi: 10.1126/science.adf8974. 
Epub 2023 Aug 3.
Aug 4, 2023
Seegren PV, Harper LR, Downs TK, Zhao XY, Viswanathan SB, Stremska ME, Olson RJ, Kennedy J, Ewald SE, Kumar P, Desai BN
Nat Aging. 
2023 Jul;
3
(7):
796-812. 
doi: 10.1038/s43587-023-00436-8. 
Epub 2023 Jun 5.
Jul 1, 2023
Concepcion AR, Wagner LE 2nd, Zhu J, Tao AY, Yang J, Khodadadi-Jamayran A, Wang YH, Liu M, Rose RE, Jones DR, Coetzee WA, Yule DI, Feske S
Nat Immunol. 
2022 Feb;
23
(2):
287-302. 
doi: 10.1038/s41590-021-01105-x. 
Epub 2022 Feb 1.
Feb 1, 2022

This study identifies LRRC8C as a novel transporter for cyclic dinucleotides (CDNs) in T cells demonstrating that: i) LRRC8C expression is induced by IL-2 signaling in T cells, ii) LRRC8C facilitates influx of CDNs such as cGAMP, activating the CDN sensor STING, iii) STING activation results in p53 accumulation, causing cell cycle arrest and apoptosis. This study establishes the LRRC8C–STING–p53 axis as a negative feedback pathway suppressing T cell responses and adaptive immunity. –ARC/SF

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