Mitani M, Cianciolo G J, Snyderman R, Yasuda M, Good R A, Day N K
Proc Natl Acad Sci U S A. 1987 Jan;84(1):237-40. doi: 10.1073/pnas.84.1.237.
Purified feline leukemia virus, UV light-inactivated feline leukemia virus, and a synthetic peptide (CKS-17) homologous to a well-conserved region of the transmembrane components of several human and animal retroviruses were each studied for their effects on IgG production by feline peripheral blood lymphocytes. Using a reverse hemolytic plaque assay, both the viable virus and the UV-inactivated feline leukemia virus, but not the CKS-17, activated B lymphocytes to secrete IgG. When staphylococcal protein A, a polyclonal B-cell activator, was used to stimulate IgG synthesis by feline lymphocytes, the viable virus, the UV-inactivated virus, and the CKS-17 peptide each strongly suppressed IgG secretion without compromising viability of the lymphocytes. These findings suggest that the immunosuppressive influences of feline leukemia virus on immunoglobulin synthesis may reside in a conserved portion of the envelope glycoprotein that includes the region homologous to CKS-17.
分别研究了纯化的猫白血病病毒、紫外线灭活的猫白血病病毒以及一种与几种人类和动物逆转录病毒跨膜成分保守区域同源的合成肽（CKS-17）对猫外周血淋巴细胞产生IgG的影响。使用反向溶血空斑试验，活病毒和紫外线灭活的猫白血病病毒均可激活B淋巴细胞分泌IgG，但CKS-17不能。当用葡萄球菌蛋白A（一种多克隆B细胞激活剂）刺激猫淋巴细胞合成IgG时，活病毒、紫外线灭活病毒和CKS-17肽均强烈抑制IgG分泌，且不影响淋巴细胞的活力。这些发现表明，猫白血病病毒对免疫球蛋白合成的免疫抑制作用可能存在于包膜糖蛋白的保守部分，该部分包括与CKS-17同源的区域。
