Journal of Experimental Medicine最新文献

Early transcriptional effects of inflammatory cytokines reveal highly redundant cytokine networks.

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-04-07 Epub Date: 2025-01-28 DOI: 10.1084/jem.20241207

Juliana J Lee, Liang Yang, Jonathan J Kotzin, Dughan Ahimovic, Michael J Bale, Peter A Nigrovic, Steven Z Josefowicz, Diane Mathis, Christophe Benoist

{"title":"Early transcriptional effects of inflammatory cytokines reveal highly redundant cytokine networks.","authors":"Juliana J Lee, Liang Yang, Jonathan J Kotzin, Dughan Ahimovic, Michael J Bale, Peter A Nigrovic, Steven Z Josefowicz, Diane Mathis, Christophe Benoist","doi":"10.1084/jem.20241207","DOIUrl":"https://doi.org/10.1084/jem.20241207","url":null,"abstract":"Inflammatory cytokines are fundamental mediators of the organismal response to injury, infection, or other harmful stimuli. To elucidate the early and mostly direct transcriptional signatures of inflammatory cytokines, we profiled all immunologic cell types by RNAseq after systemic exposure to IL1β, IL6, and TNFα. Our results revealed a significant overlap in the responses, with broad divergence between myeloid and lymphoid cells, but with very few cell-type-specific responses. Pathway and motif analysis identified several main controllers (NF-κB, IRF8, and PU.1), but the largest portion of the response appears to be mediated by MYC, which was also implicated in the response to γc cytokines. Indeed, inflammatory and γc cytokines elicited surprisingly similar responses (∼50% overlap in NK cells). Significant overlap with interferon-induced responses was observed, paradoxically in lymphoid but not myeloid cell types. These results point to a highly redundant cytokine network, with intertwined effects between disparate cytokines and cell types.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 4","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Altered X-chromosome inactivation of the TLR7/8 locus and heterogeneity of pDCs in systemic sclerosis. TLR7/8位点的x染色体失活改变和系统性硬化症中pDCs的异质性。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2024-12-13 DOI: 10.1084/jem.20231809

Yong Du, Bérénice Faz-Lopez, Marie Dominique Ah Kioon, Claire Cenac, Michael Pierides, Kimberly S Lakin, Robert F Spiera, Julie Chaumeil, Marie-Elise Truchetet, Jessica K Gordon, Jean-Charles Guéry, Franck J Barrat

{"title":"Altered X-chromosome inactivation of the TLR7/8 locus and heterogeneity of pDCs in systemic sclerosis.","authors":"Yong Du, Bérénice Faz-Lopez, Marie Dominique Ah Kioon, Claire Cenac, Michael Pierides, Kimberly S Lakin, Robert F Spiera, Julie Chaumeil, Marie-Elise Truchetet, Jessica K Gordon, Jean-Charles Guéry, Franck J Barrat","doi":"10.1084/jem.20231809","DOIUrl":"10.1084/jem.20231809","url":null,"abstract":"Systemic sclerosis (SSc) is an autoimmune disease that has a strong female predominance. Both the X-linked TLR7 and TLR8 can induce type I IFN (IFN-I) by plasmacytoid DCs (pDCs), which can promote fibrosis. We identified five subclusters of pDCs, including ISGhigh clusters that were over-represented in SSc patients. We observed that both TLR7 and TLR8 genes escape from X chromosome inactivation (XCI) at higher frequency in pDCs of SSc patients, which was associated with changes in TLR7 protein profile. Combined DNA/RNA FISH analysis revealed that the TLR7/8 locus is preferentially located outside of the inactive X (Xi) territory when TLR7 is expressed, suggesting that higher-order loop formation is linked to TLR7/8 expression from the Xi. Furthermore, the expression levels of XIST and the transcriptional repressor SPEN were reduced in SSc pDCs. Hence, our data revealed the heterogeneity of pDCs in SSc and suggested that altered XCI at the TLR7/8 locus may contribute to the chronic IFN-I activity of pDCs in female SSc patients.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11639950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kazuyo Moro: Building relationships is essential for gaining both speed and opportunities in research. Kazuyo Moro：建立关系对于获得研究速度和机会至关重要。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2024-12-04 DOI: 10.1084/jem.20242176

Montserrat Cols

引用次数: 0

RNase T2 restricts TLR13-mediated autoinflammation in vivo.

