The Role of the interleukin‐10 Subfamily Members in Immunoglobulin Production by Human B Cells
Interleukin (IL)‐10 has been shown to have various effects on B cells, including positively affecting the production of immunoglobulin A (IgA) and IgG. Several human IL‐10‐related molecules have been identified. These include IL‐19, IL‐20, IL‐22, IL‐24, IL‐26, IL‐28 and IL‐29. To determine the effec...
Gespeichert in:
Veröffentlicht in: | Scandinavian journal of immunology 2006-07, Vol.64 (1), p.40-47 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Interleukin (IL)‐10 has been shown to have various effects on B cells, including positively affecting the production of immunoglobulin A (IgA) and IgG. Several human IL‐10‐related molecules have been identified. These include IL‐19, IL‐20, IL‐22, IL‐24, IL‐26, IL‐28 and IL‐29. To determine the effects of the IL‐10 analogues on the class switch recombination in B cells, we analysed Ig production from naïve B cells stimulated with these cytokines in the presence of anti‐CD40. None of the cytokines were found to induce Ig production by themselves in the presence of anti‐CD40 Ab. However, all cytokines inhibited the production of IgA and IgG induced by anti‐CD40 Ab alone. In combination with anti‐CD40 Ab and IL‐4, IgG4 were inhibited in cultures stimulated with IL‐20, IL‐22, IL‐26, IL‐28 and IL‐29 compared with IL‐4 and anti‐CD40 Ab alone, whereas all IL‐10 analogues increased the production of total IgG. All analogues reduced anti‐CD40 Ab + transforming growth factor (TGF)‐β‐induced IgA production compared with cultures stimulated with anti‐CD40 Ab and TGF‐β alone. Together, these data show that the IL‐10‐related cytokines in combination with anti‐CD40 Ab are not by themselves directly involved in the Ig regulation in B cells. However, some of the analogues might have regulatory effects on CSR induced by CD40‐ligation in combination with IL‐4 or TGF‐β. |
---|---|
ISSN: | 0300-9475 1365-3083 |
DOI: | 10.1111/j.1365-3083.2006.01773.x |