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Facb rosette-forming cells in mice: studies on their functional significance
Immunology
|May 1, 1984
Summary
Fc-binding (Facb) receptor-bearing lymphocytes increase during secondary immune responses in mice. These cells may suppress antibody production, offering insights into rheumatoid arthritis.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Lymphocytes expressing Fc-binding (Facb) receptors for IgG are elevated in rheumatoid arthritis patients.
- The generation and function of these Fc-binding receptor (Facb-R+) lymphocytes in immune regulation are not fully understood.
Purpose of the Study:
- To investigate the generation and functional role of Fc-binding receptor (Facb-R+) lymphocytes in mice.
- To determine if these cells are involved in humoral versus cell-mediated immunity and their potential suppressive effects on antibody production.
Main Methods:
- Induction of primary and secondary immune responses in mice using various antigens (sheep erythrocytes, goat erythrocytes, chicken erythrocytes, bacterial lipopolysaccharide).
- Quantification of splenic Fc-binding receptor (Facb-R+) lymphocytes.
- Administration of Fc-binding (Facb) fragments and F(ab')2 fragments to assess their effect on plaque-forming cell (PFC) responses.
- Evaluation of delayed hypersensitivity responses.
Main Results:
- Fc-binding receptor (Facb-R+) lymphocytes were elevated in secondary humoral responses but not primary responses.
- Elevation of Fc-binding receptor (Facb-R+) lymphocytes occurred with cross-reacting antigens during secondary immunization.
- Administration of antigen-specific Fc-binding (Facb) fragments suppressed secondary antibody production, while F(ab')2 fragments did not.
- No change in Fc-binding receptor (Facb-R+) lymphocytes was observed during cell-mediated immune responses.
Conclusions:
- Fc-binding receptor (Facb-R+) lymphocytes are specifically generated during secondary humoral immune responses.
- These lymphocytes may play a suppressive role in antibody production.
- The findings provide a potential explanation for the presence of these cells in rheumatoid arthritis patients.