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Development of IgE-forming cells in vitro from rat mesenteric lymph node cells
Journal of Immunology (Baltimore, Md. : 1950)
|December 1, 1978
Summary
This study reveals that Nippostrongylus brasiliensis infection alters immune cell responses, promoting IgE antibody production. It identifies IgE-IgM double-bearing cells as key precursors for IgE-forming cells.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Immune responses to parasitic infections involve complex B and T cell interactions.
- The development of specific antibody isotypes, like IgE, is crucial for defense against helminths.
- Understanding the cellular precursors driving antibody class switching is vital for immune modulation.
Purpose of the Study:
- To investigate the impact of Nippostrongylus brasiliensis (Nb) infection on immune cell differentiation.
- To identify precursor cells involved in the development of IgM, IgG2a, and IgE-producing plasma cells.
- To determine the role of T lymphocytes and antigen priming in antibody isotype regulation.
Main Methods:
- Culturing rat mesenteric lymph node cells with pokeweed mitogen (PWM) or Nb antigen.
- Assessing the development of IgM, IgG2a, and IgE-containing cells using immunofluorescence.
- Depleting specific B cell populations (IgE- or IgM-bearing) to study precursor-product relationships.
Main Results:
- Pokeweed mitogen stimulated IgM and IgE production in normal cells, but IgM, IgG2a, and IgE in infected cells.
- Antigen stimulation of infected cells induced antigen-specific IgM, IgG2a, and IgE plasma cells, requiring primed T cells.
- Depletion of IgE- or IgM-bearing cells reduced IgE-forming cells, indicating IgE-IgM double-bearing cells are precursors.
- T cell source influenced isotype distribution: infected T cells favored IgE, while normal T cells favored IgG2a.
Conclusions:
- Nippostrongylus brasiliensis infection enhances IgE-producing cell development.
- IgE-IgM double-bearing lymphocytes are critical precursors for IgE-producing plasma cells.
- T cell populations from infected and normal rats differentially regulate B cell isotype switching.