Van Der Pouw Kraan T T, Stiekema F E, Teunissen M B, Bos J D, Kapsenberg L
Laboratory of Cell Biology Histology, University of Amsterdam, The Netherlands.
Immunology. 1989 Oct;68(2):147-53.
We examined the role of antigen-presenting B lymphocytes using panels of antigen-specific CD4+8-T-lymphocyte clones (TLC). All 19 TLC showed a class II major histocompatibility complex-encoded (HLA-II) restricted proliferation to antigen presented by antigen-presenting cells (APC) from the monocyte fraction of peripheral blood. Only six TLC were effectively activated by antigen presented by autologous B lymphocytes activated by EBV transformation. This failure of B lymphocytes was not due to: (i) a high degree of cell surface sialic acid; (ii) a low expression of the cell surface proteins HLA-II, ICAM-1 or LFA-3 that restrict antigen presentation; (iii) lack of secretion of the cytokine IL-1 or other soluble factors that may be required as secondary signals; or (iv) induction of incomplete T-cell activation resulting in the production of growth factor interleukin-2 (IL-2) or the expression of receptors for IL-2 only. These data suggest the involvement of another cell surface interaction in antigen presentation acting besides the interactions known so far.
我们使用抗原特异性CD4 + 8 - T淋巴细胞克隆(TLC)组来研究抗原呈递B淋巴细胞的作用。所有19个TLC对外周血单核细胞部分的抗原呈递细胞(APC)呈递的抗原均表现出II类主要组织相容性复合体编码(HLA - II)限制的增殖。只有6个TLC被EBV转化激活的自体B淋巴细胞呈递的抗原有效激活。B淋巴细胞的这种失败不是由于:(i)细胞表面唾液酸高度;(ii)限制抗原呈递的细胞表面蛋白HLA - II、ICAM - 1或LFA - 3的低表达;(iii)缺乏细胞因子IL - 1或其他可能作为第二信号所需的可溶性因子的分泌;或(iv)诱导不完全的T细胞激活导致生长因子白细胞介素 - 2(IL - 2)的产生或仅IL - 受体的表达。这些数据表明除了目前已知的相互作用外,另一种细胞表面相互作用参与了抗原呈递。