PROLIFERATIVE RESPONSE OF HUMAN CD4(-LYMPHOCYTES STIMULATED BY THE LECTIN JACALIN() T)

The Gal beta(1-3)GalNAc-binding lectin jacalin is known to specificall y induce the proliferation of human CD4(+) T lymphocytes in the presen ce of autologous monocytes and to interact with the CD4 molecule and b lock HIV-1 infection of CD4(+) cells. We further show that jacalin-ind uced proliferation is characterized by an unusual pattern of T cell ac tivation 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 int erleukin (IL)-1 and IL-6 did not replace the co-stimulatory activity o f 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 a bolished jacalin responsiveness. Jacalin induced interferon-gamma and high IL-6 secretion, mostly by monocytes, and no detectable IL-2 synth esis or secretion by PBMC. In contrast, jacalin-stimulated Jurkat T ce lls 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 w as 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 j acalin-competitive sugars.