Related Experiment Videos
Enhancement of B cell function as antigen-presenting cell during interplay with Th cells
K Nakamachi1, K Nagai, H Nariuchi
1Department of Allergology, University of Tokyo, Japan.
Immunobiology
|June 1, 1994
Summary
Stimulated B cells enhance their antigen-presenting cell (APC) function by interacting with T cells, leading to T cell proliferation. This interaction primes B cells to induce a stronger T cell response to antigens.
Area of Science:
- Immunology
- Cellular Biology
- T cell-B cell interactions
Background:
- C57BL/6 mouse B cells present antigens (Ag) to T cells, inducing IL-2 secretion but not proliferation.
- Spleen adherent cells act as antigen-presenting cells (APCs), inducing T cell proliferation to OVA.
- The role of B cell stimulation during Ag presentation in T cell response induction was unclear.
Purpose of the Study:
- To investigate if B cells, upon stimulation during Ag presentation, acquire enhanced APC capabilities.
- To determine if stimulated B cells can induce a proliferative Ag-specific T cell response.
Main Methods:
- B cells were cultured with OVA-specific T cell clone 34-7F, with or without prior stimulation.
- Antigen-presenting cell (APC) function was assessed by measuring T cell proliferation and IL-2 receptor (IL-2R) expression.
- Phosphatidyl inositol metabolism and IL-2 mRNA expression in T cells were analyzed.
Main Results:
- Unstimulated B cells proliferated upon culture with T cells and OVA, an effect inhibited by anti-I-Ab mAb.
- Stimulated B cells enhanced phosphatidyl inositol metabolism in T cells upon Ag presentation, unlike unstimulated B cells.
- Stimulated B cells induced IL-2R expression on T cells, leading to IL-2-dependent proliferation, independent of increased IL-2 production by T cells.
Conclusions:
- B cells receive signals from T cells during Ag presentation that enhance their APC function.
- Stimulated B cells can overcome the non-proliferative response of T cells to Ag on unstimulated B cells.
- This study demonstrates a mechanism by which B cells become potent APCs, driving T cell proliferation.