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zimring published april 15 2024 citation information j clin invest 2024 134 8 e167665 https doi org 10 1172 jci167665 view text pdf complement c3 and marginal zone b cells promote igg mediated enhancement of rbc alloimmunization in mice text pdf abstract administration of anti rhd immunoglobulin ig to decrease maternal alloimmunization antibody mediated immune suppression amis was a landmark clinical development however igg has potent immune stimulatory effects in other settings antibody mediated immune enhancement amie the dominant thinking has been that igg causes amis for antigens on rbcs but amie for soluble antigens however we have recently reported that igg against rbc antigens can cause either amis or amie as a function of an igg subclass recent advances in mechanistic understanding have demonstrated that rbc alloimmunization requires the ifn α β receptor ifnar and is inhibited by the complement c3 protein here we demonstrate the opposite for amie of an rbc alloantigen ifnar is not required and c3 enhances rbc clearance c3 deposition and antigen modulation all preceded amie and both cd4 t cells and marginal zone b cells were required we detected no significant increase in antigen specific germinal center b cells consistent with other studies of rbc alloimmunization that show extrafollicular like responses to the best of our knowledge these findings provide the first evidence of an rbc alloimmunization pathway which is ifnar independent and c3 dependent thus further advancing our understanding of rbcs as an immunogen and amie as a phenomenon authors arijita jash thomas pridmore james b collins ariel m hay krystalyn e hudson chance john luckey james c zimring hyperactive stat5 hijacks t cell receptor signaling and drives immature t cell acute lymphoblastic leukemia tobias suske marco herling richard moriggl tobias suske marco herling richard moriggl published april 15 2024 citation information j clin invest 2024 134 8 e168536 https doi org 10 1172 jci168536 view text pdf hyperactive stat5 hijacks t cell receptor signaling and drives immature t cell acute lymphoblastic leukemia text pdf abstract t cell acute lymphoblastic leukemia t all is an aggressive immature t cell cancer mutations in il7r have been analyzed genetically but downstream effector functions such as stat5a and stat5b hyperactivation are poorly understood here we studied the most frequent and clinically challenging stat5bn642h driver in t cell development and immature t cell cancer onset and compared it with stat5a hyperactive variants in transgenic mice enhanced stat5 activity caused disrupted t cell development and promoted an early t cell progenitor all phenotype with upregulation of genes involved in t cell receptor tcr signaling even in absence of surface tcr importantly tcr pathway genes were overexpressed in human t all and mature t cell cancers and activation of tcr pathway kinases was stat5 dependent we confirmed stat5 binding to these genes using chip seq analysis in human t all cells which were sensitive to pharmacologic inhibition by dual stat3 5 degraders or zap70 tyrosine kinase blockers in vitro and in vivo we provide genetic and biochemical proof that stat5a and stat5b hyperactivation can initiate t all through tcr pathway hijacking and suggest similar mechanisms for other t cell cancers thus stat5 or tcr component blockade are targeted therapy options particularly in patients with chemoresistant clones carrying stat5bn642h authors tobias suske helena sorger gabriele manhart frank ruge nicole prutsch mark w zimmerman thomas eder diaaeldin i abdallah barbara maurer christina wagner susann schönefeldt katrin spirk alexander pichler tea pemovska carmen schweicker daniel pölöske emina hubanic dennis jungherz tony andreas müller myint myat khine aung anna orlova ha thi thanh pham kerstin zimmel thomas krausgruber christoph bock mathias müller maik dahlhoff auke boersma thomas rülicke roman fleck elvin dominic de araujo patrick thomas gunning tero aittokallio satu mustjoki takaomi sanda sylvia hartmann florian grebien gregor hoermann torsten haferlach philipp bernhard staber heidi anne neubauer alfred thomas look marco herling richard moriggl cd8 t cells sustain antitumor response by mediating crosstalk between adenosine a2a receptor and glutathione gpx4 siqi chen navdeep s chandel bin zhang siqi chen navdeep s chandel bin zhang published march 5 2024 citation information j clin invest 2024 134 8 e170071 https doi org 10 1172 jci170071 view text pdf cd8 t cells sustain antitumor response by mediating crosstalk between adenosine a2a receptor and glutathione gpx4 text pdf abstract antitumor responses of cd8 t cells are tightly regulated by distinct metabolic fitness high levels of glutathione gsh are observed in the majority of tumors contributing to cancer progression and treatment resistance in part by preventing glutathione peroxidase 4 dependent gpx4 dependent ferroptosis here we show the necessity of adenosine