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2025-01-24 DOI: 10.1084/jem.20241424

Carlos Gomez-Diaz, Wilhelm Greulich, Benedikt Wefers, Meiyue Wang, Silvia Bolsega, Maike Effern, Daniel P Varga, Zhe Han, Minyi Chen, Marleen Bérouti, Natascia Leonardi, Ulrike Schillinger, Bernhard Holzmann, Arthur Liesz, Axel Roers, Michael Hölzel, Marijana Basic, Wolfgang Wurst, Veit Hornung

{"title":"RNase T2 restricts TLR13-mediated autoinflammation in vivo.","authors":"Carlos Gomez-Diaz, Wilhelm Greulich, Benedikt Wefers, Meiyue Wang, Silvia Bolsega, Maike Effern, Daniel P Varga, Zhe Han, Minyi Chen, Marleen Bérouti, Natascia Leonardi, Ulrike Schillinger, Bernhard Holzmann, Arthur Liesz, Axel Roers, Michael Hölzel, Marijana Basic, Wolfgang Wurst, Veit Hornung","doi":"10.1084/jem.20241424","DOIUrl":"10.1084/jem.20241424","url":null,"abstract":"RNA-sensing TLRs are strategically positioned in the endolysosome to detect incoming nonself RNA. RNase T2 plays a critical role in processing long, structured RNA into short oligoribonucleotides that engage TLR7 or TLR8. In addition to its positive regulatory role, RNase T2 also restricts RNA recognition through unknown mechanisms, as patients deficient in RNase T2 suffer from neuroinflammation. Consistent with this, mice lacking RNase T2 exhibit interferon-dependent neuroinflammation, impaired hematopoiesis, and splenomegaly. However, the mechanism by which RNase T2 deficiency unleashes inflammation in vivo remains unknown. Here, we report that the inflammatory phenotype found in Rnaset2-/- mice is completely reversed in the absence of TLR13, suggesting aberrant accumulation of an RNA ligand for this receptor. Interestingly, this TLR13-driven inflammatory phenotype is also fully present in germ-free mice, suggesting a role for RNase T2 in limiting erroneous TLR13 activation by an as yet unidentified endogenous ligand. These results establish TLR13 as a potential self-sensor that is kept in check by RNase T2.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The XCL1-XCR1 axis supports intestinal tissue residency and antitumor immunity. XCL1-XCR1轴支持肠道组织驻留和抗肿瘤免疫。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2025-01-22 DOI: 10.1084/jem.20240776

Amir Ferry, Kianoosh M Mempel, Alexander Monell, Miguel Reina-Campos, Nicole E Scharping, Maximilian Heeg, Kennidy K Takehara, Shiruyeh Schokrpur, Ning Kuo, Robert Saddawi-Konefka, J Silvio Gutkind, Ananda W Goldrath

{"title":"The XCL1-XCR1 axis supports intestinal tissue residency and antitumor immunity.","authors":"Amir Ferry, Kianoosh M Mempel, Alexander Monell, Miguel Reina-Campos, Nicole E Scharping, Maximilian Heeg, Kennidy K Takehara, Shiruyeh Schokrpur, Ning Kuo, Robert Saddawi-Konefka, J Silvio Gutkind, Ananda W Goldrath","doi":"10.1084/jem.20240776","DOIUrl":"10.1084/jem.20240776","url":null,"abstract":"Tissue-resident memory T cells (TRM) provide frontline protection against pathogens and emerging malignancies. Tumor-infiltrating lymphocytes (TIL) with TRM features are associated with improved clinical outcomes. However, the cellular interactions that program TRM differentiation and function are not well understood. Using murine genetic models and targeted spatial transcriptomics, we found that the CD8+ T cell-derived chemokine XCL1 is critical for TRM formation and conventional DC1 (cDC1) supported the positioning of intestinal CD8+ T cells during acute viral infection. In tumors, enforced Xcl1 expression by antigen-specific CD8+ T cells promoted intratumoral cDC1 accumulation and T cell persistence, leading to improved overall survival. Notably, analysis of human TIL and TRM revealed conserved expression of XCL1 and XCL2. Thus, we have shown that the XCL1-XCR1 axis plays a non-cell autonomous role in guiding intestinal CD8+ TRM spatial differentiation and tumor control.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 2","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2025-01-24 DOI: 10.1084/jem.20230647

Ryota Sato, Kaiwen Liu, Takuma Shibata, Katsuaki Hoshino, Kiyoshi Yamaguchi, Toru Miyazaki, Ryosuke Hiranuma, Ryutaro Fukui, Yuji Motoi, Yuri Fukuda-Ohta, Yun Zhang, Tatjana Reuter, Yuko Ishida, Toshikazu Kondo, Tomoki Chiba, Hiroshi Asahara, Masato Taoka, Yoshio Yamauchi, Toshiaki Isobe, Tsuneyasu Kaisho, Yoichi Furukawa, Eicke Latz, Kohta Nakatani, Yoshihiro Izumi, Yunzhong Nie, Hideki Taniguchi, Kensuke Miyake

