6533b7cffe1ef96bd1257c46
RESEARCH PRODUCT
A novel B cell population revealed by a CD38/CD24 gating strategy: CD38−CD24− B cells in centenarian offspring and elderly people
Mariavaleria PellicanòGraham PawelecCalogero CarusoGiuseppina Colonna-romanoDavid GoldeckAdriana MartoranaMatteo BulatiSilvio Buffasubject
AdultMaleParentsAgingCD180OffspringImmunosenescencePopulationB cell; CD38; CD24; CD180; Immunosenescence; Centenarian offspringLongevityCentenarian offspringCD38Lymphocyte ActivationCD19Article03 medical and health sciences0302 clinical medicineReference ValuesmedicineHumanseducationCD24B cell030304 developmental biologyAgedSettore MED/04 - Patologia GeneraleAged 80 and over0303 health scienceseducation.field_of_studyB cellB-LymphocytesImmunity CellularbiologyCD24 AntigenGeneral MedicineImmunosenescenceMiddle AgedAcquired immune systemADP-ribosyl Cyclase 13. Good healthmedicine.anatomical_structureImmunologybiology.proteinCytokinesFemaleGeriatrics and GerontologyCentenarianCD38030215 immunologydescription
The B cell arm of adaptive immunity undergoes significant modifications with age. Elderly people are characterized by impaired B cell responses reflected in a reduced ability to effectively respond against viruses and bacteria. Alterations of immunity with advancing age (immunosenescence) have been widely studied in centenarians who are considered a good example of successful aging. In recent years, attention has shifted to centenarian offspring (CO) as a model of people genetically advantaged for healthy aging and longevity. Here, we describe the preliminary characterization of a proposed new population of memory B cells, defined as CD19(+)CD38(-)CD24(-), which we find at higher frequencies in the elderly but less so in CO than healthy age-matched random controls. In addition, we found a decreased expression of RP105 (CD180), a toll-like receptor-associated molecule, on these cells. CD180 downregulation may potentially be a marker of immunosenescence. Moreover, we show that these CD19(+)CD38(-)CD24(-) B cells produce TNF and hypothesize that their observed expansion in the elderly might contribute to the increased inflammatory status sometimes designated "inflamm-aging."
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2012-11-07 |