Design of highly selective biological substances made use of three bas
ic components of a complex pathogenetic model of RA: the presence of a
ntigen-presenting cells, genetic defects and autoimmune aggression. Ef
forts now are directed to development of monoclonal antibodies (MAB) t
o receptors of T-cells, B lymphocytes, MAB to CD 18 and CD54, cytokine
s, search for natural inhibitors of cytokines, introduction of cytokin
es. Many of such preparations including recombinant interferons proved
clinically promising.