{"title":"RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.","authors":"Ryota Sato, Kaiwen Liu, Takuma Shibata, Katsuaki Hoshino, Kiyoshi Yamaguchi, Toru Miyazaki, Ryosuke Hiranuma, Ryutaro Fukui, Yuji Motoi, Yuri Fukuda-Ohta, Yun Zhang, Tatjana Reuter, Yuko Ishida, Toshikazu Kondo, Tomoki Chiba, Hiroshi Asahara, Masato Taoka, Yoshio Yamauchi, Toshiaki Isobe, Tsuneyasu Kaisho, Yoichi Furukawa, Eicke Latz, Kohta Nakatani, Yoshihiro Izumi, Yunzhong Nie, Hideki Taniguchi, Kensuke Miyake","doi":"10.1084/jem.20230647","DOIUrl":"10.1084/jem.20230647","url":null,"abstract":"Lysosomal stress due to the accumulation of nucleic acids (NAs) activates endosomal TLRs in macrophages. Here, we show that lysosomal RNA stress, caused by the lack of RNase T2, induces macrophage accumulation in multiple organs such as the spleen and liver through TLR13 activation by microbiota-derived ribosomal RNAs. TLR13 triggered emergency myelopoiesis, increasing the number of myeloid progenitors in the bone marrow and spleen. Splenic macrophages continued to proliferate and mature into macrophages expressing the anti-inflammatory cytokine IL-10. In the liver, TLR13 activated monocytes/macrophages to proliferate and mature into monocyte-derived KCs (moKCs), in which, the liver X receptor (LXR) was activated. In accumulated moKCs, tissue clearance genes such as MerTK, AXL, and apoptosis inhibitor of macrophage (AIM) were highly expressed, while TLR-dependent production of proinflammatory cytokines was impaired. Consequently, Rnaset2-/- mice were resistant to acute liver injuries elicited by acetaminophen (APAP) and LPS with D-galactosamine. These findings suggest that TLR13 activated by lysosomal RNA stress promotes the replenishment of tissue-protective Kupffer cells.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Autocrine TGF-β1 drives tissue-specific differentiation and function of resident NK cells. 自分泌TGF-β1驱动常驻NK细胞的组织特异性分化和功能。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2024-12-18 DOI: 10.1084/jem.20240930

Colin Sparano, Darío Solís-Sayago, Nathan Sébastien Zangger, Lukas Rindlisbacher, Hannah Van Hove, Marijne Vermeer, Frederike Westermann, Caroline Mussak, Elisa Rallo, Stanislav Dergun, Gioana Litscher, Yishu Xu, Mitchell Bijnen, Christin Friedrich, Melanie Greter, Vanda Juranić Lisnić, Burkhard Becher, Georg Gasteiger, Annette Oxenius, Sonia Tugues

{"title":"Autocrine TGF-β1 drives tissue-specific differentiation and function of resident NK cells.","authors":"Colin Sparano, Darío Solís-Sayago, Nathan Sébastien Zangger, Lukas Rindlisbacher, Hannah Van Hove, Marijne Vermeer, Frederike Westermann, Caroline Mussak, Elisa Rallo, Stanislav Dergun, Gioana Litscher, Yishu Xu, Mitchell Bijnen, Christin Friedrich, Melanie Greter, Vanda Juranić Lisnić, Burkhard Becher, Georg Gasteiger, Annette Oxenius, Sonia Tugues","doi":"10.1084/jem.20240930","DOIUrl":"10.1084/jem.20240930","url":null,"abstract":"Group 1 innate lymphoid cells (ILCs) encompass NK cells and ILC1s, which have non-redundant roles in host protection against pathogens and cancer. Despite their circulating nature, NK cells can establish residency in selected tissues during ontogeny, forming a distinct functional subset. The mechanisms that initiate, maintain, and regulate the conversion of NK cells into tissue-resident NK (trNK) cells are currently not well understood. Here, we identify autocrine transforming growth factor-β (TGF-β) as a cell-autonomous driver for NK cell tissue residency across multiple glandular tissues during development. Cell-intrinsic production of TGF-β was continuously required for the maintenance of trNK cells and synergized with Hobit to enhance cytotoxic function. Whereas autocrine TGF-β was redundant in tumors, our study revealed that NK cell-derived TGF-β allowed the expansion of cytotoxic trNK cells during local infection with murine cytomegalovirus (MCMV) and contributed to viral control in the salivary gland. Collectively, our findings reveal tissue-specific regulation of trNK cell differentiation and function by autocrine TGF-β1, which is relevant for antiviral immunity.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11654236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CCDC134 controls TLR biogenesis through the ER chaperone Gp96. CCDC134通过ER伴侣Gp96控制TLR的生物发生。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2024-12-10 DOI: 10.1084/jem.20240825

