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Fc gamma-receptor III (CD 16) is involved in NK-B cell interaction
P Lenz1, J E Gessner, C Sautes
1Department of Clinical Immunology, Hannover Medical School, Germany.
Insights
CD16 (Fc gamma RIIIA) on NK cells regulates B cell immunoglobulin production. Blocking CD16 or using Fc-specific antibodies inhibits NK-enhanced antibody responses and cytokine production.
Area of Science:
- Immunology
- Cellular Biology
- Molecular Biology
Background:
- CD16 (Fc gamma RIIIA) is a known NK cell activation molecule.
- The role of CD16 in NK-B cell interactions and immunoglobulin regulation is not fully understood.
Purpose of the Study:
- To investigate the function of CD16 in NK cell-mediated regulation of immunoglobulin production.
- To elucidate the mechanism by which CD16 influences NK-B cell interactions.
Main Methods:
- Coculture of CD16+ human NK clone CNK6 with activated B lymphocytes.
- Treatment with CD16 antibodies, recombinant soluble CD16, and Fc-specific F(ab')2 antibody fragments.
- Analysis of immunoglobulin production and mRNA expression for IFN-gamma and TNF-alpha.
Main Results:
- CD16 antibodies and Fc-specific antibodies significantly diminished NK-enhanced immunoglobulin production in a dose-dependent manner.
- Recombinant soluble CD16 suppressed NK cell-stimulated B cell antibody response.
- CD16 and Fc-specific antibodies prevented the induction of mRNA for IFN-gamma and TNF-alpha in cocultured NK and B cells.
Conclusions:
- CD16 plays a crucial role in NK-B cell interactions that enhance immunoglobulin production.
- The interaction of CD16 on NK cells with B cell-bound immunoglobulin induces NK cell cytokines (IFN-gamma, TNF-alpha), which in turn stimulate B cell immunoglobulin production.
Abstract:
CD16, the low affinity receptor for monomeric IgG (Fc gamma RIIIA), is a well characterized activation molecule on NK cells. In this study we investigated the role of CD16 in NK cell-mediated regulation of immunoglobulin production. Cocultures of the CD16+ human NK clone CNK6 and highly purified SAC/IL-2-activated B lymphocytes with various CD16 antibodies showed significantly diminished NK-enhanced immunoglobulin production in a dose-dependent manner, indicating that CD16 is relevant in NK-B cell interaction. Similarly, recombinant soluble CD16 incubated with B cells before cultures, suppressed the NK cell-stimulated B cell antibody response. Enhanced immunoglobulin production was also inhibited by Fc-specific F(ab')2 anti-body fragments. Coculture of NK cells with B lymphocytes resulted in induction of mRNA for IFN-gamma and TNF-alpha. The accumulation of mRNA for these cytokines was prevented by addition of CD16 and Fc-specific antibodies. It is proposed that interaction of CD16 on NK cells with B cell bound immunoglobulin leads to induction of cytokines in NK cells which stimulate immunoglobulin production by B cells.