Rejection of class I MHC-deficient haemopoietic cells by irradiated MHC-matched mice.

Irradiated MHC-heterozygous mice often reject bone marrow cells transplanted from one of the homozygous parental strains, a phenomenon ('hybrid resistance') that appears to violate the laws of transplantation. Rejection of parental and allogeneic marrow cells also differs from conventional T cell-mediated rejection mechanisms as it is effected by NK1.1+ cells. To account for the unusual specificity of bone marrow rejection, it has been proposed that NK1.1+ cells destroy marrow cells that fail to express the full complement of self MHC class I (MHC-I) molecules. We show here that NK1.1+ cells in normal mice reject haemopoietic transplants from mice that are deficient for normal cell-surface MHC-I expression because of a targeted mutation in the beta 2-microglobulin gene. These findings demonstrate that deficient expression of MHC-I molecules renders marrow cells susceptible to rejection.

MHC class-I antigen deficiency, malignancy and susceptibility of P815 mastocytoma to NK and macrophage killing.

A subline of the murine P815 mastocytoma passaged for a long period of time in histoincompatible hosts was found to be deficient in surface MHC class-I antigens by serological and biochemical methods. In agreement with the lack of restriction elements, this variant cell line was no longer susceptible to killing by cytotoxic T cells stimulated by and directed against the parental tumor cell line in syngeneic DBA-2 hosts. We did not observe the appearance of susceptibility to NK killing concomitantly with H-2 loss. We thus could not confirm the hypothesis of a regulatory function of H-2 structures in NK recognition/killing. Both cell lines were also resistant to lysis by mouse macrophages. The parental cell line was sensitive to rat macrophage killing, whereas the variant line had lost such sensitivity. In spite of resistance in vitro to various defense mechanisms, the variant H-2 loss tumor cell line was less tumorigenic in syngeneic hosts and exhibited a lower metastatic capacity than the parental cell line. We propose that in the H-2 loss subline, survival of cells in vivo is impeded since positive signals mediated by H-2 structures are missing, which are necessary for cell-cell contact and survival.

[A case of the bare lymphocyte syndrome with clinical manifestations of diffuse panbronchiolitis].

Touraine et al reported some cases lacking HLA-class I antigens on the cell surface of their lymphocytes as "Bare lymphocyte syndrome" (BLS). Recently we experienced a case of BLS the clinical features of which are very similar to those of diffuse panbronchiolitis (DPB). Namely, she had chronic pansinusitis, diffuse nodular shadows on her chest X-ray film, obstructive impairment of pulmonary function tests and continuous increase of cold hemagglutinin titer. The pathogenesis of DPB is not confirmed. However, this case and other cases with sino-bronchial syndrome suggest that patients with DPB may have some immunodeficiencies. In addition the immunosuppressive action of erythromycin and its effectiveness on DPB were interesting. From these points of view, we discussed the relationship between this case and DPB, and the pathogenesis of DPB.