a2a receptor a2ar signaling and the gsh gpx4 axis in orchestrating metabolic fitness and survival of functionally competent cd8 t cells activated cd8 t cells treated ex vivo with simultaneous inhibition of a2ar and lipid peroxidation acquire a superior capacity to proliferate and persist in vivo demonstrating a translatable means to prevent ferroptosis in adoptive cell therapy additionally we identify a particular cluster of intratumoral cd8 t cells expressing a putative gene signature of gsh metabolism gmgs in association with clinical response and survival across several human cancers our study addresses a key role of gsh gpx4 and adenosinergic pathways in fine tuning the metabolic fitness of antitumor cd8 t cells authors siqi chen jie fan ping xie jihae ahn michelle fernandez leah k billingham jason miska jennifer d wu derek a wainwright deyu fang jeffrey a sosman yong wan yi zhang navdeep s chandel bin zhang an ebv related cd4 tcr immunotherapy inhibits tumor growth in an hla dp5 nasopharyngeal cancer mouse model chenwei wang zibing wang lin chen chenwei wang zibing wang lin chen published february 27 2024 citation information j clin invest 2024 134 8 e172092 https doi org 10 1172 jci172092 view text pdf an ebv related cd4 tcr immunotherapy inhibits tumor growth in an hla dp5 nasopharyngeal cancer mouse model text pdf abstract adoptive transfer of t cell receptor engineered t cells tcr t is a promising strategy for immunotherapy against solid tumors however the potential of cd4 t cells in mediating tumor regression has been neglected nasopharyngeal cancer is consistently associated with ebv here to evaluate the therapeutic potential of cd4 tcr t in nasopharyngeal cancer we screened for cd4 tcrs recognizing ebv nuclear antigen 1 ebna1 presented by hla dp5 using mass spectrometry we identified ebna1567 581 a peptide naturally processed and presented by hla dp5 we isolated tcr135 a cd4 tcr with high functional avidity that can function in both cd4 and cd8 t cells and recognizes hla dp5 restricted ebna1567 581 tcr135 transduced t cells functioned in two ways directly killing hla dp5 ebna1 tumor cells after recognizing ebna1 presented by tumor cells and indirectly killing hla dp5 negative tumor cells after recognizing ebna1 presented by antigen presenting cells tcr135 transduced t cells preferentially infiltrated into the tumor microenvironment and significantly inhibited tumor growth in xenograft nasopharyngeal tumor models additionally we found that 62 of nasopharyngeal cancer patients showed 50 100 expression of hla dp on tumor cells indicating that nasopharyngeal cancer is well suited for cd4 tcr t therapy these findings suggest that tcr135 may provide a new strategy for ebv related nasopharyngeal cancer immunotherapy in hla dp5 patients authors chenwei wang jiewen chen jingyao li zhihong xu lihong huang qian zhao lei chen xiaolong liang hai hu gang li chengjie xiong bin wu hua you danyi du xiaoling wang hongle li zibing wang lin chen ectopic expression of the transcription factor onecut3 drives a complex karyotype in myelodysplastic syndromes yingwan luo gang huang hongyan tong yingwan luo gang huang hongyan tong published february 22 2024 citation information j clin invest 2024 134 8 e172468 https doi org 10 1172 jci172468 view text pdf ectopic expression of the transcription factor onecut3 drives a complex karyotype in myelodysplastic syndromes text pdf abstract chromosomal instability is a prominent biological feature of myelodysplastic syndromes mds with over 50 of patients with mds harboring chromosomal abnormalities or a complex karyotype ck despite this observation the mechanisms underlying mitotic and chromosomal defects in mds remain elusive in this study we identified ectopic expression of the transcription factor onecut3 which is associated with cks and poorer survival outcomes in mds onecut3 overexpressing cell models exhibited enrichment of several notable pathways including signatures of sister chromosome exchange separation and mitotic nuclear division with the upregulation of incenp and cdca8 genes notably dysregulation of chromosome passenger complex cpc accumulation besides the cell equator and midbody during mitotic phases consequently caused cytokinesis failure and defective chromosome segregation mechanistically the homeobox hox domain of onecut3 serving as the dna binding domain occupied the unique genomic regions of incenp and cdca8 and transcriptionally activated these 2 genes we identified a lead compound c5484617 that functionally targeted the hox domain of onecut3 inhibiting its transcriptional activity on downstream genes and synergistically resensitized mds cells to hypomethylating agents this study revealed that onecut3 promoted chromosomal instability by transcriptional activation of incenp and cdca8 suggesting potential prognostic and therapeutic roles for targeting high risk mds patients with a ck authors yingwan luo xiaomin feng wei lang weihong xu wei wang chen mei li ye shuanghong zhu lu wang xinping