Th1 and Th2 CD4+ T Cells Provide Help for B Cell Clonal Expansion and Antibody Synthesis in a Similar Manner In Vivo

Abstract

The relative ability of Th1 and Th2 T cells to help B cells remains controversial as do the mechanisms by which both T cell subsets provide help in vivo. Whether this help affects the clonal expansion and/or differentiation of B cells has been difficult to assess due to the low frequency of Ag-specific T and B lymphocytes. We have employed a novel technique to directly monitor the clonal expansion of Ag-specific T and B lymphocytes in vivo. OVA-specific TCR transgenic T lymphocytes were polarized toward a Th1 or Th2 phenotype in vitro. These cells were then transferred into syngeneic recipients, along with B cell receptor transgenic hen egg lysozyme-specific B lymphocytes. Our results indicate that Th1 and Th2 cells support B cell responses to a similar extent in vivo and that they achieve this in the same manner by migrating into B cell follicles to promote CD154-dependent B cell clonal expansion and Ab production.

Chronic TCDD exposure results in the dysregulation of gene expression in splenic B-lymphocytes and in the impairments in T-cell and B-cell differentiation in mouse model

“…B cell differentiation into the plasma cell is predominantly triggered by the contact with the T helper cells. The Th2 cells stimulate the immature B cells to proliferate into the antibody secreting plasma cells while Th1 cells promote the production of IgG (Licona-Limón et al, 2013;MacLeod et al, 2011;Smith et al, 2000). The TCDD exposure has led to a dramatic reduction in both Th1 and Th2 cells; that alone is expected to cause a partial arrest in B cell maturation into plasma cells.…”

Cells, Molecules and Mechanisms Involved in the Neuro-Immune Interaction

“…On the other hand, effector CD4 + T cells not only contribute to efficient activation of CD8 + T cells (Bennett et al, 1998;Ridge et al, 1998;Schoenberger et al, 1998) and B cells (Smith et al, 2000), but they also regulate the function of several cells of the innate immune system, such as macrophages and NK cells (figure 2). Depending on the signals that DCs provide to T cells in addition to antigenic pMHC, they can promote the differentiation of distinct CD4 + T cell subsets, including T helper 1 (Th1), Th2 and Th17 (figure 3).…”

Characterization of the anticollagen antibody response in a new model of chronic polyarthritis

“…Lymph nodes from DO11.10 mice were pooled, and CD4ϩ T cells were purified by negative selection, as described previously (24,28). Th1 cell differentiation was induced by culturing CD4ϩ T cells with antigen-presenting cells in the presence of OVA 323-339 (Genosys), interleukin-12 (IL-12; PeproTech), and anti-IL-4 monoclonal antibody (R&D Systems), as described previously (24,28).…”

“…Lymph nodes from DO11.10 mice were pooled, and CD4ϩ T cells were purified by negative selection, as described previously (24,28). Th1 cell differentiation was induced by culturing CD4ϩ T cells with antigen-presenting cells in the presence of OVA 323-339 (Genosys), interleukin-12 (IL-12; PeproTech), and anti-IL-4 monoclonal antibody (R&D Systems), as described previously (24,28). The proportion of CD4ϩKJ1.26ϩ DO11.10 T cells was determined by flow cytometric analysis, and 2 ϫ 10 6 Th1 DO11.10 cells were injected intravenously into recipient mice, as described previously (24,28).…”

“…Th1 cell differentiation was induced by culturing CD4ϩ T cells with antigen-presenting cells in the presence of OVA 323-339 (Genosys), interleukin-12 (IL-12; PeproTech), and anti-IL-4 monoclonal antibody (R&D Systems), as described previously (24,28). The proportion of CD4ϩKJ1.26ϩ DO11.10 T cells was determined by flow cytometric analysis, and 2 ϫ 10 6 Th1 DO11.10 cells were injected intravenously into recipient mice, as described previously (24,28). One day following the adoptive transfer, all of the recipient mice were immunized subcutaneously in the scruff with OVA emulsified with Freund's complete adjuvant (CFA; Sigma-Aldrich), and 10 days later, mice were challenged with a subcutaneous injection of 100 g of heat-aggregated OVA (HAO) in 50 l of phosphate buffered saline (PBS), as described previously (24), into 1 hind limb, near the ankle joint.…”