CD8+ (suppressor/cytotoxic) lymphocytes block replication of HIV-1 or the simian immunodeficiency virus of macaques (SIVmac) in PBL of infected individuals. We now show that these CD8+ lymphocytes undergo clonal expansion in vivo after AIDS virus infection of the individual, suggesting they may be antigen-specific T cells. These CD8+ cells block replication of virus in autologous but not MHC class I-mismatched PBL. The inhibitory lymphocytes express the integrin family molecule 4B4 and the CTL-associated S6F1 epitope of LFA-1. Finally, physical contact is required for the CD8+ lymphocyte-mediated inhibition of AIDS virus replication, since this inhibitory function is blocked by anti-LFA-1 and anti-CD8 mAbs. These studies suggest that the cell that inhibits AIDS virus replication in PBL of infected individuals is a CTL.

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S U M M A R YThe human palatine tonsils have surface and crypt stratified epithelium and may be initiated via the epithelium to mount immune responses to various presenting antigens. Here we investigated the expression and function of tight junctions in the epithelium of human palatine tonsils from patients with tonsillar hypertrophy or recurrent tonsillitis. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, -7, -8, and -14 mRNAs were detected in tonsillar hypertrophy. Occludin and claudin-14 were expressed in the uppermost layer of the tonsil surface epithelium, whereas ZO-1, JAM-1, and claudin-1, -4, and -7 were found throughout the epithelium. In the crypt epithelium, claudin-4 was preferentially expressed in the upper layers. In freeze-fracture replicas, short fragments of continuous tight junction strands were observed but never formed networks. In the crypt epithelium of recurrent tonsillitis, the tracer was leaked from the surface regions where occludin and claudin-4 disappeared. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, and -14, but not claudin-7, mRNAs were decreased in recurrent tonsillitis compared with those of tonsillar hypertrophy. These studies suggest unique expression of tight junctions in human palatine tonsillar epithelium, and the crypt epithelium may possess an epithelial barrier different from that of the surface epithelium.

Rhesus monkeys infected with the simian immunodeficiency virus of macaques (SICVK) demonstrate significant virologic and clinical improvement as a result of treatment with human recombinant soluble CD4 (rsCD4). We show that human rsCD4 does not efficiently inhibit SIV1 replication in bone marrow macrophages of rhesus monkeys and does not snificantly augment bone marrow hematopoietic colony formation in vitro. However, plasma of human rsCD4-treated rhesus monkeys does exhibit sicant anti-SIV activity in vitro. Plasma of these animals efficiently blocks