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Regulatory effects mediated by OKT8+ subsets on B cell response in the elderly
S Antonaci1, E Jirillo, M Gallitelli
1Istituto di Medicina Clinica, University of Bari Medical School, Italy.
Mechanisms of Ageing and Development
|November 1, 1987
Summary
T cell function declines with age, impacting B cell responsiveness. Aged donors show reduced B cell antibody production, with specific T cell subsets contributing to this age-related immune dysfunction.
Area of Science:
- Immunology
- Gerontology
Background:
- T cell-mediated B cell responsiveness is crucial for adaptive immunity.
- Age-related immune decline (immunosenescence) can impair T cell function and antibody production.
Purpose of the Study:
- To investigate the impact of aging on T cell-dependent B cell responsiveness.
- To identify specific T cell subsets and mechanisms involved in age-related changes in B cell function.
Main Methods:
- Utilized a Pokeweed mitogen (PWM)-driven differentiation system with peripheral blood mononuclear cells (PBMC) from 50 aged donors.
- Assessed plaque-forming cell (PFC) generation in response to T cell subset manipulation (OKT4+, OKT8+, OKT8+M1+, OKT8+M1-).
- Investigated the role of soluble suppressive factors and the effect of indomethacin.
Main Results:
- Aged donors exhibited significantly lower PFC generation compared to young donors.
- OKT4+ T cell addition partially restored B cell response in aged donors, but not to levels seen in young donors.
- Both OKT8+M1+ and OKT8+M1- subsets suppressed B cell response in aged donors, whereas only OKT8+M1+ cells suppressed in young donors.
- Soluble suppressive factors were identified as mediators of OKT8+M1--mediated suppression in aged individuals.
Conclusions:
- Aging is associated with altered T cell-B cell interactions, leading to impaired B cell responsiveness.
- Specific T cell subsets, particularly OKT8+M1- cells, exert suppressive effects on B cell function in the elderly through soluble factors.
- These findings highlight age-related changes in immune regulation impacting humoral immunity.