Figure 1. Transcription factor and HIV-1 p24 expression in the lung using immunohis- tochemistry. (A) Immunoperoxidase stain- ing of normal lung with C/EBP polyclonal antibody. (B) Immunoperoxidase staining of uninvolved lung of an HIV-1–TB-coin- fected patient with C/EBP polyclonal an- tibody (1,000 ). (C) Involved lung seg- ment of the same HIV-1–TB patient with C/EBP polyclonal antibody (1,000 ). (D) Involved lung segment from a second HIV-1–TB patient with C/EBP poly- clonal antibody (200 ). (E) Uninvolved lung segment of an HIV-1–TB coinfected patient with p65 NF- B immunoperoxi- dase staining (1,000 ). (F) Involved lung segment of an HIV-1–TB coinfected pa- tient with p65 NF- B immunoperoxidase staining (1,000 ). (G) HIV-1 p24 immu- noperoxidase staining of a transbronchial lung biopsy (400 ). (H) HIV-1 p24 immu- noperoxidase staining of a lung section of HIV-1– TB involved lung (1,000 ). When resting syngenic blood lymphocytes were added to the AM, there was stable expression of inhibitory C/EBP after 4 d in culture (Fig. 2 A, lanes 4 and 5). This demonstrates that alteration of C/EBP expression was not an artifact of cell culture. Therefore, with regard to C/EBP expression, the addition of activated lympho- cytes to AM from uninvolved lung, reproduced the state of activation found in AM from lung segments involved with TB. To test if lymphocyte contact was required to produce loss of inhibitory C/EBP , lymphocytes and AM were separated by a porous 0.4- m insert. In the absence of di- rect contact, Con A–activated lymphocytes did not re- duce inhibitory C/EBP expression in AM (Fig. 2 A, lane 6). Similar results were obtained when allogenic lym- phocytes, stimulated to produce soluble factors by MHC incompatibility, were added to the upper chamber of the insert and macrophages were cocultured in the lower chamber (unpublished data). These data suggest that the loss of inhibitory C/EBP expression in AM requires lymphocyte contact. We next tested if activated lymphocytes could stimulate HIV-1 replication in AM isolated from AIDS patients with no lung disease. These cells had been provirally infected in 498 Contact and Cytokines Are Needed for Maximal HIV Replication