Regulatory B cells in CVID patients fail to suppress multifunctional IFN-gamma+TNF-alpha(+)CD4(+) T cells differentiation
| Authors | |
|---|---|
| Year of publication | 2015 |
| Type | Article in Periodical |
| Magazine / Source | Clinical Immunology |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.1016/j.clim.2015.06.013 |
| Field | Immunology |
| Keywords | B cell; Common variable immunodeficiency (CVID); Cytokine production; Flow cytometry; T cell |
| Description | Common variable immunodeficiency (CVID) refers to primary hypogammaglobulinemia with unknown pathogenesis. Although there is evidence for intrinsic B cell defects in some CVID patient groups, various abnormalities in cytokine production by T cells in CVID patients are frequently observed. Here, we demonstrate a relationship in the production of pro-inflammatory Th1 cytokines and regulatory B cells producing IL-10 between CVID patients and healthy controls. We describe CD19+CD24hiCD38hiIL-10+ regulatory B cells generated after T cell stimulation of human peripheral blood lymphocytes ex vivo are able to suppress IFN-gamma+TNF-alpha+ producing CD4+ T cells. This process is impaired in CVID patients, who present with both low numbers of CD19+CD24hiCD38hiIL-10+ B cells and increased numbers of IFN-gamma+TNF-alpha+CD4+ T cells. Disruption of the regulatory B cell response to T cell stimulation explains the excessive T cell activation regarded as an immunoregulatory abnormality that is a frequent finding in CVID patients. |
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