Léa Bernaleau, Michaela Drobek, Fenja Blank, Philipp Walch, Maeva Delacrétaz, Ales Drobek, Marta Monguió-Tortajada, Petr Broz, Olivia Majer, Manuele Rebsamen

{"title":"CCDC134 controls TLR biogenesis through the ER chaperone Gp96.","authors":"Léa Bernaleau, Michaela Drobek, Fenja Blank, Philipp Walch, Maeva Delacrétaz, Ales Drobek, Marta Monguió-Tortajada, Petr Broz, Olivia Majer, Manuele Rebsamen","doi":"10.1084/jem.20240825","DOIUrl":"10.1084/jem.20240825","url":null,"abstract":"Toll-like receptors (TLRs) are central to initiate immune responses against invading pathogens. To ensure host defense while avoiding aberrant activation leading to pathogenic inflammation and autoimmune diseases, TLRs are tightly controlled by multilevel regulatory mechanisms. Through a loss-of-function genetic screen in a reporter cell line engineered to undergo cell death upon TLR7-induced IRF5 activation, we identified here CCDC134 as an essential factor for TLR responses. CCDC134 deficiency impaired endolysosomal TLR-induced NF-κB, MAPK, and IRF5 activation, as well as downstream production of proinflammatory cytokines and type I interferons. We further demonstrated that CCDC134 is an endoplasmic reticulum (ER)-resident interactor of Gp96 (HSP90B1/Grp94), an ER chaperone essential for folding and trafficking of plasma membrane and endolysosomal TLRs. CCDC134 controlled Gp96 stability as its loss led to Gp96 hyperglycosylation and ER-associated protein degradation (ERAD)-mediated clearance. Accordingly, CCDC134 deficiency impaired the folding, maturation, and trafficking of TLRs, resulting in blunted inflammatory responses upon stimulation. Altogether, this study reveals CCDC134 as a central regulator of the chaperone Gp96, thereby controlling TLR biogenesis and responses.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanosensing regulates pDC activation in the skin through NRF2 activation. 机械感应通过NRF2激活调节皮肤中pDC的激活。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2024-12-13 DOI: 10.1084/jem.20240852

Vidyanath Chaudhary, Bikash Mishra, Marie Dominique Ah Kioon, Yong Du, Lionel B Ivashkiv, Mary K Crow, Franck J Barrat

{"title":"Mechanosensing regulates pDC activation in the skin through NRF2 activation.","authors":"Vidyanath Chaudhary, Bikash Mishra, Marie Dominique Ah Kioon, Yong Du, Lionel B Ivashkiv, Mary K Crow, Franck J Barrat","doi":"10.1084/jem.20240852","DOIUrl":"10.1084/jem.20240852","url":null,"abstract":"Plasmacytoid DCs (pDCs) infiltrate the skin, chronically produce type I interferon (IFN-I), and promote skin lesions and fibrosis in autoimmune patients. However, what controls their activation in the skin is unknown. Here, we report that increased stiffness inhibits the production of IFN-I by pDCs. Mechanistically, mechanosensing activates stress pathways including NRF2, which induces the pentose phosphate pathway and reduces pyruvate levels, a product necessary for pDC responses. Modulating NRF2 activity in vivo controlled the pDC response, leading to resolution or chronic induction of IFN-I in the skin. In systemic sclerosis (SSc) patients, although NRF2 was induced in skin-infiltrating pDCs, as compared with blood pDCs, the IFN response was maintained. We observed that CXCL4, a profibrotic chemokine elevated in fibrotic skin, was able to overcome stiffness-mediated IFN-I inhibition, allowing chronic IFN-I responses by pDCs in the skin. Hence, these data identify a novel regulatory mechanism exerted by the skin microenvironment and identify points of dysregulation of this mechanism in patients with skin inflammation and fibrosis.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11639951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tissue-resident NK cells do their own glandscaping. 组织内NK细胞会自行美化环境。

IF 12.6 1区医学

Journal of Experimental Medicine Pub Date : 2025-03-03 Epub Date: 2025-01-03 DOI: 10.1084/jem.20242253

Jacob A Myers, Shanelle P Reilly, Laurent Brossay

引用次数: 0