Proliferative response of human CD4+ T lymphocytes stimulated by the lectin jacalin

The Galβ(1–3)GalNAc‐binding lectin jacalin is known to specifically induce the proliferation of human CD4+ T lymphocytes in the presence of autologous monocytes and to interact with the CD4 molecule and block HIV‐1 infection of CD4+ cells. We further show that jacalin‐induced proliferation is characterized by an unusual pattern of T cell activation and cytokine production by human peripheral blood mononuclear cells (PBMC). A cognate interaction between T cells and monocytes was critical for jacalin‐induced proliferation, and human recombinant interleukin (IL)‐1 and IL‐6 did not replace the co‐stimulatory activity of monocytes. Blocking studies using monoclonal antibodies (mAb) point out the possible importance of two molecular pathways of interaction, the CD2/LFA‐3 and LFA‐1/ICAM‐1 pathways. One out of two anti‐CD4 mAb abolished jacalin responsiveness. Jacalin induced interferon‐γ and high IL‐6 secretion, mostly by monocytes, and no detectable IL‐2 synthesis or secretion by PBMC. In contrast, jacalin‐stimulated Jurkat T cells secreted IL‐2. CD3− Jurkat cell variants failed to secrete IL‐2, suggesting the involvement of the T cell receptor/CD3 complex pathway in jacalin signaling. IL‐2 secretion by CD4− Jurkat variant cells was delayed and lowered. In addition to CD4, jacalin interacts with the CD5 molecule. Jacalin‐CD4 interaction and the proliferation of PBMC, as well as IL‐2 secretion by Jurkat cells were inhibited by specific jacalin‐competitive sugars.