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S Fairchild

Publications and source records attributed to S Fairchild.

23 records · Page 2Linked to original sources
PubMed1991

The genetic basis of negative selection of Tcrb-V11+ T cells.

Non-H-2 genes responsible for negative selection of Tcrb-V11+ T cells were examined using backcross mice of various strains with C58, which does not delete Tcrb-V11+ T cells. Two independently segregating genes were found: one leading to partial deletion was closely linked to Ly-2/Ly-3 on chromosome 6, and the second giving virtually complete deletion has not yet been mapped. The A strain had only the former, whereas BALB/c, BALB.K, B10.BR, CBA-T6, C3H/He, and DBA/2 expressed both of these genes. Although a gene(s) of the NIH strain led only to partial deletion, the chromosomal localization of the gene(s) has not yet been determined: no informative polymorphic molecules are expressed from genes on chromosome 6 of this strain.

Animals↗
PubMed1989

Two monoclonal antibodies specific for the T cell receptor V alpha 8.

Two monoclonal antibodies, KT50 and KT65, specific for V alpha 8 have been established. This was determined as follows: (a) 4 T cell clones, C6, R1, G22 and I9, out of 43 T cell clones with various antigen specificities, major histocompatibility complex restrictions and V beta usages not only bound KT50 and KT65 but also expressed V alpha 8 mRNA, (b) KT50 and KT65 precipitated molecules from the clone C6 similar to the T cell receptor molecules precipitated in C6 cells by KT11 (anti-V beta 11) or KTL2 (anti-Ti) and (c) KT50 and KT65 were mitogenic and induced cytotoxicity. All strains of mice so far examined have populations of KT50+ and KT65+ T cells of 1.4%-3.6% and 0.9%-2.6%, respectively. Different H-2 haplotypes were not observed to affect the number of cells expressing KT50 or KT65. In addition KT15 (anti-CD8), without cross-linking to KT50 or KT65, augmented proliferation triggered by KT50 or KT65.

Animals↗
PubMedDate not supplied

H-Y responses of non-obese diabetic (NOD) mice.

Female non-obese diabetic (NOD) mice were tested for their ability to make responses to the male-specific (H-Y) transplantation antigen. In vivo assessment of this ability was made using skin graft rejection. A proportion (60%) spontaneously rejected NOD male tail skin by 80 days post-transplantation. The detection of the generation of H-Y-specific cytotoxic T cells, following in vivo priming and secondary in vitro restimulation, was carried out using a conventional 51Cr release assay. Female NOD mice primed either by skin grafting, intraperitoneal (i.p.) or footpad (f.p.) injection of male NOD spleen cells could be induced to make anti-H-Y cytotoxic responses, but not every immunized mouse responded. The nature of the H-Y-reactive T cells was investigated further by the in vitro isolation of T-cell clones of which some were H-Y specific.

Animals↗