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Additional resources for Annual Review of Immunology Volume 12 1994
Sample text
12:1-62. org by HINARI on 08/30/07. For personal use only. " For me, Talmage and Lederberg began to point the way out; Jerne and Burner, while making important contributions, remained mired in the Landsteiner legacy. All of this said, we are left to wondcr why Talmageand/or Lederberg did not derive Protecton theory (4, 25). In fact, it might moreappropriately be asked, what took us so long, some 30 years, to see where Lederberg (37) and Talmage(38) were leading; the momentshould have been ripe tie recognition to effector function.
Werefer to these cells as initial state or i-cells (iB and iT). Theyhave no effector function at this stage; they receive signals, they do not send them. In order to be referred to as "unispecific," the i-cell population must be over 95%haplotype excluded. Lastly, i-cells must have two pathways open to them, one resulting in effectors (induction) and one resulting in death (tolerance); it is only whenin the i-state that a SINSdecision can be made. 3. The interaction of the antigen-receptor (BAr for B cells, TAr for cells) with antigen results in a signal to the i-cell (iB/iT) that is referred to as Signal [1].
Important for this exchange was the first attempt on our part to tie together two decision functions, the S/NS discrimination and the determination of the class of this response (59, 60). In 1978, as I described elsewhere (3, foreword), the formalization of the concept of restrictive recognition of antigen by Langman(61) led us (62) to redefine the mechanism of the eTH-iT/iB interaction as due to two unispecific cells in which the effector T helper (eTH) initiated and sent Signal [2] via the class II-restricting element on the target iT/iB-cell.
