Although natural killer (NK) cells are thought to give the host a spontaneous resistance against tumours and have been postulated to act in vivo as surveillor cells, definitive data in support of these hypotheses has not been obtained. Recently the beige (bg) mouse, a morphological homologue of the human Chediak-Higashi (CH) syndrome, was shown to be deficient in NK activity. Specifically, spleen cells of bg mice were demonstrated to be incapable of in vitro natural cytotoxicity against tumour cells. We report here that a tumour line, modified to be sensitive to NK cytotoxicity by in vitro culture, demonstrated in vivo an increased growth rate, faster induction time and an increased metastatic capability in bg compared to control mice. This was not found with a tumour line insensitive to NK activity (without in vitro culture). In vivo activation of NK cells in bg and control mice resulted in a decrease in tumour growth rate and metastatic frequency. These results demonstrate that NK cells have an important function in the host's control of tumour growth and metastasis.
The serum susceptibility of 64 isolates of Haemophilus somnus from cattle was determined in a bactericidal assay with undiluted fresh or inactivated bovine serum with serial dilutions of bacterial suspension in RPMI 1640 medium. A total of 27 strains isolated from cattle with clinical disease (4 with thromboembolic meningoencephalitis, 13 with pneumonia, and 10 with reproductive failure) were compared with 35 strains from asymptomatic carriers (11 from the vagina and 24 from the prepuce). Essentially, al clinical isolates were serum resistant, whereas approximately 25% of preputial isolates were serum susceptible, as judged after 1 h of incubation in serum; a majority of vaginal isolates showed delayed serum susceptibility. Lysozyme played no role in serum killing, and the alternative complement pathway played only a minor role. Iron saturation, however, appeared to impart greater serum resistance to serum-susceptible strains from the vagina and prepuce. Perhaps the serum-susceptible strains from carriers would be useful vaccine candidates, but resistant strains from carriers may be pathogenic.
Control of a naturally occurring lentivirus, equine infectious anemia virus (EIAV), occurs in most infected horses and involves MHC class I-restricted, virus-specific CTL. Two minimal 12-aa epitopes, Env-RW12 and Gag-GW12, were evaluated for presentation by target cells from horses with an equine lymphocyte Ag-A1 (ELA-A1) haplotype. Fifteen of 15 presented Env-RW12 to CTL, whereas 11 of 15 presented Gag-GW12. To determine whether these epitopes were presented by different molecules, MHC class I genes were identified in cDNA clones from Arabian horse A2152, which presented both epitopes. This horse was selected because it is heterozygous for the SCID trait and is used to breed heterozygous females. Offspring with SCID are used as recipients for CTL adoptive transfer, and normal offspring are used for CTL induction. Four classical and three putative nonclassical full-length MHC class I genes were found. Human 721.221 cells transduced with retroviral vectors expressing each gene had equine MHC class I on their surface. Following peptide pulsing, only cells expressing classical MHC class I molecule 7-6 presented Env-RW12 and Gag-GW12 to CTL. Unlabeled peptide inhibition of 125I-labeled Env-RW12 binding to 7-6-transduced cells demonstrated that Env-RW12 affinity was 15-fold higher than Gag-GW12 affinity. Inhibition with truncated Env-RW12 demonstrated that amino acid positions 1 and 12 were necessary for binding, and single substitutions identified positions 2 and 3 as possible primary anchor residues. Since MHC class I 7-6 presented both epitopes, outbred horses with this allele can be immunized with these epitopes to optimize CTL responses and evaluate their effectiveness against lentiviral challenge.
Craniomandibular osteopathy is a disease of several breeds of dogs, principally West Highland White and Scottish terriers. It is characterized by a non-neoplastic proliferation of bone on the ramus of the mandible and/or the tympanic bulla. The disease in various respects resembles Paget's disease and infantile cortical hyperostosis of humans. A retrospective pedigree analysis of a kindred of West Highland White terriers was performed to determine if the trait was inherited and to determine mode of inheritance. This study indicated that in West Highland White terriers, the condition is an autosomal recessive trait.
The phenotypes with respect to congenital myasthenia gravis of 132 smooth fox terrier dogs from 25 matings were analyzed. These included both prospective and retrospective matings. It was determined that congenital myasthenia gravis in the smooth fox terrier dog breed is inherited in an autosomal recessive manner with complete penetrance. We propose the symbol mg for the gene for congenital myasthenia gravis in the smooth fox terrier. Attempts to maintain live affected dogs to adulthood were unsuccessful and it is concluded that this is a lethal trait.
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