Follicular helper T cell signature of replicative exhaustion, apoptosis, and senescence in common variable immunodeficiency.
Giulia MilardiBiagio Di LorenzoJolanda GerosaFederica BarzaghiGigliola Di MatteoMaryam OmraniTatiana JofraIvan MerelliMatteo BarcellaMatteo FilippiniAnastasia ContiFrancesca FerruaFrancesco Pozzo GiuffridaFrancesca DionisioPatrizia Rovere QueriniSarah MarktelAndrea AssanelliSimona PiemonteseImmacolata BrigidaMatteo ZoccolilloEmilia CirilloGiuliana GiardinoMaria Giovanna DanieliFernando SpecchiaLucia PacilloSilvia Di CesareCarmela GiancottaFrancesca RomanoAlessandro MatareseAlfredo Antonio ChettaMatteo TrimarchiAndrea LaurenziMaurizio De PellegrinSilvia DarinDavide MontinMaddalena MarinoniRosa Maria DellepianeValeria SordiVassilios LougarisAngelo VaccaRaffaella MelziRita NanoChiara AzzariLucia BongiovanniClaudio PignataCaterina CancriniAlessandro PlebaniLorenzo PiemontiConstantinos PetrovasRaffaella Di MiccoMaurilio PonzoniAlessandro AiutiMaria Pia CicaleseGeorgia FousteriPublished in: European journal of immunology (2022)
Common variable immunodeficiency (CVID) is the most frequent primary antibody deficiency whereby follicular helper T (Tfh) cells fail to establish productive responses with B cells in germinal centers. Here, we analyzed the frequency, phenotype, transcriptome, and function of circulating Tfh (cTfh) cells in CVID patients displaying autoimmunity as an additional phenotype. A group of patients showed a high frequency of cTfh1 cells and a prominent expression of PD-1 and ICOS as well as a cTfh mRNA signature consistent with highly activated, but exhausted, senescent, and apoptotic cells. Plasmatic CXCL13 levels were elevated in this group and positively correlated with cTfh1 cell frequency and PD-1 levels. Monoallelic variants in RTEL1, a telomere length- and DNA repair-related gene, were identified in four patients belonging to this group. Their blood lymphocytes showed shortened telomeres, while their cTfh were more prone to apoptosis. These data point toward a novel pathogenetic mechanism in CVID, whereby alterations in DNA repair and telomere elongation might predispose to antibody deficiency. A Th1, highly activated but exhausted and apoptotic cTfh phenotype was associated with this form of CVID.
Keyphrases
- cell cycle arrest
- dna repair
- induced apoptosis
- cell death
- end stage renal disease
- high frequency
- dna damage
- ejection fraction
- newly diagnosed
- chronic kidney disease
- endoplasmic reticulum stress
- oxidative stress
- prognostic factors
- peritoneal dialysis
- gene expression
- transcranial magnetic stimulation
- stem cells
- pi k akt
- single cell
- genome wide
- mesenchymal stem cells
- signaling pathway
- endothelial cells
- poor prognosis
- long non coding rna
- big data
- anti inflammatory
- artificial intelligence
- replacement therapy