Wiley J A, Harmsen A G
Trudeau Institute, Inc., Saranac Lake, NY 12983, USA.
J Immunol. 1995 Oct 1;155(7):3525-9.
The role of the CD40-CD40 ligand (CD40L) interaction in resolution of Pneumocystis carinii (PC) pneumonia (PCP) was assessed in a PC-infected severe combined immunodeficiency (SCID) mouse reconstitution model using an anti-CD40L mAb to block CD40L. SCID mice infected with PC were reconstituted with unfractionated spleen cells from immunocompetent donors and given either anti-CD40L mAb or an irrelevant control mAb. Mice given the control mAb resolved the PC infection, whereas those given the anti-CD40L mAb did not. That anti-CD40L mAb also inhibited PC-specific IgG production is consistent with the possibility that cognate CD4+ T cell-B cell interactions are important in PCP resolution. The experiment was then repeated, except that the PC-infected SCID mice were reconstituted with purified CD4+ T cells only. Again, the control mAb-treated group resolved the PCP, whereas mice treated with anti-CD40L mAb did not. In the second experiment, inhibition of resolution of PCP in the anti-CD40L mAb group was not the result of blocking CD4+ T cell-dependent activation of PC-specific B cells. The results are consistent with the possibility that resistance to PCP may involve interaction between B cells and CD4+ T cells via the CD40-CD40L pathway. However, results additionally indicate that inhibition of CD40-CD40L interaction ablates resistance to PCP by inhibiting the interaction of T cells with some cell other than B cells.
在卡氏肺孢子虫(PC)肺炎(PCP)感染的严重联合免疫缺陷(SCID)小鼠重建模型中,使用抗CD40L单克隆抗体(mAb)阻断CD40L,评估CD40 - CD40配体(CD40L)相互作用在PCP消退中的作用。用来自免疫活性供体的未分级脾细胞重建感染PC的SCID小鼠,并给予抗CD40L mAb或无关对照mAb。给予对照mAb的小鼠清除了PC感染,而给予抗CD40L mAb的小鼠则没有。抗CD40L mAb也抑制PC特异性IgG的产生,这与同源CD4 + T细胞 - B细胞相互作用在PCP消退中很重要的可能性一致。然后重复该实验,不同的是用纯化的CD4 + T细胞重建感染PC的SCID小鼠。同样,对照mAb处理组清除了PCP,而用抗CD40L mAb处理的小鼠则没有。在第二个实验中,抗CD40L mAb组中PCP消退的抑制不是阻断CD4 + T细胞依赖性激活PC特异性B细胞的结果。这些结果与对PCP的抵抗力可能涉及B细胞和CD4 + T细胞通过CD40 - CD40L途径相互作用的可能性一致。然而,结果还表明,抑制CD40 - CD40L相互作用通过抑制T细胞与B细胞以外的某些细胞的相互作用而消除了对PCP的抵抗力。