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H Balner

Publications and source records attributed to H Balner.

At least 73 records · Page 4Linked to original sources
PubMed1976

Inhibition of human monocyte spreading. An in vitro test for immunosuppressive potency of antihum lymphocyte globulin.

Monocytes from human peripheral blood, when incubated in vitro, spread onto the surface of the glass. Horse antihuman lymphocyte globulin (ALG) added to the incubation chamber inhibits the spreading, while normal horse globulin (NHG) does not. The inhibition depends on the concentration of ALG admixed to the mononuclear blood cells. Eleven coded samples of antihuman ALG were assayed for the ability to inhibit monocyte spreading. This potential was then compared to the in vivo immunosuppressive effect of the same samples determined by the prolongation of skin allograft survival in subhuman primates. It was found that the in vitro inhibitory acttivity correlated rather well with the in vivo immunosuppression, Therefore, the inhibition of monocyte spreading is proposed as an additional test system for the in vitro evaluation of the immunosuppressive potential of antihuman ALG.

Animals↗
PubMed1975

Mapping of the immune response genes in the major histocompatibility complex of the Rhesus monkey.

Interest in the Ir genes of rheus monkeys stems from their phylogenetic relationship to man and the extensive data already available on the major histocompatibility complex of the monkey. At least two independent dominant H-linked Ir genes have been identified in the rhesus. These genes control the ability of monkeys to respond to the random linear copolymer of glutamyl alanine (GA), or the dinitrophenyl conjugate of glutamyl lysine (DNP-GL). These synthetic polymers can elicit weak delayed-type skin reactions and strong humoral responses in some monkeys. In a series of unrelated monkeys phenotyped for the serologically defined RhL-A specificities of both segregant series, there were no correlations between any RhL-A specificity and responder status to the GA or DNP-GL polymers. However, segregation analysis of 21 rhesus families sired by 3 fathers indicated the capacity of the offspring to form antibodies was associated with genes coded for in the RhL-A complex. In three monkeys, verified recombination within the RhL-A complex between the genes coding for the serologically defined determinants (SD loci) and the gene(s) controlling the lymphocyte-activating determinants (Lad loci) responsible for mixed lymphocyte reactivity was established. In two of these monkeys the immune response genes controlling the DNP-GL response segregated with the Lad genes, while in the third case the Ir-GL gene segregated with the SD loci, tentatively localizing the Ir-GL gene between the SD and Lad loci. In addition, we have shown that genetically distinct genes control responsiveness to DNP-GL and GA. These genes were separated by recombination, thus one monkey inherited the Lad, Ir-GL, and SD loci from one paternal haplotype and by crossing over inherited the gene controlling GA responsiveness from the other paternal haplotype. The fine structure mapping of the RhL-A gene complex is compared with the H-2 and HL-A gene complexes. Several striking similarities were noted.

Alanine↗
PubMed1975

Progress in rhesus histocompatibility typing resulting from the Second International Nonhuman Primate Histocompatibility Workshop (1973).

The Second International Nonhuman Primate Histocompatibility Workshop permitted comparison of rhesus monkey alloantisera developed in various laboratories on a single common panel of related and unrelated monkeys. Analysis of the data permits the conclusion that at least nine specificities are recognized by more than one laboratory, including six at the first locus and three at the second locus.

Animals↗