美国专科医生问我，我回答到：“I didn’t finish all of the interviews either but suspected there was something behind him to create a conspiracy [Shocked]” （大意：我还沒有看完全部的访谈，但是怀疑在他背后有人故意制造这种阴谋论）
美国医生朋友吃惊盖茨基金会怎么会雇他，我说：“I don’t think he had any credible experiences with Gates foundation, he claims to be a counsel with them but probably only had a phone conversation [Chuckle]”（大意：我不认为他在盖茨基金会拥有任何靠谱的经历，他声称自己是盖茨基金会的顾问，那顾问经历可能是打过一次电话而已）
这里主要的原因是因为我们的获得性免疫所产生的抗体，是通过免疫球蛋白的VDJ基因重排实现的。免疫球蛋白重链和轻链的可变区都可以贡献抗体的多样性，产生重链的V, D, J三类基因分别有40，25和6个，也就是说重链可以产生40 X 25 X 6 =6000个拥有不同的可变区的基因以及相应的多样化抗体。以此为原则算出轻链有320个不同可变区的基因。我们将重链与轻链同时考虑时，仅从重链与轻链的基因重排就能产生320 X 6000 = 1.9 X 1,000,000种不同的抗体。这只是通过基因重排，我们还沒有考虑体细胞的基因点突变，那是产生多样化抗体的关健，所以加起来数目是会上亿的。人类能产生的特异性抗体的数量是无限的，根本不能与抗生素类比。
“Two models were proposed to explain the role of MHC class I molecules controlling target cell resistance/susceptibility to NK cell lysis. The first model, the receptor inhibition model, stated that a putative receptor specific for MHC class I molecules on the NK cell will transmit an inhibitory signal that will turn off NK cell activation. The second model, the target interference model, postulated that ligands on target cells for activating NK cell receptors will be masked by the expression of MHC class I molecules, making them unable to trigger NK cell activation. Although there was some evidence supporting one model or the other, neither was conclusive at the time.
To validate the receptor inhibition model, it was important to identify the inhibitory receptor(s) expressed on NK cells that would block NK cell activation. In 1989, Yokoyama had cloned the receptor recognized by the A1 mAb from an EL4 expression library. He showed that the receptor was a type II transmembrane protein that belonged to the C-type lectin family and that this new receptor was a member of a family of highly related molecules (14, 15). Yokoyama was convinced that Ly49 (currently named Ly49A) must be involved in NK cell recognition (16).
The fact that Ly49 belonged to a polymorphic family that was expressed on subsets of NK cells and the lack of knowledge regarding the molecular mechanisms involved in NK cell recognition were key factors for Yokoyama to focus his work on the role of Ly49 on NK cells (16). A logical step was to purify Ly49+ NK cells and compare them with Ly49? NK cells. They observed that there were no phenotypic differences between the Ly49+ and the Ly49? NK cells. They also observed that the classical NK cell target YAC-1 and other target cells were killed equally by both subsets. However, they found a considerable number of target cells that were not killed by the Ly49+ NK cells while they were very susceptible to killing by the Ly49? subset. Moreover, the resistant target cells could not be lysed by other mechanisms, including Ab-dependent cellular cytotoxicity and redirected lysis, suggesting that a global block on NK cell activation was occurring. When they analyzed the mouse origin of the target cells, they found a correlation between the MHC class I expression on the target cells and their resistance/susceptibility to NK cell attack. Targets from H-2d and H-2k background were resistant to killing by Ly49+ NK cells. Those results suggested that Ly49 is a receptor for an Ag of those haplotypes. This was the moment when Yokoyama made the connection with K?rre’s “missing self” hypothesis (16). To demonstrate that specific MHC class I products were responsible for determining NK cell resistance by Ly49+ NK cells, they transfected a susceptible cell line with cDNAs encoding several class I molecules. Only the one encoding for H-2Dd, but not H-2Kd or H-2Ld, was able to confer resistance to killing by Ly49+ NK cells, but not by Ly49? NK cells. To demonstrate further that there was an interaction between Ly49 and H-2Dd, they made cytotoxic assays in the presence of blocking Abs. The killing of resistant target cells by Ly49+ NK cells was restored if mAb against Ly49 or the α1/α2 domains of Dd were present in the assay, whereas Abs against the α3 domain could not restore the killing. Soon after Yokoyama’s description of the first mouse NK inhibitory receptor, Moretta’s group identified the first inhibitory receptors on human NK cells, the p58 (later named KIR2DL) molecules (17).
As a testimony to the relevance of his work, in 2001 Wayne Yokoyama received the Novartis Prize for Immunology, along with Klas K?rre and Lorenzo Moretta, for his description of the first NK cell inhibitory receptor specific for MHC class molecules. According to Rolf Zinkernagel, chairman of the selection committee, the three of them received the prize for “their scientific contributions… to our better understanding of the NK cell physiology and mechanisms of natural resistance against tumours and infections, not only conceptionally and experimentally, but also personally” (18).
Today, Yokoyama’s lab is still producing magnificent and provocative papers, some of them discovering new roles for the Ly49 family of receptors. Two great examples are the identification of Ly49H as the activating receptor involved in the resistance to murine CMV infection (19) and the role of the Ly49 inhibitory receptors in the development of NK self-tolerance (20). We, the scientific community, and I, personally, owe Wayne much for his commitment and interest in doing good science and pursuing new questions and answers. Our intellect is well nourished with Yokoyama’s contributions.”
最近比利时人Geert Vanden Bossche建立网站，发布很少证据支持的科学手稿，他也接受采访，只传递一个信息：接种新冠疫苗将会为我们带来灾难性的后果。他还对世界卫生组织发表公开信，要求立即终止新冠疫苗的接种计划。