美國專科醫生問我，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：我還沒有看完全部的訪談，但是懷疑在他背後有人故意製造這種陰謀論）
美國醫生朋友吃驚蓋茨基金會怎麽會雇他，我說：“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：我不認為他在蓋茨基金會擁有任何靠譜的經曆，他聲稱自己是蓋茨基金會的顧問，那顧問經曆可能是打過一次電話而已）
這裏主要的原因是因為我們的獲得性免疫所產生的抗體，是通過免疫球蛋白的VDJ基因重排實現的。免疫球蛋白重鏈和輕鏈的可變區都可以貢獻抗體的多樣性，產生重鏈的V, D, J三類基因分別有40，25和6個，也就是說重鏈可以產生40 X 25 X 6 =6000個擁有不同的可變區的基因以及相應的多樣化抗體。以此為原則算出輕鏈有320個不同可變區的基因。我們將重鏈與輕鏈同時考慮時，僅從重鏈與輕鏈的基因重排就能產生320 X 6000 = 1.9 X 1,000,000種不同的抗體。這隻是通過基因重排，我們還沒有考慮體細胞的基因點突變，那是產生多樣化抗體的關健，所以加起來數目是會上億的。人類能產生的特異性抗體的數量是無限的，根本不能與抗生素類比。
“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.”
美國專科醫生問我，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：我還沒有看完全部的訪談，但是懷疑在他背後有人故意製造這種陰謀論）
美國醫生朋友吃驚蓋茨基金會怎麽會雇他，我說：“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：我不認為他在蓋茨基金會擁有任何靠譜的經曆，他聲稱自己是蓋茨基金會的顧問，那顧問經曆可能是打過一次電話而已）
這裏主要的原因是因為我們的獲得性免疫所產生的抗體，是通過免疫球蛋白的VDJ基因重排實現的。免疫球蛋白重鏈和輕鏈的可變區都可以貢獻抗體的多樣性，產生重鏈的V, D, J三類基因分別有40，25和6個，也就是說重鏈可以產生40 X 25 X 6 =6000個擁有不同的可變區的基因以及相應的多樣化抗體。以此為原則算出輕鏈有320個不同可變區的基因。我們將重鏈與輕鏈同時考慮時，僅從重鏈與輕鏈的基因重排就能產生320 X 6000 = 1.9 X 1,000,000種不同的抗體。這隻是通過基因重排，我們還沒有考慮體細胞的基因點突變，那是產生多樣化抗體的關健，所以加起來數目是會上億的。人類能產生的特異性抗體的數量是無限的，根本不能與抗生素類比。
最近比利時人Geert Vanden Bossche建立網站，發布很少證據支持的科學手稿，他也接受采訪，隻傳遞一個信息：接種新冠疫苗將會為我們帶來災難性的後果。他還對世界衛生組織發表公開信，要求立即終止新冠疫苗的接種計劃。