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The Journal of Immunology, Vol 155, Issue 7 3525-3529, Copyright © 1995 by American Association of Immunologists
ARTICLES |
JA Wiley and AG Harmsen
Trudeau Institute, Inc., Saranac Lake, NY 12983, USA.
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.
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