zhou huimin zeng liya ma yanling ren jie jin rongzhen xu gang huang hongyan tong vhl loss reprograms the immune landscape to promote an inflammatory myeloid microenvironment in renal tumorigenesis melissa m wolf w kimryn rathmell jeffrey c rathmell melissa m wolf w kimryn rathmell jeffrey c rathmell published april 15 2024 citation information j clin invest 2024 134 8 e173934 https doi org 10 1172 jci173934 view text pdf vhl loss reprograms the immune landscape to promote an inflammatory myeloid microenvironment in renal tumorigenesis text pdf abstract clear cell renal cell carcinoma ccrcc is characterized by dysregulated hypoxia signaling and a tumor microenvironment tme highly enriched in myeloid and lymphoid cells loss of the von hippel lindau vhl gene is a critical early event in ccrcc pathogenesis and promotes stabilization of hif whether vhl loss in cancer cells affects immune cells in the tme remains unclear using vhl wt and vhl ko in vivo murine kidney cancer renca models we found that vhl ko tumors were more infiltrated by immune cells tumor associated macrophages tams from vhl deficient tumors demonstrated enhanced in vivo glucose consumption phagocytosis and inflammatory transcriptional signatures whereas lymphocytes from vhl ko tumors showed reduced activation and a lower response to anti programmed cell death 1 anti pd 1 therapy in vivo the chemokine cx3cl1 was highly expressed in human ccrcc tumors and was associated with vhl deficiency deletion of cx3cl1 in cancer cells decreased myeloid cell infiltration associated with vhl loss to provide a mechanism by which vhl loss may have contributed to the altered immune landscape here we identify cancer cell specific genetic features that drove environmental reprogramming and shaped the tumor immune landscape with therapeutic implications for the treatment of ccrcc authors melissa m wolf matthew z madden emily n arner jackie e bader xiang ye logan vlach megan l tigue madelyn d landis patrick b jonker zaid hatem kaylee k steiner dakim k gaines bradley i reinfeld emma s hathaway fuxue xin m noor tantawy scott m haake eric jonasch alexander muir vivian l weiss kathryn e beckermann w kimryn rathmell jeffrey c rathmell granulocytic myeloid derived suppressor cell activity during biofilm infection is regulated by a glycolysis hif1a axis christopher m horn kevin l garvin tammy kielian christopher m horn kevin l garvin tammy kielian published february 29 2024 citation information j clin invest 2024 134 8 e174051 https doi org 10 1172 jci174051 view text pdf granulocytic myeloid derived suppressor cell activity during biofilm infection is regulated by a glycolysis hif1a axis text pdf abstract staphylococcus aureus is a leading cause of biofilm associated prosthetic joint infection pji a primary contributor to infection chronicity is an expansion of granulocytic myeloid derived suppressor cells g mdscs which are critical for orchestrating the antiinflammatory biofilm milieu single cell sequencing and bioinformatic metabolic algorithms were used to explore the link between g mdsc metabolism and s aureus pji outcome glycolysis and the hypoxia response through hif1a were significantly enriched in g mdscs interfering with both pathways in vivo using a 2 deoxyglucose nanopreparation and granulocyte targeted hif1a conditional ko mice respectively attenuated g mdsc mediated immunosuppression and reduced bacterial burden in a mouse model of s aureus pji in addition single cell rna seq scrna seq analysis of granulocytes from pji patients also showed an enrichment in glycolysis and hypoxia response genes these findings support the importance of a glycolysis hif1a axis in promoting g mdsc antiinflammatory activity and biofilm persistence during pji authors christopher m horn prabhakar arumugam zachary van roy cortney e heim rachel w fallet blake p bertrand dhananjay shinde vinai c thomas svetlana g romanova tatiana k bronich curtis w hartman kevin l garvin tammy kielian the hiv 1 reservoir landscape in persistent elite controllers and transient elite controllers carmen gasca capote xu g yu ezequiel ruiz mateos carmen gasca capote xu g yu ezequiel ruiz mateos published february 20 2024 citation information j clin invest 2024 134 8 e174215 https doi org 10 1172 jci174215 view text pdf clinical medicine the hiv 1 reservoir landscape in persistent elite controllers and transient elite controllers text pdf abstract background persistent controllers pcs maintain antiretroviral free hiv 1 control indefinitely over time while transient controllers tcs eventually lose virological control it is essential to characterize the quality of the hiv reservoir in terms of these phenotypes in order to identify the factors that lead to hiv progression and to open new avenues toward an hiv cure methods the characterization of hiv 1 reservoir from peripheral blood mononuclear cells was performed using next generation sequencing techniques such as full length individual and ...
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