Brooks J W, Hamilton-Easton A M, Christensen J P, Cardin R D, Hardy C L, Doherty P C
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
J Virol. 1999 Nov;73(11):9650-4. doi: 10.1128/JVI.73.11.9650-9654.1999.
Respiratory challenge with the murine gammaherpesvirus 68 (gammaHV-68) results in productive infection of the lung, the establishment of latency in B lymphocytes and other cell types, transient splenomegaly, and prolonged clonal expansion of activated CD8(+) CD62L(lo) T cells, particularly a Vbeta4(+) CD8(+) population that is found in mice with different major histocompatibility complex (MHC) haplotypes. Aspects of the CD8(+)-T-cell response are substantially modified in mice that lack B cells, CD4(+) T cells, or the CD40 ligand (CD40L). The B-cell-deficient mice show no increase in Vbeta4(+) CD8(+) T cells. Similar abrogation of the Vbeta4(+) CD8(+) response is seen following antibody-mediated depletion of the CD4(+) subset, through the numbers of CD8(+) CD62L(lo) cells are still significantly elevated. Virus-specific CD4(+)-T-cell frequencies are minimal in the CD40L(-/-) mice, and the Vbeta4(+) CD8(+) population remains unexpanded. Apparently B-cell-CD4(+)-T-cell interactions play a part in the gammaHV-68 induction of both splenomegaly and non-MHC-restricted Vbeta4(+) CD8(+)-T-cell expansion.
用鼠γ疱疹病毒68(γHV - 68)进行呼吸道攻击会导致肺部产生感染、在B淋巴细胞和其他细胞类型中建立潜伏状态、出现短暂性脾肿大以及活化的CD8(+)CD62L(lo)T细胞的长期克隆性扩增,特别是在具有不同主要组织相容性复合体(MHC)单倍型的小鼠中发现的Vβ4(+)CD8(+)群体。在缺乏B细胞、CD4(+)T细胞或CD40配体(CD40L)的小鼠中,CD8(+)-T细胞反应的各个方面会发生显著改变。B细胞缺陷型小鼠的Vβ4(+)CD8(+)T细胞没有增加。在通过抗体介导耗尽CD4(+)亚群后,也会出现类似的Vβ4(+)CD8(+)反应的消除,不过CD8(+)CD62L(lo)细胞的数量仍然显著升高。在CD40L(-/-)小鼠中,病毒特异性CD4(+)-T细胞频率极低,并且Vβ4(+)CD8(+)群体仍未扩增。显然,B细胞与CD4(+)T细胞之间的相互作用在γHV - 68诱导脾肿大和非MHC限制性Vβ4(+)CD8(+)-T细胞扩增中发挥作用。